Abramo, F., S. Bo, M.G. Canese, and A. Poli (1995). Regional distribution of lesions in the central nervous system of cats infected with feline immunodeficiency virus. AIDS Research and Human Retroviruses 11(10): 1247-1253. ISSN: 0889-2229.
Abstract: Neuropathological examination of the central nervous system of 13 naturally and 13 experimentally feline immunodeficiency virus (FIV)-infected cats revealed diffuse gliosis of gray and white matter and vacuolar myelinopathy in a large proportion of infected animals, sometimes associated with lymphocytic meningitis. Multinucleated giant cell formation, the hallmark of multifocal giant cell encephalitis in HIV infection, was never observed. Morphometric analysis confirmed a marked increase of GFAP reactivity in infected cats. Gliosis was mainly present in cortical structures of frontal, parietal, and occipital lobes. Only one naturally infected animal evidenced clinical symptoms of neurological damage. This study confirms that FIV provides an interesting model for studying HIV-induced cortical and subcortical brain pathology believed to be the cause of the neurological manifestations frequently observed in AIDS patients.
Descriptors: central nervous system, feline acquired immunodeficiency syndrome, immunodeficiency virus, feline, cats, meninges.

Albert, M., F. Schuster, S. Schulze, B. Pontz, W. Roeschinger, A. Muntau, C. Peters, D. Stachel, I. Schmid, and R. Haas (2001). Successful allogeneic t-cell-depleted peripheral blood stem cell transplantation (pbsct) in a child with alpha-mannosidosis. Blood 98(11 Part 2): 373b. ISSN: 0006-4971.
NAL Call Number: RB145.A1B57
Descriptors: clinical, alpha mannosidosis, feline animal model, stem cell, human disease, digestive system disease, metabolic disease, surgical method, therapeutic method.
Notes: Meeting Information: 43rd Annual Meeting of the American Society of Hematology, Part 2, Orlando, Florida, USA; December 7-11, 2001.

Alex, J.C. (2004). The application of sentinel node radiolocalization to solid tumors of the head and neck: A 10-year experience. The Laryngoscope 114(1): 2-19. ISSN: 0023-0852X.
Abstract: OBJECTIVES/HYPOTHESIS: The goals of the research study were to develop an easily mastered, accurate, minimally invasive technique of sentinel node radiolocalization with biopsy (SNRLB) in the feline model; to compare it with blue-dye mapping techniques; and to test the applicability of sentinel node radiolocalization biopsy in three head and neck tumor types: N0 malignant melanoma, N0 Merkel cell carcinoma, and N0 squamous cell carcinoma. STUDY DESIGN: Prospective consecutive series studies were performed in the feline model and in three head and neck tumor types: N0 malignant melanoma (43 patients), N0 Merkel cell carcinoma (8 patients), and N0 squamous cell carcinoma (20 patients). METHODS: The technique of sentinel node radiolocalization with biopsy was analyzed in eight felines and compared with blue-dye mapping. Patterns of sentinel node gamma emissions were recorded. Localization success rates were determined for blue dye and sentinel node with radiolocalization biopsy. In the human studies, all patients had sentinel node radiolocalization biopsy performed in a similar manner. On the morning of surgery, each patient had sentinel node radiolocalization biopsy of the sentinel lymph node performed using an intradermal or peritumoral injection of technetium Tc 99m sulfur colloid. Sentinel nodes were localized on the skin surface using a handheld gamma detector. Gamma count measurements were obtained for the following: 1) the "hot" spot/node in vivo before incision, 2) the hot spot/node in vivo during dissection, 3) the hot spot/node ex vivo, 4) the lymphatic bed after hot spot/node removal, and 5) the background in the operating room. The first draining lymph node(s) was identified, and biopsy of the node was performed. The radioactive sentinel lymph node(s) was submitted separately for routine histopathological evaluation. Preoperative lymphoscintigrams were performed in patients with melanoma and patients with Merkel cell carcinoma. In patients with head and neck squamous cell carcinoma, the relationship between the sentinel node and the remaining lymphatic basin was studied and all patients received complete neck dissections. The accuracy of sentinel node radiolocalization with biopsy, the micrometastatic rate, the false-negative rate, and long-term recurrence rates were reported for each of the head and neck tumor types. In the melanoma study, the success of sentinel node localization was compared for sentinel node radiolocalization biopsy, blue-dye mapping, and lymphoscintigraphy. In the Merkel cell carcinoma study, localization rates were evaluated for sentinel node radiolocalization biopsy and lymphoscintigraphy. In the head and neck squamous cell carcinoma study, the localization rate of sentinel node radiolocalization biopsy and the predictive value of the sentinel node relative to the remaining lymphatic bed were determined. All results were analyzed statistically. RESULTS: Across the different head and neck tumor types studied, sentinel node radiolocalization biopsy had a success rate approaching 95%. Sentinel node radiolocalization biopsy was more successful than blue-dye mapping or lymphoscintigraphy at identifying the sentinel node, although all three techniques were complementary. There was no instance of a sentinel node-negative patient developing regional lymphatic recurrence. In the head and neck squamous cell carcinoma study, there was no instance in which the sentinel node was negative and the remaining lymphadenectomy specimen was positive. CONCLUSION: In head and neck tumors that spread via the lymphatics, it appears that sentinel node radiolocalization biopsy can be performed with a high success rate. This technique has a low false-negative rate and can be performed through a small incision. In head and neck squamous cell carcinoma, the histological appearance of the sentinel node does appear to reflect the regional nodal status of the patient.
Descriptors: carcinoma, merkel cell secondary, squamous cell carcinoma, head and neck neoplasms, lymphatic system, lymphatic system, secondary melanoma, sentinel lymph node biopsy, skin neoplasms, adult, aged, aged 80 and over, merkel cell carcinoma, radionuclide imaging, cats, dyes, lymphatic metastasis, melanoma radionuclide imaging, middle aged, radiopharmaceuticals diagnostic use, rosaniline dyes diagnostic use, scintillation counting instrumentation, technetium tc 99m sulfur colloid diagnostic use, time factors.

Andaluz, N., M. Zuccarello, and K.R. Wagner (2002). Experimental animal models of intracerebral hemorrhage. Neurosurgery Clinics of North America 13(3): 385-393. ISSN: 1042-3680.
Abstract: Experimental animal ICH models are able to reproduce the overall important pathophysiologic events documented in human ICH, including edema development, markedly reduced metabolism, and tissue pathologic responses. Thus, ICH models serve as an important tool for new understanding of the mechanisms underlying brain injury after an intracerebral bleed. Currently, ongoing studies in several laboratories using these models investigating secondary inflammatory responses as well as intracellular signaling and molecular events are expected to provide therapeutic targets for treating ICH. Future studies should also be directed at one aspect of ICH modeling that has received little attention--potential differences in the hemostatic systems and physical and biochemical properties of clots in animals that might make their susceptibility to aspiration and/or fibrinolytic drugs and rates of rehemorrhage different than in human beings. Also, future efforts should be directed toward the development of a model that mimics the pathophysiologic processes that lead to spontaneous ICH, progression of hemorrhage, and the recurrence of bleeding in human beings. This model would not only provide better understanding of the dynamic events leading to ICH and tissue injury but should also lead to the development of highly effective pharmacologic and surgical treatments.
Descriptors: cerebral hemorrhage, animal disease models, brain supply, brain, brain, cats, cerebral hemorrhage, cerebrovascular circulation, dogs, haplorhini, rabbits, rats, swine.

Aoyagi, Y., R.B. Stein, V.K. Mushahwar, and A. Prochazka (2004). The role of neuromuscular properties in determining the end point of a movement. Institute of Electrical and Electronics Engineers Transactions Neural Systems and Rehabilitation Engineering 12(1): 12-23. ISSN: 1534-4320.
Abstract: How does the activation of several muscles combine to produce reliable multijoint movements? To study this question, we stimulated up to six sites in muscles, nerves, and the spinal cord. Flexion and extension of the hip, knee, and ankle were elicited in anesthetized and decerebrate cats. The movements occurred largely in the sagittal plane against a constant spring load and covered most of the passive range of motion of the cat's limb. The movements of the end-point (foot) were compared with predictions based on vectorial summation of end-point movements elicited by stimulating single electrodes. The lengths of the movements produced by stimulating more than one site exceeded what was expected from linear summation for small movements (<3 cm) and showed a less than linear summation for large movements (>11 cm). The data were compared with muscle and limb models. Since the deviations from linearity were predictable as a function of distance, adjustments might easily be learned by trial and error. The summation was less complete for spinal stimulation, compared to nerve and muscle stimulation, so spinal circuits do not appear to compensate for the nonlinearities. Movements were elicited from positions of the limb not only in a neutral position, but also in front and behind the neutral position. A degree of convergence was seen, even with stimulation of some individual muscles, but the convergence increased as more muscles were stimulated and more joints were actively involved. This suggests that convergence to an equilibrium-point arises at least partly from muscle properties. In conclusion, there are deviations from linear vectorial summation, and these deviations increase when more muscles are stimulated. The convergence to an equilibrium-point may simplify the computations needed to produce movements involving many muscles.
Descriptors: electric stimulation, models, neurological, movement, muscle contraction, muscle, skeletal, musculoskeletal equilibrium, peripheral nerves, spinal cord, anesthesia, cats, computer simulation, decerebrate state, electric stimulation therapy, hindlimb, muscle, skeletal innervation, range of motion, articular, spinal nerve roots, unconsciousness.

Arts, M., F. Bemelmans, and A. Cools (1998). Activation of n-methyl-d-aspartate receptors in the feline retrorubral nucleus elicits orofacial dyskinesia. European Journal of Pharmacology 349(1): 23-31. ISSN: 0014-2999.
NAL Call Number: QP901 .E8
Descriptors: neural coordination, orofacial dyskinesia, nervous system disease, feline, model, NMDA, DPI, dopamine receptor agonist, caudate nucleus, retroubral nucleus, dopamine.

Aubin, M.L., C.C. Powell, J.R. Gionfriddo, and A.D. Fails (2003). Ultrasound biomicroscopy of the feline anterior segment. Veterinary Ophthalmology 6(1): 15-17. ISSN: 1463-5216.
NAL Call Number: SF891 .V47
Abstract: Ultrasound biomicroscopy was performed on enucleated feline globes as a model for use in vivo. Quantitative measurements were obtained from the anterior segment using a 50-MHz transducer. Mean values from 26 feline globes were axial corneal thickness, 0.74 mm; anterior chamber depth, 4.20 mm; distance from the first ciliary process to the limbus, 3.17 mm; angle recess, 0.38 mm; angle opening distance, 1.05 mm; iris base width 0.38 mm; iris middle width 0.52 mm; iris tip width 0.13 mm, and iris-lens overlap, 0.69 mm. Distinctive features of the feline anterior segment include a relatively wide iridocorneal angle and deep anterior chamber.
Descriptors: anterior eye segment, cats, anterior eye segment ultrasonography, reference values.

Avanzini, G., F. Panzica, and M. de Curtis (2000). The role of the thalamus in vigilance and epileptogenic mechanisms. Clinical Neurophysiology 111(2): S19-S26. ISSN: 1388-2457.
Abstract: OBJECTIVES: The most relevant results of studies on the anatomo-physiological substrate of the thalamic rhythmogenic mechanisms responsible for sleep spindles and spike-wave discharges are reviewed. METHODS: The reviewed experiments have been carried out in cats, rodents and other mammals with either in vivo or in vitro electrophysiological recording. RESULTS: The rhythmic bilateral and synchronous EEG activities underlying sleep spindles and spike-wave discharges have been found to be correlated with oscillatory patterns involving mutually interconnected cortical and thalamic neurons. These rhythmic patterns are generated in thalamic neurons when the membrane potential, which is modulated by aminergic and cholinergic systems, is set to a level where the low threshold calcium current is de-inactivated. The pacemaker structure responsible for the initiation of the thalamo-cortical oscillatory activities has been identified as the reticular thalamic nucleus, a GABAergic structure projecting exclusively to the other thalamic nuclei. Experiments carried out in GAERS (genetic absence epilepsy rat from Strasbourg) demonstrated in this rat model of inherited absence epilepsy an enhancement of the pacemaker properties of the thalamic nucleus, due to a genetically determined increase in the low threshold calcium current, which is responsible for the pathological synchronization underlying spike-wave discharges. CONCLUSIONS: Recent experiments confirm the longstanding hypothesis that spindles and spike-wave discharges share common mechanisms involving thalamo-cortical circuitry. Due to its unusual anatomic and functional organization the nucleus reticularis thalami plays a crucial role as pacemaker of these rhythmic EEG activities.
Descriptors: arousal, epilepsy, sleep, thalamus.

Avoli, M. (1995). Feline generalized penicillin epilepsy. Italian Journal of Neurological Sciences 16(1-2): 79-82. ISSN: 0392-0461.
Abstract: Feline generalized penicillin epilepsy represents an experimental model of generalized spike-and-wave discharges occurring during clinical absence attacks. Spike-and-wave discharges of feline generalized penicillin epilepsy also have a pharmacological profile that is similar to that encountered in human absence attacks. Studies on the respective roles played by the thalamus and cortex in the generation of spike-and-wave discharges indicate that both structures are important in the elaboration of such generalized activity. Moreover, GABAA-mediated, intracortical inhibitory mechanisms are preserved and eventually enhanced at a time when generalized spike-and-wave discharges of feline generalized penicillin epilepsy are recorded. A preservation of GABA-mediated mechanisms in pure absence epilepsy might explain the differences in prognostic outlook that characterizes this type of epilepsy from seizures in which GABAergic mechanisms break down (e.g., generalized convulsive and partial epileptic attacks).
Descriptors: epilepsy, absence, cats, animal disease models, electroencephalography, evoked potentials, neural inhibition, penicillins, reproducibility of results, gamma aminobutyric acid.

Aye, M.M., S. Izumo, S. Inada, Y. Isashiki, H. Yamanaka, K. Matsumuro, Y. Kawasaki, Y. Sawashima, J. Fujiyama, K. Arimura, and M. Osame (1998). Histopathological and ultrastructural features of feline hereditary cerebellar cortical atrophy: a novel animal model of human spinocerebellar degeneration. Acta Neuropathologica 96(4): 379-387. ISSN: 0001-6322.
Descriptors: histopathology, disease models, animal models, atrophy, cerebellum, degeneration, hereditary diseases, electron microscopy, brain diseases, nervous system diseases, cats.

Bakker, J. and M.J. Baum (2000). Neuroendocrine regulation of GnRH release in induced ovulators. Frontiers in Neuroendocrinology 21(3): 220-262. ISSN: 0091-3022.
Descriptors: gonadorelin, ovulation, follicular pHase, hormones, luteinizing hormone, neurotransmitters, ovary, LH, GnRH.

Baranov, V.M., M.A. Tikhonov, A.N. Kotov, Z. Donina, and I.N. Lavrov (2001). The effect of complex barometric exposure on hemodynamics during simulation of the physiological impacts microgravity in animals [Vliianie kompleksnogo barovozdeistviia na gemodinamiku u zhivotnykh pri modelirovanii fiziologicheskikh effektov mikrogravitasii]. Aviakosmicheskaia i Ekologicheskaia Meditsina [Aerospace and Environmental Medicine] 35(1): 55-60. ISSN: 0233-528X.
Abstract: In experiments with anesthetized cats effects of breathing under negative pressure (BNP, -5 cm of water column) combined with lower body negative pressure (LBNP, -20 cm of water column) on the cardiorespiratory reactions to postural simulation of the hemodynamic shifts in microgravity were studied. Evidence was obtained that this complex barometric exposure of tilted animals (-30 degrees) imitated the central and peripheral hemodynamics characteristic of tilt at the calculated inclination of +6 degrees up to +12 degrees. Extrapolation of the experimental data on the orthodox physiological model of microgravity (HDT, -6 degrees) allows an assumption that the protocol of complex barometric exposure tested in this experiment transforms the hemodynamic parameters under study to the levels close to those in the vertical body. Results of the investigation infer an additive character of the complex barometric exposure (LBNP + BNP) and its utility as a model of orthostatic g-loads.
Descriptors: hypokinesia, weightlessness, cats, cerebrovascular circulation, head down tilt, hemodynamic processes, lower body negative pressure.
Language of Text: Russian.

Baratta, R.V., M. Solomonow, G. Nguyen, and R. D'Ambrosia (2000). Characterization of load-length-velocity relationships of nine different skeletal muscles. Journal of Biomechanics 33(3): 381-5. ISSN: 0021-9290.
NAL Call Number: TA166. J6
Abstract: A three-dimensional characterization of muscle load, length and velocity was obtained from nine muscles in the cat's hind limb through contractions where the muscles shortened against inertial-gravitational loads. A model based on the load-length characteristic and second-order dynamics describes shortening velocity related to load and length under these conditions. We conclude that this model describes well contraction velocity as function of length and load under inertial-gravitational load conditions, with correlation coefficients higher than 0.9 in most of the tested muscles.
Descriptors: muscle, skeletal, biomechanics, cats, electric stimulation, kinetics, biological models, muscle contraction, tibia, weight bearing.

Barr, M.C., S. Huitron Resendiz, M. Sanchez Alavez, S.J. Henriksen, and T.R. Phillips (2003). Escalating morphine exposures followed by withdrawal in feline immunodeficiency virus-infected cats: a model for HIV infection in chronic opiate abusers. Drug and Alcohol Dependence 72(2): 141-9. ISSN: 0376-8716.
Abstract: Opiate abuse is a risk factor for human immunodeficiency virus (HIV) infection. Because the direct effects of opiates on HIV infection are difficult to determine epidemiologically, animal models of lentivirus infection are relied upon to study the effects of opiates in the absence of confounding factors. Morphine, the predominant metabolite of heroin, is used in most experimental systems examining heroin abuse. In this study, morphine treatment of feline immunodeficiency virus (FIV)-infected cats modeled a typical pattern of escalating drug use interspersed with withdrawals. Plasma cortisol levels were measured for evidence of stress associated with morphine withdrawal. In the morphine-treated cats, cortisol levels peaked at time points corresponding to morphine withdrawal and returned to baseline levels during treatment and several weeks after the final withdrawal. Morphine-treated cats displayed clear behavioral and physical signs of opiate exposure and evidence of withdrawal when the drug was stopped. Morphine-exposed cats did not experience enhanced severity of FIV-related disease; in fact, morphine demonstrated a protective effect on FIV-associated changes in brainstem auditory evoked potentials. Our research suggests that opiate exposure is unlikely to adversely affect the progression of acute lentivirus infection and might be beneficial in controlling associated neurological disease.
Descriptors: animal disease models, HIV infections, feline immunodeficiency virus, lentivirus infections, lentivirus infections, morphine, opioid related disorders, substance withdrawal syndrome, cats, chronic disease, drug administration schedule, evoked potentials, auditory, brain stem, hydrocortisone, morphine, morphine, severity of illness index, substance withdrawal syndrome, time factors, viremia, viremia.

Barron, B.A. (1999). Opioid peptides and the heart. Cardiovascular Research 43(1): 13-6. ISSN: 0008-6363.
Abstract: The heart is a complex neuroendocrine (opioids, NPY, VIP) or mechanoendocrine (ANP) organ. Opioid peptides and receptors are present in the heart and nerves such that they can easily modulate cardiac function. Cardiac opioids may have autocrine, paracrine and endocrine function. The challenge is to find the signal that turns them on and then what they do in the face of an overwhelmingly redundant system making knock-out technology hard to interpret. Determining the cardiac release of opioids in an intact system still requires a larger animal model.
Descriptors: myocardium, opioid peptides, receptors, opioid, adrenal medulla, cats, animal disease models, dogs, guinea pigs, opioid peptides biosynthesis, rats, receptors, opioid, swine.

Barthez, P.Y., D.J. Chew, and S.P. DiBartola (2001). Simplified methods for estimation of 99mTc-pentetate and 131-I-orthoiodohippurate plasma clearance in dogs and cats. Journal of Veterinary Internal Medicine 15(3): 200-8. ISSN: 0891-6640.
NAL Call Number: SF601 .J65
Abstract: The purpose of this study was to evaluate simplified methods for estimation of Technetium Tc 99m (99mTc)-pentetate and orthoiodohippurate I 131 (131I-OIH) plasma clearance in dogs and cats with 1 and 2 blood samples. Plasma clearances were calculated after a bolus injection of 1.85-11.1 MBq of 99mTc-pentetate and 131I-OIH with a 2-compartment model based on a 12-point curve as a reference method in 21 dogs and 18 cats. Three 2-sample and 3 single-sample methods were investigated. The method yielding the smallest standard deviation of the difference between the reference method and the simplified method was selected as the optimal one. Linear regression analysis was performed between the reference method and the simplified method and coefficient of determination (R2) was calculated. For 99mTc-pentetate plasma clearance, the optimal 2-sample method was the one with a mono-compartment model with samples taken at specific times. For 131I-OIH plasma clearance, the estimation was improved slightly by raising the clearance calculated with a mono-compartment model to the power of an empirically determined parameter. The optimal single-sample method was the one with a linear quadratic regression between the volume of distribution of the tracer at a specific time and the clearance calculated with 12 samples. Two-sample methods performed significantly better than did single-sample methods. The conclusion is made that 99mTc-pentetate and 131I-OIH plasma clearances can be estimated in dogs and cats with 1 or 2 blood samples with a reasonable margin of error compared to plasma clearances calculated with a 2-compartment model and 12 blood samples.
Descriptors: cats, dogs, iodine radioisotopes, iodohippuric acid, radiopharmaceuticals, technetium tc 99m pentetate, area under curve, injections, intravenous, iodine radioisotopes, iodine radioisotopes, iodohippuric acid, metabolic clearance rate, radiopharmaceuticals, radiopharmaceuticals, technetium tc 99m pentetate, technetium tc 99m pentetate.

Baylor, J.E., W.J. Mcfeely, and P.J. Antonelli (1999). Central nervous system metabolic activity after cochlear implantation in the feline neonatal model. Otolaryngology: Head and Neck Surgery 121(4): 361-366. ISSN: 0194-5998.
Abstract: OBJECTIVE: To determine the effects of deafening and cochlear implant stimulation on central nervous system (CNS) metabolic activity in the feline neonate model. BACKGROUND: Deafening of fetal animals has been shown to result in acute, profound depression of CNS glucose metabolism, in both auditory structures and the cerebral hemispheres. Preliminary studies have suggested that electrical stimulation of the auditory system may increase central nervous metabolic activity after deafening. The purpose of this study was to investigate this possibility. METHODS: This was a prospective, randomized, blinded, and controlled animal study of 13 random-source newborn kittens. It was set in an animal research facility for otologic disorders. OUTCOME: Deoxyglucose metabolism (assessed with autoradiograph densitometry) of brain cross-sections of normal, deafened, and deafened and cochlear-implanted animals after 6 weeks of auditory stimulation or deprivation. RESULTS: Chronic deafening did not result in a profound reduction in CNS metabolic activity. Cochlear implantation and electrical stimulation did not significantly raise the level of CNS metabolic activity within either auditory pathways or the cerebral hemispheres. CONCLUSIONS: Deafening is not associated with significant chronic reduction in CNS metabolic activity. Other parameters of CNS activity and maturation may be necessary to assess the effects of cochlear implantation and stimulation in animal models.
Descriptors: auditory pathways, brain, cochlear implantation, deafness, energy, animals, newborn, audiometry, evoked response, autoradiography, cats, deoxyglucose, sensory deprivation.

Bazhenov, M., I. Timofeev, M. Steriade, and T.J. Sejnowski (1998). Computational models of thalamocortical augmenting responses. Journal of Neuroscience 18(16): 6444-6465. ISSN: 0270-6474.
Descriptors: computational biology, mathematical biology, nervous system, neural coordination, intracortical inhibition, cortical model, thalamocortical augmenting responses, computational models, in vivo validation, anethetized cats, thalmic cells.

Bertalanffy, H., N. Yamaguchi, M. Ishikawa, T. Kawase, and S. Toya (1994). A new model for in vivo observation of the feline spinal microcirculation: the closed spinal window. Neurosurgery 34(2): 316-21. ISSN: 0148-396X.
Abstract: A new experimental model is described that uniquely allows the in vivo observation and quantification of vascular caliber changes on the dorsal surface of the feline spinal cord. The model consists of a rectangular Plexiglas window that is sutured to the lumbar dura and is supported by a special holder. Inlet and outlet tubes attached to the window serve for topical applications of mock cerebrospinal fluid or vasoactive agents to the surface of the cord and for continuous monitoring of intrathecal pressure. Pial vessels below the window were observed at 200-fold magnification with the aid of a microvideo camera. Spinal arterioles reacted to hypercarbia and superfusion with acetylcholine solution in a manner similar to cerebral arterioles. Tests with increased intrathecal pressure showed that the window remained watertight between 25 and 130 mm Hg, with an average leakage pressure of 57.8 +/- 33.5 mm Hg. To promote the use of this model in other laboratories, the authors give a detailed description of the closed spinal window preparation and report their experiences gained from 50 experiments. It is concluded that the closed spinal window is a highly reproducible model, suitable for the study of the feline spinal microcirculation for several hours in vivo.
Descriptors: microcirculation, skin window technique, spinal cord supply, cats, pia mater supply, vascular resistance.

Bhattacherjee, P., C.A. Paterson, J.M. Spellman, G. Graff, and J.M. Yanni (1999). Pharmacological validation of a feline model of steroid-induced ocular hypertension. Archives of Ophthalmology 117(3): 361-4. ISSN: 0003-9950.
Abstract: OBJECTIVE: To validate pharmacologically the feline model of steroid-induced ocular hypertension. METHODS: Serial studies were conducted in domesticated adult female cats trained to accept topical ocular drug administration and pneumotonometry. To establish intraocular pressure (IOP) values for each study, measurements were performed at the same time of day for 6 consecutive days. Beginning on day 7, cats received either steroid or vehicle administered topically to both eyes three times a day for approximately 28 days. The IOP measurements were performed daily. RESULTS: After 5 to 7 days of treatment with 0.1% dexamethasone or 1.0% prednisolone acetate, IOP began to increase, reaching peak values within 2 weeks. These values were sustained throughout dosing but declined rapidly to baseline upon cessation of treatment. Maximum IOPs for the dexamethasone- and prednisolone-treated groups averaged 4.5 +/- 0.3 mm Hg (n = 12) greater than the mean IOP value obtained in vehicle-treated cats. Cats treated with 0.25% fluorometholone, 1.0% loteprednol etabonate, and 1.0% rimexolone exhibited increases of 0.6, 1.2, and 1.7 mm Hg, respectively. These values were significantly lower than those observed following treatment with dexamethasone or prednisolone. CONCLUSIONS: The ocular hypertensive effects of selected anti-inflammatory topical ocular steroids in this model are consistent with clinical findings. CLINICAL RELEVANCE: This feline model is a useful tool for assessing the potential IOP liability of novel anti-inflammatory steroids.
Descriptors: animal disease models, glucocorticoids, ocular hypertension, topical administration, androstadienes, androstadienes, cats, dexamethasone, dexamethasone, fluorometholone, fluorometholone, glucocorticoids, intraocular pressure, ocular hypertension, ophthalmic solutions, ophthalmic solutions, prednisolone, prednisolone, pregnadienes, pregnadienes, random allocation, reproducibility of results, tonometry, ocular.

Bice, D.E., J. Seagrave, and F.H. Green (2000). Animal models of asthma: potential usefulness for studying health effects of inhaled particles. Inhalation Toxicology 12(9): 829-62. ISSN: 0895-8378.
Abstract: Asthma is now recognized to be a chronic inflammatory disease that affects the whole lung. Incidence appears to be increasing despite improved treatment regimens. There is substantial epidemiological evidence suggesting a relationship between the incidence and severity of asthma (e.g., hospitalizations) and exposure to increased levels of air pollution, especially fine and ultrafine particulate material, in susceptible individuals. There have been a few studies in animal models that support this concept, but additional animal studies to test this hypothesis are needed. However, such studies must be performed with awareness of the strengths and weaknesses of the currently available animal models. For studies in mice, the most commonly used animal, a broad spectrum of molecular and immunological tools is available, particularly to study the balance between Th1 and Th2 responses, and inbred strains may be useful for genetic dissection of susceptibility to the disease. However, the mouse is a poor model for bronchoconstriction or localized immune responses that characterize the human disease. In contrast, allergic lung diseases in dogs and cats may more accurately model the human condition, but fewer tools are available for characterization of the mechanisms. Finally, economic issues as well as reagent availability limit the utility of horses, sheep, and primates.
Descriptors: air pollutants, asthma, animal disease models, inhalation exposure, asthma, asthma, cats, dogs, guinea pigs, horses, mice, rabbits, rats, sheep, species specificity.

Bidawid, S., N. Malik, O. Adegbunrin, S.A. Sattar, and J.M. Farber (2003). A feline kidney cell line-based plaque assay for feline calicivirus, a surrogate for norwalk virus. Journal of Virological Methods 107(2): 163-167. ISSN: 0166-0934.
NAL Call Number: QR355 .J6
Descriptors: cell based plaque assay, bioassay techniques, laboratory techniques, cell culture, tissue culture, feline calcivirus, feline kidney cells, CrFK, Norwalk virus model.

Bidawid, S., N. Malik, O. Adegbunrin, S.A. Sattar, and J.M. Farber (2004). Norovirus cross-contamination during food handling and interruption of virus transfer by hand antisepsis: experiments with feline calicivirus as a surrogate. Journal of Food Protection 67(1): 103-109. ISSN: 0362-028X.
NAL Call Number: 44.8 J824
Descriptors: disinfectants, food contamination, food handlers, food safety, ham, hands, lettuces, microbial contamination, stainless steel, washing, feline calicivirus, Lactuca sativa.

Biourge, V.C., J.M. Groff, R.J. Munn, C.A. Kirk, T.G. Nyland, V.A. Madeiros, J.G. Morris, and Q.R. Rogers (1994). Experimental induction of hepatic lipidosis in cats. American Journal of Veterinary Research 55(9): 1291-1302. ISSN: 0002-9645.
NAL Call Number: 41.8 Am3A
Abstract: The effect of long-term voluntary fasting on hematologic variables, biochemical profiles, and liver histologic findings was assessed in 15 obese cats (> 40% overweight). Clinical signs and laboratory results consistent with hepatic lipidosis were observed in 12 of 15 cats after 5 to 7 weeks of fasting, and were associated with 30 to 35% reduction of initial body weight. Histologic examination of successive liver biopsy specimens revealed that obesity was not associated with liver parenchymal lipid accumulation, but that fasting resulted in lipidosis in all 15 cats. The long-term fast was associated with an early (after 2 to 4 weeks of fasting) and significant (P < 0.05) reduction in serum urea, glucose, and albumin concentrations, and RBC mass. Fasting for 5 to 7 weeks was associated with a significant (P < 0.05) increase in hepatic-associated enzyme activities and in total and direct serum bilirubin concentrations. Significant (P < 0.05) changes in serum alkaline phosphatase developed as early as 3 weeks before the onset of hyperbilirubinemia. Except for development of hepatic lipidosis, cats appeared to tolerate the fast without other adverse effect. This study confirmed that long-term fasting may induce clinical hepatic lipidosis in obese cats. Fasting appears to induce a syndrome of hepatic lipidosis that is indistinguishable from feline idiopathic hepatic lipidosis and may be an appropriate model to study the pathophysiologic features and treatment of hepatic lipidosis.
Descriptors: cats, lipidosis, disease models, fasting, hematology, liver, histopathology, symptoms, body weight, enzyme activity.

Birder, L.A., A. Wolf-Johnston, C.A. Buffington, J.R. Roppolo, W.C. de Groat, and A.J. Kanai (2005). Altered inducible nitric oxide synthase expression and nitric oxide production in the bladder of cats with feline interstitial cystitis. The Journal of Urology 173(2): 625-9. ISSN: 0022-5347.
Abstract: PURPOSE: Alterations in nitric oxide (NO) levels have been demonstrated in some humans with interstitial cystitis (IC) as well as in chemically induced animal models of cystitis. Thus, in the current study we investigated whether inducible NO synthase (iNOS) mediated NO production is altered in the bladder of cats with a naturally occurring model of IC termed feline IC (FIC). MATERIALS AND METHODS: We examined iNOS expression using Western immunoblotting and baseline NO production using an NO microsensor from smooth muscle and mucosal bladder strips in 9 healthy cats and 6 diagnosed with FIC. RESULTS: There was a significant increase in baseline NO production in cats with FIC compared with that in healthy cats in smooth muscle and mucosal strips. This production was not ablated in the absence of extracellular Ca (100 microM egtazic acid) or following incubation with the calmodulin antagonist trifluoroperazine (20 microM), indicating iNOS mediated Ca independent NO production. Release was significantly decreased following incubation with the NOS antagonist L-NAME (N-nitro-L-arginine methyl ester) (100 microM). Furthermore, immunoblotting revealed a trend toward increased iNOS expression in smooth muscle and mucosal strips from FIC cats but not from healthy cats. CONCLUSIONS: In light of previous findings that the barrier property of the urothelial surface is disrupted in FIC and iNOS mediated increase in NO alters barrier function in other types of epithelium our findings suggest that iNOS dependent NO production may have a role in epithelial barrier dysfunction in FIC.
Descriptors: bladder, cystitis, interstitial, nitric oxide biosynthesis, nitric oxide synthase biosynthesis, cats.

Blatt, D.R., W.A. Friedman, F.J. Bova, D.P. Theele, and J.P. Mickle (1994). Temporal characteristics of radiosurgical lesions in an animal model. Journal of Neurosurgery 80(6): 1046-55. ISSN: 0022-3085.
Abstract: To characterize the temporal course of radiosurgical lesions, 19 cats were irradiated in an animal linear accelerator radiosurgical device. The animals were followed clinically and, at 3.5, 6, 12, 18, 23, 29, and 63 weeks, were studied with gadolinium-enhanced magnetic resonance (MR) imaging. They were then sacrificed after Evans blue dye perfusion, and gross pathological and histopathological studies were performed. Mild neurological deficits developed between 3.5 and 4.5 weeks, correlating with the onset of mass effect both grossly and radiographically and with the maximum amount of white matter edema on T2-weighted MR imaging and microscopic examination. Clinical improvement occurred within several weeks as these resolved. The lesions were of similar size at all time intervals. Gadolinium-enhanced MR imaging demonstrated lesions with peripheral areas of enhancement and central nonenhancing regions which correlated histologically with areas of vascular proliferation and radiation necrosis, respectively. In the early lesions at 3.5 and 6 weeks, necrosis and edema were predominant. From 12 to 29 weeks, an intermediate stage was observed, with resorption of the necrotic debris as evidenced by progressive cavitation and microglial response and by increased perilesional vascularity. At 63 weeks, resorption was still taking place, but gliosis and diminution of the vascular response were seen.
Descriptors: brain surgery, radiation injuries, radiosurgery, brain, brain radiation effects, brain edema diagnosis, brain edema, brain edema, cats, animal disease models, magnetic resonance imaging, necrosis, radiation injuries diagnosis, radiation injuries, time factors.

Bonyhadi, M.L., L. Su, J. Auten, J.M. McCune, and H. Kaneshima (1995). Development of a human thymic organ culture model for the study of HIV pathogenesis. AIDS Research and Human Retroviruses 11(9): 1073-80. ISSN: 0889-2229.
Abstract: The development of effective therapies for the treatment of AIDS would be facilitated by a better understanding of HIV pathogenesis in vivo. While some aspects of pathogenesis may be assessed by standard tissue culture assays, in vivo animal models may provide clues to other aspects of HIV-mediated progression toward AIDS. Current animal models include primate models for the study of simian immunodeficiency virus (SIV) and HIV, SCID-hu and hu-PBL SCID mouse models for the study of HIV, and feline models for the study of feline immunodeficiency virus (FIV). In general these models are costly and labor intensive. We have developed a simple human fetal thymic organ culture (TOC) system that is permissive for HIV infection and that exhibits pathology similar to that observed in vivo. A key feature of this system is the time-dependent destruction of thymocytes typified by the preferential loss of CD4-expressing cells. HIV-mediated thymocyte destruction occurs by a process involving programmed cell death. We have infected TOC with a panel of HIV isolates and found that the resulting viral replicative and pathogenic profiles are similar to those seen in the SCID-hu Thy/Liv mouse, yet different from profiles observed in standard PHA-blast tissue culture assays. In addition, we find that TOC may be used to assess efficacy of antiviral agents such as AZT (3'-azido-3'-deoxythymidine) and ddI (2',3'-dideoxyinosine) in blocking both viral replication and virus-induced pathology. These results indicate that this model is amenable to the systematic manipulation, analysis, and characterization of a variety of HIV virus isolates and antiviral therapies.
Descriptors: HIV infections, HIV 1 pathogenicity, biological models, thymus gland, antiviral agents, apoptosis, cd4 cd8 ratio, cd4 positive t lymphocytes, cd4 positive t lymphocytes, cats, didanosine, drug evaluation, preclinical, fetus, HIV infections, HIV infections, HIV 1, HIV 1, mice, organ culture techniques, organ culture techniques standards, thymus gland, thymus gland, time factors, virus replication, zidovudine.

Borostyankoi, Z. and K. Senyi (2000). A szemtengely-beallitodas idobeli lefolyasa muvi kancsal macskakban [Time-course of interocular alignment in artificially esotropic cats]. Orvosi Hetilap 141(35): 1929-32. ISSN: 0030-6002.
Abstract: Strabismus induced by eye-muscle surgery is a widely accepted experimental model of discordant binocular vision. Up to now, no attention was paid to the progress of strabismus in the postsurgical period, although, the grade of the developing strabismus is strongly influenced by the loss of binocularity in the visual system. Following lateral rectus laminotomy of 2-week-old kittens, the Hirschberg method and prisms were used to assess interocular alignment. The angle of deviation was measured weekly. During the first postoperative weeks, cats fixated still alternally, while by the end of the second postnatal month, when compared to healthy controls, operated cats were unable to align their eyes parallelly. They also showed persistent esotropy (+35 +/- 7 delta) that developed with a characteristic time-course. The interocular misalignment in artificially strabismic kittens develop gradually, and does not simply appear after the operation. The nature of this pathological process resembles the normal development of eye-movements in kittens, as well as in primate infants. Therefore, the surgery for strabismus in experimental animals at the earliest time point during the sensitive period are recommended, in order to provide ample time-window window for the effective development of the "strabismic visual system".
Descriptors: convergence, ocular, strabismus, strabismus surgery, cats, animal disease models, esotropia, esotropia surgery, time factors.
Language of Text: Hungarian.

Boskov, D., M. Jocic, K. Jovanovic, M. Ljubisavljevic, and R. Anastasijevic (1994). Membrane potential changes of skeletomotor neurons in response to random stretches of the triceps surae muscles in decerebrate cats. Biological Cybernetics 71(4): 333-339. ISSN: 0340-1200.
Descriptors: cell biology, models, simulations, computational biology, muscular system, nervous system, neural coordination, wiener kernel, membrane potential, skelatomotor neurons, triceps surae muscles.

Bragg, D.C., T. Childers, J. Boles, M. Tompkins, W. Tompkins, and R. Meeker (2000). The choroid plexus and AIDS-related CNS disease. Journal of Neurovirology 6(5): 444. ISSN: 1355-0284.
Descriptors: immune system, infection , nervous system, neural coordination, AIDS, feline, model , viral disease.

Brellou, G., I. Vlemmas, S. Lekkas, and N. Papaioannou (2005). Immunohistochemical investigation of amyloid beta-protein (Abeta) in the brain of aged cats. Histology and Histopathology 20(3): 725-31. ISSN: 0213-3911.
Abstract: To clarify the immunohistochemical features of amyloid deposits and cerebral amyloid angiopathy (CAA), the distribution of the amyloid beta-protein subtypes Abeta40, Abeta42, Abeta43 and Abeta precursor protein (APP) were examined in the brains of fourteen aged cats (7.5-21 year-old). Two types of plaques were detected. The first type was characterized by ASS positive antigenic material and detected in the cortical layers of the frontal and parietal lobes of all examined cats. The second type was characterized by diffuse positive immune staining representing diffuse plaques, which were detected only in the very aged cats (17-21 years old) and distributed throughout the cortical layers of the parietal lobes. Vascular amyloid and the amyloid deposits were strongly positive-stained with the antibody Abeta42. APP was exhibited in neurons and axons while the staining was stronger in the very aged cats (17-21 years old). Our findings suggest that the feline forms a spontaneous model for understanding the early changes of normal brain aging and the early stage of amyloid beta-protein deposition.
Descriptors: cats, amyloid deposits, brain, alzheimers, Abeta, angiopathy, plaques.

Briquet, S., J. Richardson, C. Vanhee Brossollet, and C. Vaquero (2001). Natural antisense transcripts are detected in different cell lines and tissues of cats infected with feline immunodeficiency virus. Gene 267(2): 157-164. ISSN: 0378-1119.
NAL Call Number: QH442 .A1G4
Abstract: Feline immunodeficiency virus (FIV) is a lentivirus inducing an AIDS-like disease in cats, thus providing an interesting model for AIDS study. FIV and HIV-1 possess a similar genomic arrangement of structural and non-structural genes, whose expression is regulated by related genetic mechanisms. On the DNA strand complementary to the HIV-1 envelope messenger, an open reading frame (ORF) has been identified which encompasses the Rev Responsive Element (RRE), a cis-acting element critical to HIV gene expression. This ORF was highly conserved among HIV-1 isolates and had the potential to encode a hydrophobic protein. A corresponding antisense transcript was detected in cells infected with HIV-1, and appeared to encode an antisense protein. In the present study, we have identified a well-conserved antisense ORF, also coincident with the RRE region, in the genome of 21 FIV isolates. The predicted protein, 103 amino acids in length, is highly hydrophobic, as is the case for that of HIV-1. In addition, we have shown that a corresponding transcript, complementary to the transmembrane sequence of the FIV envelope gene, was produced in different cellular and viral contexts, that is, ex vivo and in vivo in FIV infected cell lines and tissues of infected cats, respectively. Expression of antisense transcripts might therefore be of general importance in the natural history of retroviruses.
Descriptors: feline immunodeficiency virus, antisense RNA, amino acid sequence, cats, cell line, gene expression regulation, ENV gene products, lentivirus infections, molecular sequence data, open reading framessequence alignment, tissue distribution, genetic transcription.

Broder, C.C. and R.G. Collman (1997). Chemokine receptors and hiv. Journal of Leukocyte Biology 62(1): 20-29. ISSN: 0741-5400.
NAL Call Number: QP185 .R4
Descriptors: immune system, cell biology, AIDS, CCR5 gene, chemokine receptor, HIV 1, feline immunodeficiency virus.

Brooks, A.I., C.S. Stein, S.M. Hughes, J. Heth, P.M.J. McCray, S.L. Sauter, J.C. Johnston, D.A. Cory Slechta, H.J. Federoff, and B.L. Davidson (2002). Functional correction of established central nervous system deficits in an animal model of lysosomal storage disease with feline immunodeficiency virus-based vectors. Proceedings of the National Academy of Sciences of the United States of America 99(9): 6216-6221. ISSN: 0027-8424.
NAL Call Number: 500 N21P
Abstract: Gene transfer vectors based on lentiviruses can transduce terminally differentiated cells in the brain; however, their ability to reverse established behavioral deficits in animal models of neurodegeneration has not previously been tested. When recombinant feline immunodeficiency virus (FIV)-based vectors expressing beta-glucuronidase were unilaterally injected into the striatum of adult beta-glucuronidase deficient [mucopolysaccharidosis type VII (MPS VII)] mice, an animal model of lysosomal storage disease, there was bihemispheric correction of the characteristic cellular pathology. Moreover, after the injection of FIV-based vectors expressing beta-glucuronidase into brains of beta-glucuronidase-deficient mice with established impairments in spatial learning and memory, there was dramatic recovery of behavioral function. Cognitive improvement resulting from expression of beta-glucuronidase was associated with alteration in expression of genes associated with neuronal plasticity. These data suggest that enzyme replacement to the MPS VII central nervous system goes beyond restoration of beta-glucuronidase activity in the lysosome, and imparts improvements in plasticity and spatial learning.
Descriptors: central nervous system diseases, gene transfer techniques, feline immunodeficiency virus, lysosomal storage diseases, animal behavior, brain, central nervous system, cognition, genetic vectors, glucuronidase, learning, memory, mice, mucopolysaccharidosis vii, oligonucleotide array sequence analysis, phenotype, polymerase chain reaction, transgenes.

Brown, D.E., M.A. Thrall, S.U. Walkley, S. Wurzelmann, D.A. Wenger, R.W. Allison, and C.A. Just (1996). Metabolic abnormalities in feline Niemann-Pick type C heterozygotes. Journal of Inherited Metabolic Disease 19(3): 319-330. ISSN: 0141-8955.
NAL Call Number: RC627.8J68
Abstract: Niemann-Pick disease type C (NPC) is an autosomal recessive neurovisceral lysosomal storage disorder in which cholesterol lipidosis results from defective intracellular transport of unesterified cholesterol. The primary molecular defect of NPC is unknown; regulatory mechanisms of cholesterol metabolism are impaired, resulting in retarded esterification of exogenous cholesterol with accumulation of unesterified cholesterol in lysosomes and secondary storage of glycolipids and sphingomyelin. In obligate heterozygotes from a feline NPC model, cultured skin fibroblasts challenged with exogenously derived cholesterol exhibited intermediate rates of cholesterol esterification and accumulation of unesterified cholesterol. Liver lipid analyses of obligate heterozygote cats demonstrated intermediate cholesterol and sphingomyelin concentrations. Vacuolated skin fibroblasts were found in 2 of 3 heterozygote cats, and occasional cortical neurons exhibited intracellular inclusions immunoreactive for GM2-ganglioside. Ultrastructural studies provided evidence of storage in liver and brain. We believe these morphological and biochemical findings are the first example of manifestations of CNS abnormalities in a genetic carrier for a neuronal storage disease.
Descriptors: Niemann-Pick diseases, brain, cats, cholesterol, heterozygote, liver.

Brown, I.E. and G.E. Loeb (2000). Measured and modeled properties of mammalian skeletal muscle: IV. dynamics of activation and deactivation. Journal of Muscle Research and Cell Motility 21(1): 33-47. ISSN: 0142-4319.
NAL Call Number: QP321. J59
Abstract: The interactive effects of length and stimulus frequency on rise and fall times and on sag were investigated in fast-twitch feline caudofemoralis at normal body temperature. The length and stimulus frequency ranges studied were 0.8 1.2 L0 and 15 60 pps. Isometric rise times were shortest under two sets of conditions: short lengths + low stimulus frequencies and long lengths + high stimulus frequencies. In contrast the isometric fall time relationship showed a single minimum at short lengths + low stimulus frequencies. Velocity was shown to have an additional effect on fall time, but only at higher stimulus frequencies (40 60 pps): fall times were shorter during movement in either direction as compared to isometric. The effects of sag were greatest at shorter lengths and lower stimulus frequencies during isometric stimulus trains. Potential mechanisms underlying this last effect were investigated by comparing isometric twitches elicited prior to and immediately following a sag-inducing stimulus train. Post-sag twitches produced less force, reached peak force earlier and initially decayed more quickly compared to pre-sag twitches. However, the final rate of force decay and the initial rate of force rise (during the first 15 ms) were unaffected by sag. We construct a logical argument based on these findings to hypothesize that the predominant mechanism underlying sag is an increase in the rate of sarcoplasmic calcium ion removal. All of the above findings were used to construct a model of activation dynamics for fast-twitch muscle, which was then extrapolated to slow-twitch muscle. When coupled with a previous model of kinematic dynamics, the complete model produced accurate predictions of the forces actually recorded during experiments in which we applied concurrent dynamic changes in length. velocity and stimulus frequency.
Descriptors: action potentials, muscle contraction, muscle fibers, fast twitch, muscle, skeletal, cats, electric stimulation, biological models, muscle fibers, slow twitch, time factors.

Brown, I.E. and G.E. Loeb (1999). Measured and modeled properties of mammalian skeletal muscle. I. The effects of post-activation potentiation on the time course and velocity dependencies of force production. Journal of Muscle Research and Cell Motility 20(5-6): 443-456. ISSN: 0142-4319.
NAL Call Number: QP321.J59
Descriptors: muscular system, feline caudofemoralis muscle, myosin regulatory light chain, cross bridge dynamics, force dispotentiation .

Bruninga, K., L. Riedy, A. Keshavarzian, and J. Walter (1998). The effect of electrical stimulation on colonic transit following spinal cord injury in cats. Spinal Cord 36(12): 847-53. ISSN: 1362-4393.
Abstract: The effect of direct electrical stimulation on colinic transit and manometric recordings following spinal cord injury were assessed in five adult male cats. Intra-colonic catheters were surgically placed, stimulating electrodes were sutured to the colonic serosa and a laminectomy with spinal cord clamping at a T4 level was done to induce spinal cord injury (SCI). Twenty radiopaque markers were inserted through an intra-colonic catheter located 1 cm distal to the cecum and were monitored with daily fluoroscopy as a measure of colonic transit. Transit measurements were compared before SCI, after SCI and after SCI with electrical stimulation of 40 pps, 1 ms, and 0-50 mA. Colonic transit following SCI was significantly prolonged (P<0.05) when compared to the transit before SCI. Electrical stimulation following SCI improved colonic transit to values not significantly different from those before SCI. Spontaneous colonic phasic motor activity was similar both before and after SCI. Manometric defection patterns were also observed to be similar before SCI and after SCI with electrical stimulation. Based on our scoring criteria, the most frequent response to electrical stimulation was an abdominal contraction. These findings demonstrate that colonic transit is prolonged following SCI and that direct electrical stimulation of the colon following SCI improves colonic transit in an animal model.
Descriptors: colon, electric stimulation, gastrointestinal transit, spinal cord injuries, cats, constipation, constipation therapy, electric stimulation therapy.

Buchman, S.R., S.P. Bartlett, I.L.3. Wornom, and L.A. Whitaker (1994). The role of pressure on regulation of craniofacial bone growth. The Journal of Craniofacial Surgery 5(1): 2-10. ISSN: 1049-2275.
Abstract: The regulatory role of pressure on growth and differentiation of the craniofacial skeleton is largely unknown. We devised an experimental model to determine if the graded application of pressure could exert a trophic influence on craniofacial bone, allowing deliberate alteration and reshaping of the facial skeleton. To examine this question, 18 kittens were used to determine the adverse morphological sequelae after orbital evisceration and to compare the ability to remedy such facial deformity with the use of an inert implant or pressure-induced tissue expansion. In addition to detailed craniometric measurements of the cranial, orbital, and midfacial regions, histological analyses as well as radiographic and gross morphological comparisons were evaluated. Our results demonstrate a severe asymmetry and constriction in the orbital and midfacial regions resulting from orbital evisceration in the growing kitten. Placement of an inert implant will help to ameliorate only some of these adverse sequelae, whereas graded application of pressure appears to direct craniofacial bone growth, resulting in normal bony histology and improved facial form. We affirm that regional growth disturbances can alter normal facial development and that the regulatory role of pressure on bone growth can be exploited to dynamically correct abnormal craniofacial anatomy.
Descriptors: facial asymmetry, maxillofacial development, orbit evisceration, pressure, analysis of variance, cats, cepHalometry, facial bones growth and development, prostheses and implants, tissue expansion.

Buerke, M., A.S. Weyrich, T. Murohara, C. Queen, C.K. Klingbeil, M.S. Co, and A.M. Lefer (1994). Humanized monoclonal antibody DREG-200 directed against I-selectin protects in feline myocardial reperfusion injury. The Journal of Pharmacology and Experimental Therapeutics 271(1): 134-142. ISSN: 0022-3565.
NAL Call Number: 396.8 J82
Abstract: Polymorphonuclear leukocytes (i.e. neutrophils) significantly mediate damage in myocardial ischemia followed by reperfusion. In the present study, the cardioprotective effects of a humanized form of a monoclonal antibody directed against L-selectin designated monoclonal antibody (mAb) HuDREG-200 were examined in a feline model of 90-min myocardial ischemia followed by 270 min of reperfusion. In preliminary studies, flow cytometric analysis indicated that HuDREG-200 binds to feline neutrophils. In vitro administration of mAb HuDREG-200 significantly inhibited (P < .01) adherence of unstimulated neutrophils to ischemic-reperfused coronary endothelium in a concentration-dependent manner. Humanized DREG-200 (2 mg/kg) administered 10 min before reperfusion significantly attenuated myocardial necrosis compared to an isotype-matched humanized control mAb (HuABL364) which does not bind to L-selectin (14 +/- 3 vs. 29 +/- 3% necrosis/area-at-risk, P < .01), representing a 52% reduction in myocardial necrosis. This myocardial preservation also was related to reduced creatine kinase release and improved recovery of cardiac contractility (i.e. left ventricular dP/dtmax). Moreover, endothelial function, as assessed by relaxation to acetylcholine, also was significantly preserved in ischemic-reperfused coronary arteries isolated from cats treated with mAb HuDREG-200 compared to mAb HuABL364 (68 +/- 6 vs. 18 +/- 5, P < .01). Thus, a humanized anti-L-selectin mAb appears to be an effective means of preserving the ischemic myocardium from reperfusion injury and of preserving myocardial contractile function, at least during the early reperfusion period.
Descriptors: monoclonal antibodies, myocardial reperfusion injury, cats, cell adhesion, vascular endothelium, hemodynamic processes, I selectin, leukocyte count, neutrophils.

Buerke, M., A.S. Weyrich, Z. Zheng, F.C. Gaeta, M.J. Forrest, and A.M. Lefer (1994). Sialyl Lewisx-containing oligosaccharide attenuates myocardial reperfusion injury in cats. The Journal of Clinical Investigation 93(3): 1140-1148. ISSN: 0021-9738.
NAL Call Number: 448.8 J8295
Abstract: Neutrophil (PMN) adhesion to the vascular endothelium is an important mechanism of myocardial reperfusion injury. The adhesion process is initially mediated by selectins (e.g., P- and L-selectin), and monoclonal antibodies directed against these adhesion molecules exert cardioprotective activity in ischemia/reperfusion models. The counterreceptors for these selectins are thought to be carbohydrate-containing moieties. In this connection, we studied the effect of a soluble sialyl Lewisx-containing oligosaccharide (SLex-OS) on PMN-endothelial interactions in a feline model of myocardial ischemia/reperfusion (MI/R). SLex-OS (10 mg/kg), administered 10 min before R, significantly reduced myocardial necrosis compared with its vehicle 270 min after reperfusion (6 +/- 1% vs. 35 +/- 4% of area at risk, P < 0.01). The cardioprotection was confirmed by significantly lower plasma creatine kinase activities in SLex-OS vs. vehicle-treated cats (P < 0.01). Cardiac contractility (dP/dt max) of cats receiving SLex-OS was significantly preserved after 270 min of R (97 +/- 2% vs. 78 +/- 5% of initial, P < 0.01). Furthermore, endothelium-dependent relaxation to acetylcholine in coronary artery rings isolated from MI/R cats treated with SLex-OS was significantly preserved (73 +/- 7% vs. 22 +/- 6% vasorelaxation, P < 0.01). In vitro PMN adherence to coronary vascular endothelium after 270 min of R was significantly attenuated in the SLex-OS-treated group compared with the vehicle group (14 +/- 5 vs. 91 +/- 12 PMN/mm2, P < 0.01). Our results indicate that a SLex-OS is cardioprotective and preserves coronary endothelial function after MI/R, indicating an important role of sialyl Lewisx in PMN accumulation, endothelial dysfunction, and myocardial injury in myocardial ischemia/reperfusion.
Descriptors: CD1 antigens5, myocardial reperfusion injury, oligosaccharides, cats, cell adhesion, coronary vessels, vascular endothelium, hemodynamic processes, leukocytes, neutrophils.

Buhler, B., Y.C. Lin, G. Morris, A.J. Olson, C.H. Wong, D.D. Richman, J.H. Elder, and B.E. Torbett (2001). Viral evolution in response to the broad-based retroviral protease inhibitor TL-3. Journal of Virology 75(19): 9502-8. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Abstract: TL-3 is a protease inhibitor developed using the feline immunodeficiency virus protease as a model. It has been shown to efficiently inhibit replication of human, simian, and feline immunodeficiency viruses and therefore has broad-based activity. We now demonstrate that TL-3 efficiently inhibits the replication of 6 of 12 isolates with confirmed resistance mutations to known protease inhibitors. To dissect the spectrum of molecular changes in protease and viral properties associated with resistance to TL-3, a panel of chronological in vitro escape variants was generated. We have virologically and biochemically characterized mutants with one (V82A), three (M46I/F53L/V82A), or six (L24I/M46I/F53L/L63P/V77I/V82A) changes in the protease and structurally modeled the protease mutant containing six changes. Virus containing six changes was found to be 17-fold more resistant to TL-3 in cell culture than was wild-type virus but maintained similar in vitro replication kinetics compared to the wild-type virus. Analyses of enzyme activity of protease variants with one, three, and six changes indicated that these enzymes, compared to wild-type protease, retained 40, 47, and 61% activity, respectively. These results suggest that deficient protease enzymatic activity is sufficient for function, and the observed protease restoration might imply a selective advantage, at least in vitro, for increased protease activity.
Descriptors: evolution, molecular, protease inhibitors, retroviridae, retroviridae, amino acid sequence, cats, genome, viral, molecular sequence data.

Burgi, P.Y. and N.M. Grzywacz (1994). Model for the pharmacological basis of spontaneous synchronous activity in developing retinas. Journal of Neuroscience 14(12): 7426-39. ISSN: 0270-6474.
Abstract: Spontaneous waves of bursts of action potentials propagate across the ganglion-cell surface of developing retinas. A recent biophysical model postulated that this propagation is mediated by an increase in extracellular K+, following its ejection from ganglion cells during action potentials. Moreover, the model hypothesized that bursts might terminate due to the accumulation of intracellular Ca2+ and the subsequent activation of a Ca(2+)-dependent K+ conductance in the cells' dendrites. Finally, the model proposed that an excitatory synaptic drive causes a neuromodulation of the waves' properties. To test the feasibility of the model, we performed computer simulations of the network of developing ganglion cells under control and pharmacological-manipulation conditions. In particular, we simulated the effects of neostigmine, Cs+ and TEA, low Ca2+ concentrations, and Co2+. A comparison of the simulations with electrophysiological and pharmacological experimental data recently obtained in turtles (Sernagor and Grzywacz, 1993a), and cats and ferrets (Meister et al., 1991; Wong et al., 1993), showed that the model for the most part is consistent with the behavior of developing retinas. Moreover, modifications of the model to allow for GABAergic inputs onto ganglion cells (Sernagor and Grzywacz, 1994) and poor [K+]out buffering (Connors et al., 1982) improved the model's fits. These results lent further support to important roles of extracellular K+ concentration and synaptic drive for the propagation of waves.
Descriptors: aging, models, neurological, retina growth and development, retina, cesium, cobalt, computer simulation, electrophysiology, potassium channel blockers, retina, retinal ganglion cells, tetraethylammonium, tetraethylammonium compounds.

Burkhard, M.J. and G.A. Dean (2003). Transmission and immunopathogenesis of FIV in cats as a model for HIV. Current HIV Research 1(1): 15-29. ISSN: 1570-162X.
Abstract: The feline immunodeficiency virus (FIV) model provides a system to study lentivirus transmission, virus kinetics, pathogenesis, host responses, and immune dysfunction in a natural, out-bred host, under controlled conditions with specific-pathogen-free animals. The diversity of primary FIV strains can be exploited to mirror the range of disease manifestations associated with HIV infection. FIV is infectious via intravenous, intraperitoneal, intradermal, or subcutaneous injection as well as by atraumatic instillation onto the oral, vaginal, or rectal mucosa. Together, these features allow investigators to model specific aspects of HIV infection in a highly relevant and relatively inexpensive animal model. Well-developed areas of the FIV model include: (1) transmission of cell-associated as well as cell-free virus; (2) mucosal infectivity and immunopathogenesis; (3) vertical transmission; (4) acquired immunodeficiency including defects of the innate immune system; (5) thymic dysfunction; (6) neurotropism and neuropathogenesis; (7) host-virus interactions and the role of specific gene products; (8) efficacy of antiviral therapy; and (9) efficacy and immune correlates of experimental vaccines. This review will encompass areas specific to transmission and immunopathogenesis.
Descriptors: animal disease models, feline acquired immunodeficiency syndrome, feline acquired immunodeficiency syndrome transmission, HIV infections, HIV infections transmission, HIV 1 growth and development, feline immunodeficiency virus growth and development, cats, disease transmission, horizontal, disease transmission, vertical, feline acquired immunodeficiency syndrome, HIV infections, HIV 1, feline immunodeficiency virus, virus replication.

Burns, A.S., M.A. Lemay, and A. Tessler (2005). Abnormal spontaneous potentials in distal muscles in animal models of spinal cord injury. Muscle and Nerve 31(1): 46-51. ISSN: 0148-639X.
Descriptors: human spinal cord injury, animal models, cats, surgical transections, nervous system disease, stroke, vascular disease, fibrillation potential, spinal cord lesions.

Byers, S., J.D. Nuttall, A.C. Crawley, J.J. Hopwood, K. Smith, and N.L. Fazzalari (1997). Effect of enzyme replacement therapy on bone formation in a feline model of mucopolysaccharidosis type VI. Bone 21(5): 425-31. ISSN: 8756-3282.
NAL Call Number: RC930 B65
Abstract: A range of skeletal abnormalities are evident in mucopolysaccharidosis type VI (MPS VI, Maroteaux-Lamy syndrome) including short stature and dysostosis multiplex, resulting from a deficiency in the lysosomal hydrolase N-acetylgalactosamine-4-sulphatase (4S). In this article, bone pathology was assessed in a feline model of MPS VI to evaluate the efficacy of enzyme replacement therapy (ERT) as a treatment modality for this genetic disorder. Osteopenia is clearly evident in MPS VI animals, with bone mineral volume (BV/TV) falling well below that of normal animals (4.39% vs. 20.11%, respectively). Trabecular bone architecture was also affected in MPS VI with fewer, thinner, and more widely spaced trabeculae apparent. Bone formation rate (BFR/BS) was also lower in MPS VI animals than controls (0.0011 mm3/mm2 per day vs. 0.008 mm3/mm2 per day, respectively). Vertebral and tibial bone length in MPS VI animals progressively fell behind normal values with increasing age, as did cortical bone thickness. Vertebral body shape was also altered. ERT with recombinant human 4S (rh4S) resulted in a vertebral BV/TV of 8.23% in animals treated with an intravenous enzyme dose of 1 mg/kg and a BV/TV of 14.33% in animals treated with a dose of 5 mg/kg. BFR/BS also increased to 0.0034 mm3/mm2 per day in animals treated with enzyme doses of either 1.0 or 5.0 mg/kg rh4S. All other affected histomorphometric parameters also improved with ERT to a level intermediate between MPS VI untreated animals and normals. However, individual animals treated with 0.2 mg/kg rh4S intravenously or 1.0 mg/kg rh4S administered subcutaneously did not exhibit an improvement over untreated MPS VI animals. Vertebral and tibial bone lengths, tibial cortical bone thickness, and vertebral body shape also responded to ERT, with a trend away from the untreated group. Thus, ERT had a positive effect on bone development in MPS VI animals that was dependent upon the dose of enzyme administered and the route of administration.
Descriptors: bone density, chondro 4 sulfatase, mucopolysaccharidosis vi, bone density, bone development, metabolic bone diseases, metabolic bone diseases, cats, animal disease models, injections, intravenous, injections, subcutaneous, lumbar vertebrae, lumbar vertebrae, electron microscopy, mucopolysaccharidosis vi, osteoblasts, osteoblasts ultrastructure, osteocytes, osteocytes ultrastructure, recombinant proteins.

Calabrese, E.J. (2001). Adrenergic receptors: biphasic dose responses. Critical Reviews in Toxicology 31(4-5): 523-38. ISSN: 1040-8444.
Abstract: Agonists and antagonists of the adrenergic receptor system were assessed for their capacity to affect dose-response relationships across biological model, tissue and endpoint. U shaped dose responses were commonly reported, affecting multiple endpoints such as smooth muscle contraction/relaxation, memory, blood pressure, sexual behavior, platelet aggregation, and others. In six of the endpoints studied, mechanistic foundations of the biphasic nature of the dose response were established. The quantitative features of the dose-response relationships indicated that the maximum stimulatory responses, with but one exception, were less than twofold greater than the controls. The range of stimulatory responses was generally within 10- to 1000-fold, except for the platelet aggregation endpoint where the range was 10(3) to 10(5).
Descriptors: adrenergic agonists, adrenergic antagonists, muscle contraction, receptors, adrenergic, receptors, adrenergic, pressure, cats, dose response relationship, drug, memory, biological models, muscle, smooth, muscle, smooth, platelet aggregation, rabbits, rats, sexual behavior.

Campbell, D.J., J.M. Rawlings, S. Koelsch, J. Wallace, J.J. Strain, and B.M. Hannigan (2004). Age-related differences in parameters of feline immune status. Veterinary Immunology and Immunopathology 100(1-2): 73-80. ISSN: 0165-2427.
NAL Call Number: SF757.2. V38
Abstract: In order to assess age-related differences in feline immune status, 101 domestic short haired cats were assigned to two groups, adult (2-5 years, n=50) and senior (10-14 years, n=51). Analyses of leucocyte populations, lymphocyte subsets, complement activity, serum immunoglobulins and acute-phase proteins were undertaken and revealed significant differences between the two groups. The senior group had significantly lower WBC, lymphocyte and eosinophil counts than the adult group. Neutrophil, monocyte and basophil counts did not differ between the groups. Flow cytometry analysis, in combination with differential WBC data, revealed that the absolute values (cells/l) of T-cells, B-cells and natural killer (NK) cells were significantly lower in the older animals. While serum immunoglobulins IgA and IgM were higher in the senior group when compared with the adult group, no significant differences were observed in complement activity or in serum acute-phase proteins. Our findings suggest that age-related changes to parameters of immune status in the feline model are likely to follow a similar pattern to those observed in other long-lived mammalian species.
Descriptors: cats, age factors, apolipoproteins, colorimetry, complement, enzyme linked immunosorbent assay, flow cytometry, haptoglobins, immunodiffusion, immunoglobulins, leukocyte count, lymphocyte subsets, serum amyloid a protein, nonparametric statistics.

Cao, Y., P. Xie, and Y. Xing (2001). Role of endogenous cholinergic nerve in esophageal dysmotility with reflux esophagitis. Chinese Journal of Internal Medicine [Zhonghua Nei Ke Za Zhi] 40(10): 670-2. ISSN: 0578-1426.
Abstract: OBJECTIVE: To study the role of endogenous cholinergic nerve in esophageal dysmotility with reflux esophagitis in a feline model. METHODS: In 16 healthy cats under ketamine anesthesia (20 mg/kg), the abdominal parts of lower esophageal sphincter were cut open to establish the animal model for reflux esophagitis; esophageal motility was measured respectively preoperation and post-esophagitis. The activities of choline acetyltransferase (CHAT) and acetylcholinesterase(ACHE) in medial and distal esophageal body muscle was measured respectively with spectrophotometry, and compared to the normal cats(n = 8). RESULTS: Reflux esophagitis can make distal esophageal peristaltic amplitude decrease, the distal esophageal peristaltic amplitude of cats with reflux esophagitis [above LES 1 cm: (22.65 +/- 16.53) mm Hg; above LES 3 cm:(39.94 +/- 14.78) mm Hg, P < 0.0001] was significantly lower than that of normal cats [above LES 1 cm: (63.71 +/- 21.34) mm Hg; above LES 3 cm: (73.65 +/- 23.42) mm Hg] and the conducting velocity of distal esophagus was slower than that of normal cats [(1.04 +/- 0.36) cm/s vs (1.39 +/- 0.46) cm/s, P < 0.05]. In the esophagus of reflux esophagitis group, CHAT activity was lower in the model, especially in the distal part [(81.01 +/- 22.03) U/g vs (230.13 +/- 30.10) U/g, P < 0.0001] and ACHE activity remains unchanged. CONCLUSION: CHAT activity and pressure level were lower in the distal esophagus with reflux esophagitis compared to the normal cats. This study supported that reflux esophagitis can results in dysmotility of the distal esophagus and the abnormality of endogenous cholinergic innervation is one of the important mechanisms as far as the disorder of esophageal movement in reflux esophagitis.
Descriptors: cholinergic fibers, esophageal motility disorders, esophagitis, gastresophageal reflux, acetylcholinesterase, cats, choline o acetyltransferase, animal disease models, esophageal motility disorders, esophagitis, esophgus, esophgus innervation, esophgus, gastresophageal reflux.
Language of Text: Chinese.

Capra, N.F. and J.Y. Ro (2000). Experimental muscle pain produces central modulation of proprioceptive signals arising from jaw muscle spindles. Pain 86(1-2): 151-62. ISSN: 1083-0707.
Abstract: The aim of the present study was to investigate the effects of intramuscular injection with hypertonic saline, a well-established experimental model for muscle pain, on central processing of proprioceptive input from jaw muscle spindle afferents. Fifty-seven cells were recorded from the medial edge of the subnucleus interpolaris (Vi) and the adjacent parvicellular reticular formation from 11 adult cats. These cells were characterized as central units receiving jaw muscle spindle input based on their responses to electrical stimulation of the masseter nerve, muscle palpation and jaw stretch. Forty-five cells, which were successfully tested with 5% hypertonic saline, were categorized as either dynamic-static (DS) (n=25) or static (S) (n=20) neurons based on their responses to different speeds and amplitudes of jaw movement. Seventy-six percent of the cells tested with an ipsilateral injection of hypertonic saline showed a significant modulation of mean firing rates (MFRs) during opening and/or holding phases. The most remarkable saline-induced change was a significant reduction of MFR during the hold phase in S units (100%, 18/18 modulated). Sixty-nine percent of the DS units (11/16 modulated) also showed significant changes in MFRs limited to the hold phase. However, in the DS neurons, the MFRs increased in seven units and decreased in four units. Finally, five DS neurons showed significant changes of MFRs during both opening and holding phases. Injections of isotonic saline into the ipsilateral masseter muscle had little effect, but hypertonic saline injections made into the contralateral masseter muscle produced similar results to ipsilateral injections with hypertonic saline. These results unequivocally demonstrate that intramuscular injection with an algesic substance, sufficient to produce muscle pain, produces significant changes in the proprioceptive properties of the jaw movement-related neurons. Potential mechanisms involved in saline-induced changes in the proprioceptive signals and functional implications of the changes are discussed.
Descriptors: central nervous system, muscle spindles, myofascial pain syndromes, proprioception, signal transduction, brain stem, cats, electric stimulation, hypertonic solutions, jaw, masseter muscle, neural pathways, receptors, sensory, stimulation, chemical.

Carlson-Kuhta, P., J.R. Villablanca, and L.D. Loopuijt (1997). Innervation of the caudate nucleus, thalamus and red nucleus by the remaining sensorimotor cortex in cats with fetal or neonatal unilateral frontal cortex removal. Developmental Brain Research 98(2): 234-46. ISSN: 0165-3806.
Abstract: We studied the projections to the caudate nuclei, thalami and red nuclei from the remaining sensorimotor cortex in adult cats that had sustained a unilateral frontal cortex resection prenatally or neonatally. Four cats had the lesion at age E 50-55 and six animals sustained the ablation at age P 8-14 (seven cats were intact controls). All cats grew to young adulthood and then received injections of tritiated leucine-proline in the remaining sensorimotor cortex. Injection sites and axon terminal fields were reconstructed using autoradiography-processed tissue. In all cats the label filled a similar extent of the right pericruciate cortex. Terminal field densities in the subcortical nuclei were estimated using computer-based video software. Three medial-lateral sectors at five coronal levels were examined in the caudate nucleus. Three nuclear groups were analyzed in the thalamus (intralaminary, ventralis lateralis and ventrobasal complex). For the red nucleus, the four quadrants were examined at four coronal levels. The main goal of the study was to assess possible changes in the cortical innervation of the nuclei ipsilateral to the lesion. Therefore, the mean particle counts per nucleus (and per area or sector of nuclei) and per animal group were used to calculate percentage values for the decussated (crossed, or contralateral to the injection site) as a function of the non-decussated (uncrossed, or ipsilateral to the injection site) innervation. The percentage values for the crossed projections were: (a) for the entire caudate nucleus, 61.3% for the intact. 56.7% for the fetal-lesioned and 42.7% for the neonatal-lesioned cats, with no statistical differences between groups; (b) for the thalamus the proportion of crossed projections was minimal fluctuating between a low 0.06-0.16% for the nucleus ventralis lateralis and a high of 2.01-3.46% for the intralaminary nuclei, with the highest values belonging to the lesioned groups but with no significant differences between groups: (c) for the entire red nucleus, 1.98%, 12.74% (P < 0.05) and 6.76% for the intact, fetal- and neonatal-lesioned cats respectively. In the lesioned cats, the topography of the distribution of the axon terminals was bilaterally the same as in the controls. In conclusion, only the red nucleus of the frontal-lesioned cats showed an increased crossed innervation from the remaining sensorimotor cortex but this was relatively weak and statistically significant only for the fetal-lesioned animals. These results as well as the literature suggest that: (a) the crossed corticorubral projections in fetal cats may represent true reinnervation (i.e., newly originated, no preexisting terminals); (b) the relative paucity of the crossed projections in the present cats as compared to the extensive reorganization of subcortical terminals seen after cerebral hemispherectomy (our original postnatal lesion model) may be due to the much smaller size of the present cortical lesion which presumably induced only a limited amount of subcortical nuclear deafferentation.
Descriptors: brain mapping, caudate nucleus, frontal lobe, red nucleus, somatosensory cortex, thalamus, animals, newborn, cats, embryonic and fetal development, laterality, microinjections, neural pathways, somatosensory cortex embryology, somatosensory cortex growth and development.

Cartee, L.A. (2000). Evaluation of a model of the cochlear neural membrane. II: comparison of model and physiological measures of membrane properties measured in response to intrameatal electrical stimulation. Hearing Research 146(1-2): 153-66. ISSN: 0378-5955.
Abstract: This study examines existing equation sets describing neural membrane ionic currents, such as the Hodgkin-Huxley (1952) equations, used to define the membrane currents in a numerical model of the auditory neuron and determines their adequacy for modeling the summation and refraction properties of auditory neurons in response to electrical stimulation. Specifically, the summation and refraction time constants of each equation set are compared to physiological measures of these time constants. Since previous studies have shown the cell body and peripheral process of the auditory neuron may influence the measurement of neural time constants, the physiological time constants used for comparison are those which were recorded using intrameatal electrical stimulation. The intrameatal electrode should stimulate the neuron in an area where the axon has a uniform geometry. Accordingly, the neural model used to duplicate this experiment was also of uniform geometry. Of the membrane equation sets evaluated, none was clearly superior for modeling both the refraction and summation properties of the auditory neuron, though some equation sets were capable of accurately modeling either the refraction or the summation properties, provided operating temperatures were adjusted to provide appropriate kinetics.
Descriptors: cochlea innervation, cochlear nerve, models, neurological, auditory threshold, cats, cell membrane, cochlear implants, electric stimulation, evaluation studies, evoked potentials, auditory, brain stem, neurons.

Carter, T.J. (2004). Modelling management strategies to improve cat welfare. Animal Welfare 13(Supplement): S239. ISSN: 0962-7286.
NAL Call Number: HV4701 .A557
Descriptors: population studies, models and simulations, computational biology, matrix population model, mathematical and computer techniques, neutering , animal welfare, population growth, population management.

Chiu, Y.T., Y.T. Chen, N.N. Lin, C.C. Cheng, C.L. Gong, F.C. Cheng, S. Hsu, C.S. Chi, and Y.C. Fu (2005). Sympathetic activity and myocardial damage after stimulation of dorsal medulla and vagotomy in a novel animal model. International Journal of Cardiology 100(3): 401-7. ISSN: 0167-5273.
Abstract: Many kinds of brain lesions cause sympathetic hyperexcitation and myocardial damage. A novel animal model was developed for the correlation of sympathetic excitation with ventricular dysfunction and myocardial damage. Six cats (3.23+/-0.26 kg) under intraperitoneal urethane-chloralose anesthesia were artificially ventilated and bilaterally vagotomized. They underwent an electrical stimulation of unilateral dorsal medulla for 180 min (monopolar square-wave pulses, 10 Hz, 10 V, 0.5 ms). Mean blood pressure, heart rate plasma concentration of norepinephrine and left ventricular size and ejection fraction were measured at 0, 5, 15, 30, 60, 90, 120 and 180 min. Mean blood pressure (mm Hg), heart rate (beats/min) and norepinephrine (pg/ml) increased abruptly from 128+/-15, 203+/-22 and 353+/-123 to 234+/-26, 240+/-13 and 4727+/-2159 at 5 min after electrical stimulation (all p<0.01). The left ventricles showed significant dilatation (end-diastolic diameter: from 1.35+/-0.13 to 1.84+/-0.21 cm, p=0.006; end-systolic diameter: from 0.65+/-0.20 to 1.54+/-0.24 cm, p=0.002) and hypokinesia (ejection fraction: from 88.9+/-6.4% to 37.3+/-8.7%, p<0.001). Cardiac pathology revealed myocardial hemorrhage, cardiomyocyte apoptosis and coagulative myocytolysis (contraction band necrosis), characterized by sarcoplasmic coagulation, granulation and disruption. In conclusions, the present experiment develops a novel animal model in which stimulation of the pressor area in the dorsal medulla in vagotomized cats produces sympathetic hyperexcitation accompanied with myocardial dysfunction and damage. This model may be applicable for studying protective effect of drugs on myocardial dysfunction and damage caused by sympathetic hyperexcitation occurring in brain diseases.
Descriptors: cats, myocardial damage, dorsal medulla, vagotomy, electrical stimulation.

Chong, N.H., R.A. Alexander, K.C. Barnett, A.C. Bird, and P.J. Luthert (1999). An immunohistochemical study of an autosomal dominant feline rod/cone dysplasia (Rdy cats). Experimental Eye Research 68(1): 51-7. ISSN: 0014-4835.
Descriptors: apoptosis, photoreceptors, vertebrate, retina, retinal degeneration, animals, newborn, cats, cell count, animal disease models, glial fibrillary acidic protein, immunohistochemistry, in situ nick end labeling, opsin, photoreceptors, vertebrate, retina, retinal degeneration, rods retina, synaptopHysin, time factors.

Chong, N.H., R.A. Alexander, L. Waters, K.C. Barnett, A.C. Bird, and P.J. Luthert (1999). Repeated injections of a ciliary neurotrophic factor analogue leading to long-term photoreceptor survival in hereditary retinal degeneration. Investigative Ophthalmology and Visual Science 40(6): 1298-305. ISSN: 0146-0404.
Abstract: PURPOSE: To determine whether ciliary neurotrophic factor (CNTF) or brain-derived neurotrophic factor (BDNF) treatment leads to long-term photoreceptor survival in hereditary retinal degeneration. METHODS: An autosomal dominant feline model of rod-cone dystrophy was used throughout the study with two normal animals. In the first experiment, intravitreal injections of a human CNTF analogue (Axokine; Regeneron Pharmaceuticals, Tarrytown, NY) were administered to one eye of each animal (n = 10) beginning on postnatal day 10 and were repeated every 4 weeks. Clinical and histopathologic examinations were performed at 5.5, 9.5, and 13.5 weeks. In the second experiment, animals (n = 17) were randomly assigned to receive intravitreal injections of either Axokine (at half the initial dose), human BDNF, or the vehicle for Axokine to one eye at 5.5 weeks. The same therapy was repeated every 4 weeks in each group. Clinical and histopathologic examinations were performed at 9.5, 13.5, and 17.5 weeks. Photoreceptor survival was assessed by cell counting. Apoptotic cells were identified by morphology and a modified TdT-dUTP terminal nick-end labeling (TUNEL) technique. In the third experiment, two normal animals were treated with Axokine as in the first experiment. Glial fibrillary acidic protein ((GFAP) immunohistochemistry was performed to assess glial cell reaction. RESULTS: In the first two experiments, Axokine significantly prolonged photoreceptor survival (P < 0.01) and reduced the presence of apoptotic cells (P < 0.05) and TUNEL-positive cells (P < 0.05). In the second experiment, results in the the BDNF- and sham-injected eyes were not significantly different from those in the untreated eyes. Minimal posterior subcapsular cataract and mild retinal folds were found in all Axokine-treated eyes in both dystrophic and normal animals. These complications were milder in the second experiment when injections were started later and at a reduced dose. GFAP immunolabeling was also increased in all Axokine-treated eyes. CONCLUSIONS: Axokine, but not BDNF, delays photoreceptor loss in this hereditary retinal degeneration. Repeated injections maintain the protective effect.
Descriptors: ciliary neurotropHic factor, nerve tissue proteins, photoreceptors, vertebrate, photoreceptors, vertebrate, retinal degeneration, retinal degeneration, brain derived neurotropHic factor, cataract, cats, cell count, cell survival, cell survival, glial fibrillary acidic protein, immunohistochemistry, injections, photoreceptors, vertebrate, retina, retinal degeneration, retinitis pigmentosa, retinitis pigmentosa.

Chow, J.K., H.L. Seldon, and G.M. Clark (1995). Experimental animal model of intracochlear ossification in relation to cochlear implantation. The Annals of Otology, Rhinology and Laryngology 166: 42-5. ISSN: 0003-4894.
Descriptors: cochlea, cochlear implants, ossification, heterotopic, cats, evoked potentials, auditory, brain stem, ossification, heterotopic.

Chowdhury, V., J.W. Morley, and M.T. Coroneo (2004). Surface stimulation of the brain with a prototype array for a visual cortex prosthesis. Journal of Clinical Neuroscience 11(7): 750-755. ISSN: 0967-5868.
Abstract: We are developing a neural prosthesis to electrically stimulate the visual cortex to restore basic visual perceptions to blind patients. The effects on cortical excitation of different stimulus configurations using a prototype electrode array are presented. Cats underwent a bilateral craniotomy to expose the cortex. An array for brain stimulation was placed on the surface of the right hemisphere. Cortical stimulation was undertaken in a variety of configurations while measuring the evoked responses that propagated through transcallosal pathways, at a homologous region on the contralateral hemisphere. Cortical excitation elicited by stimulation with a particular paradigm could be assessed by measuring the spatial spread and amplitudes of evoked responses in the contralateral hemisphere. Results from this transcallosal model have allowed us to examine the spatial and amplitude effects of cortical stimulation with our prototype electrode array and will aid in developing a neuroprosthesis for blind patients.
Descriptors: neural prosthesis, visual cortex, vision, blindness.

Chowdhury, V., J.W. Morley, and M.T. Coroneo (2004). An in-vivo paradigm for the evaluation of stimulating electrodes for use with a visual prosthesis. The Australian and New Zealand Journal of Surgery 74(5): 372-8. ISSN: 1445-1433.
Abstract: BACKGROUND: Electrical stimulation of the visual cortex with surface electrodes is able to elicit basic visual perceptions in blind patients. The development of a visual prosthesis for the blind will require an in-vivo model for the optimization of cortical neurostimulation with multielectrode arrays. METHODS: In anaesthetized cats a bilateral craniotomy was performed and the dura was removed to expose the cerebral cortex. A prototype stimulating electrode array was placed on a gyrus in one hemisphere, and the transcallosal evoked response (TER) to cortical stimulation by this electrode array was recorded at a homologous region in the contralateral hemisphere. RESULTS: The stimulating electrode array elicited TER of short latency (6.9 ms) in the contralateral hemisphere. Bipolar stimulation of adjacent electrodes on the array evoked similar TER regardless of the polarity of stimulation. Electrodes spread apart on the array caused higher amplitude TER than electrodes placed close together. Multielectrode stimulation evoked lower amplitude TER than bipolar stimulation. CONCLUSIONS: This transcallosal model of cortical neurostimulation is a useful method to evaluate electrode arrays and stimulation techniques in the development of a visual prosthesis.
Descriptors: electric stimulation, electrodes, implanted, visual cortex, cats, pHospHenes.

Chung, K.I., T.S. Chung, R.D. White, H.J. Weinmann, T.H. Lim, B.I. Choi, and J.H. Suh (2001). Viable myocardium in reperfused acute myocardial infarction: rest and stress first-pass mr imaging. Journal of Korean Medical Science 16(3): 294-302. ISSN: 1011-8934.
Abstract: Feasibility of identifying viable myocardium in rest and stress magnetic resonance imaging (MRI) was evaluated using 3 hr occlusion and 30 min reperfusion model of left anterior descending (LAD) coronary artery in 12 felines. At rest MRI, viable myocardium confirmed by 2,3,5-triphenyl tetrazolium chloride (TTC)-staining showed rapid signal intensity (SI) rise followed by gradual decline not significantly different from normal myocardium that the two hyperperfused regions were distinguishable only from the hypoperfused nonviable myocardium. At stress MRI, hyperemia induced perfusion change was most pronounced in normal myocardium with earlier and greater peak enhancement followed by brisk 'washout' phase while minimally augmented enhancement in viable myocardium was still in 'washin' phase. From these findings, it was concluded that viable myocardium is identified in rest and stress MRI as redistributing hypo- perfusion compared to persistent hyper-perfusion of the normal myocardium and the persistent hypo-perfusion of the nonviable myocardium.
Descriptors: heart radiography, hyperemia radiography, myocardial infarction radiography, myocardial reperfusion injury radiography, cats, magnetic resonance imaging, stress.

Cloak, C.C., L. Chang, T. Ernst, M.C. Barr, S. Huitron Resendiz, M. Sanchez Alavez, T.R. Phillips, and S. Henriksen (2004). Methamphetamine and AIDS: Proton magnetic resonance studies in a feline model of human disease. Journal of Neuroimmunology 147(1-2): 16-20. ISSN: 0165-5728.
Abstract: Potential interactions between psychostimulant drugs and infection with feline immunodeficiency virus (FIV) on brain metabolism were evaluated. Four groups of cats were studied: control, FIV positive, methamphetamine (MA) exposed, and FIV positive plus MA exposed. Frontal gray matter, frontal white matter, and caudate brain extracts were studied with proton magnetic resonance spectroscopy (1HMRS). In the frontal white matter, FIV-infected cats showed decreases in creatine and choline, while MA-treated cats had elevated gamma-aminobutyric acid (GABA). The decreased glutamate in FIV cats normalized with MA exposure. FIV and MA both affect brain metabolites individually and combined. 1HMRS is useful for evaluating the effects of FIV and drug abuse in the brain.
Descriptors: acquired immunodeficiency syndrome, acquired immunodeficiency syndrome, brain, brain, feline immunodeficiency virus, magnetic resonance spectroscopy, methampHetamine, brain, brain, brain, cats, choline, creatine, animal disease models, infection, random allocation, gamma aminobutyric acid.

Collins, C.A. and J.E. Morgan (2003). Duchenne's muscular dystrophy: animal models used to investigate pathogenesis and develop therapeutic strategies. International Journal of Experimental Pathology 84(4): 165-72. ISSN: 0959-9673.
Abstract: Duchenne's muscular dystrophy (DMD) is a lethal childhood disease caused by mutations of the dystrophin gene, the protein product of which, dystrophin, has a vital role in maintaining muscle structure and function. Homologues of DMD have been identified in several animals including dogs, cats, mice, fish and invertebrates. The most notable of these are the extensively studied mdx mouse, a genetic and biochemical model of the human disease, and the muscular dystrophic Golden Retriever dog, which is the nearest pathological counterpart of DMD. These models have been used to explore potential therapeutic approaches along a number of avenues including gene replacement and cell transplantation strategies. High-throughput screening of pharmacological and genetic therapies could potentially be carried out in recently available smaller models such as zebrafish and Caenorhabditis elegans. It is possible that a successful treatment will eventually be identified through the integration of studies in multiple species differentially suited to addressing particular questions.
Descriptors: animal disease models, muscular dystrophy, animal, muscular dystrophy, duchenne, dogs, gene therapy, mice, mice, inbred MDX, muscular dystrophy, animal therapy, muscular dystrophy, duchenne therapy.

Cotter, L.A., H.E. Arendt, S.P. Cass, B.J. Jian, D.F.2. Mays, O.C.J. , K.A. Wilkinson, and B.J. Yates (2004). Effects of postural changes and vestibular lesions on genioglossal muscle activity in conscious cats. Journal of Applied Physiology 96(3): 923-30. ISSN: 8750-7587.
NAL Call Number: 447.8J825
Abstract: Previous studies in humans showed that genioglossal muscle activity is higher when individuals are supine than when they are upright, and prior experiments in anesthetized or decerebrate animals suggested that vestibular inputs might participate in triggering these alterations in muscle firing. The present study determined the effects of whole body tilts in the pitch (nose-up) plane on genioglossal activity in a conscious feline model and compared these responses with those generated by roll (ear-down) tilts. We also ascertained the effects of a bilateral vestibular neurectomy on the alterations in genioglossal activity elicited by changes in body position. Both pitch and roll body tilts produced modifications in muscle firing that were dependent on the amplitude of the rotation; however, the relative effects of ear-down and nose-up tilts on genioglossal activity were variable from animal to animal. The response variability observed might reflect the fact that genioglossus has a complex organization and participates in a variety of tongue movements; in each animal, electromyographic recordings presumably sampled the firing of different proportions of fibers in the various compartments and subcompartments of the muscle. Furthermore, removal of labyrinthine inputs resulted in alterations in genioglossal responses to postural changes that persisted until recordings were discontinued approximately 1 mo later, demonstrating that the vestibular system participates in regulating the muscle's activity. Peripheral vestibular lesions were subsequently demonstrated to be complete through the postmortem inspection of temporal bone sections or by observing that vestibular nucleus neurons did not respond to rotations in vertical planes.
Descriptors: consciousness, posture, tongue, vestibule, cats, pHaryngeal muscles.

Crawley, A.C., D.A. Brooks, V.J. Muller, B.A. Petersen, E.L. Isaac, J. Bielicki, B.M. King, C.D. Boulter, A.J. Moore, N.L. Fazzalari, D.S. Anson, S. Byers, and J.J. Hopwood (1996). Enzyme replacement therapy in a feline model of Maroteaux-Lamy syndrome. The Journal of Clinical Investigation 97(8): 1864-1873. ISSN: 0021-9738.
NAL Call Number: 448.8 J8295
Descriptors: disease models, recombination, mucopolysaccharidosis, enzymes, mucopolysaccharides, cats.

Crawley, A.C., K.H. Niedzielski, E.L. Isaac, R.C. Davey, S. Byers, and J.J. Hopwood (1997). Enzyme replacement therapy from birth in a feline model of mucopolysaccharidosis type VI. The Journal of Clinical Investigation 99(4): 651-62. ISSN: 0021-9738.
NAL Call Number: 448.8 J8295
Abstract: We report evidence of a dose responsive effect of enzyme replacement therapy in mucopolysaccharidosis type VI cats from birth, at the clinical, biochemical, and histopathological level. Cats treated with weekly, intravenous recombinant human N-acetylgalactosamine-4-sulfatase at 1 and 5 mg/kg, were heavier, more flexible, had greatly reduced or no spinal cord compression, and had almost normal urinary glycosaminoglycan levels. There was near normalization or complete reversal of lysosomal storage in heart valve, aorta, skin, dura, liver, and brain perivascular cells. No reduction in lysosomal vacuolation was observed in cartilage or cornea; however, articular cartilage was thinner and external ear pinnae were larger in some treated cats. Degenerative joint changes were not obviously delayed in treated cats. Skeletal pathology was reduced, with more normalized bone dimensions and with more uniform bone density and trabecular pattern clearly visible on radiographs by 5 to 6 mo; however, differences between 1 and 5 mg/kg dose rates were not clearly distinguishable. At a dose of 0.2 mg/kg, disease was not significantly altered in the majority of parameters examined. Lysosomal storage was present in all tissues examined in the midterm mucopolysaccharidosis type VI fetus and increased rapidly in extent and severity from birth.
Descriptors: chondro 4 sulfatase, mucopolysaccharidosis vi, animals, newborn, aorta, thoracic, aorta, thoracic ultrastructure, cats, chondro 4 sulfatase, chondro 4 sulfatase, animal disease models, disease progression, glycosaminoglycans urine, injections, intravenous, mitral valve, mitral valve ultrastructure, mucopolysaccharidosis vi, mucopolysaccharidosis vi radiography.

Crawley, A.C., G. Yogalingam, V.J. Muller, and J.J. Hopwood (1998). Two mutations within a feline mucopolysaccharidosis type VI colony cause three different clinical phenotypes. The Journal of Clinical Investigation 101(1): 109-19. ISSN: 0021-9738.
NAL Call Number: 448.8 J8295
Abstract: Mucopolysaccharidosis type VI (MPS VI) is a lysosomal storage disease caused by a deficiency of N-acetylgalactosamine-4-sulfatase (4S). A feline MPS VI model used to demonstrate efficacy of enzyme replacement therapy is due to the homozygous presence of an L476P mutation in 4-sulfatase. An additional mutation, D520N, inherited independently from L476P and recently identified in the same family of cats, has resulted in three clinical phenotypes. L476P homozygotes exhibit dwarfism and facial dysmorphia due to epiphyseal dysplasia, abnormally low leukocyte 4S/betahexosaminidase ratios, dermatan sulfaturia, lysosomal inclusions in most tissues including chondrocytes, corneal clouding, degenerative joint disease, and abnormal leukocyte inclusions. Similarly, D520N/D520N and L476P/D520N cats have abnormally low leukocyte 4S/betahexosaminidase ratios, mild dermatan sulfaturia, lysosomal inclusions in some chondrocytes, and abnormal leukocyte inclusions. However, both have normal growth and appearance. In addition, L476P/D520N cats have a high incidence of degenerative joint disease. We conclude that L476P/D520N cats have a very mild MPS VI phenotype not previously described in MPS VI humans. The study of L476P/D520N and D520N/ D520N genotypes will improve understanding of genotype to phenotype correlations and the pathogenesis of skeletal dysplasia and joint disease in MPS VI, and will assist in development of therapies to prevent lysosomal storage in chondrocytes.
Descriptors: mucopolysaccharidosis vi, mucopolysaccharidosis vi, mutation, arthrograpHy, cats, chondro 4 sulfatase, dermatan sulfate, animal disease models, genotype, joints, leukocytes, leukocytes, mucopolysaccharidosis vi, mucopolysaccharidosis vi radiography, pedigree, phenotype, beta n acetylhexosaminidase.

Crouser, E.D., M.W. Julian, D.V. Blaho, and D.R. Pfeiffer (2002). Endotoxin-induced mitochondrial damage correlates with impaired respiratory activity. Critical Care Medicine 30(2): 276-84. ISSN: 0090-3493.
Abstract: OBJECTIVE: This study was designed to determine whether mitochondrial function in a systemic organ is acutely impaired in a resuscitated model of sepsis (endotoxemia, lipopolysaccharide) and the relationship, if any, between this impairment and the extent of mitochondrial ultrastructural damage that occurs. DESIGN: Perspective, controlled laboratory investigation. SETTING: Animal laboratory in a university research institute. SUBJECTS: Adult male cats. INTERVENTIONS: A well-established feline model of acute endotoxemia was used wherein measures were taken to minimize tissue hypoxia. After lipopolysaccharide (3 mg/kg intravenously, n = 9) or isotonic saline vehicle (control, n = 5) administration, liver samples were obtained at 4 hrs posttreatment, and mitochondrial ultrastructure and respiratory function were assessed. Mitochondrial ultrastructural injury was graded on a scale of 0 (no injury) to 5 (severe injury), and mitochondrial respiration was evaluated by using standard techniques. MEASUREMENTS AND MAIN RESULTS: Significant mitochondrial injury was apparent by 4 hrs, but only in the lipopolysaccharide-treated group (2.5 +/- 0.2 vs. 1.3 +/- 0.2, p <.001) and despite maintenance of tissue oxygen availability. In addition, lipopolysaccharide treatment reduced the rate of state 3 (adenosine 5'-diphosphate-dependent) respiration, especially at complex IV (40% inhibition), and increased the rate of state 4 (adenosine 5'-diphosphate-independent) respiration, reflecting partial uncoupling of mitochondrial oxidative phosphorylation. Finally, a significant correlation was demonstrated between the severity of ultrastructural injury and the magnitude of mitochondrial respiratory dysfunction after lipopolysaccharide treatment and despite resuscitation efforts. CONCLUSION: Mitochondrial function is significantly impaired during acute sepsis, and this impairment is strongly associated with the extent of mitochondrial ultrastructural abnormalities present in the tissues. These findings in conjunction with those previously shown suggest that mitochondrial functional impairment may contribute to the pathogenesis of altered oxygen metabolism in systemic organs during sepsis.
Descriptors: mitochondria, liver, mitochondria, liver ultrastructure, mitochondrial diseases, oxidative phosphorylation, sepsis, cats, linear models, lipopolysaccharides, electron microscopy, oxygen, spectropHotometry.

Crouser, E.D., M.W. Julian, D.M. Weinstein, R.J. Fahy, and J.A. Bauer (2000). Endotoxin-induced ileal mucosal injury and nitric oxide dysregulation are temporally dissociated. American Journal of Respiratory and Critical Care Medicine 161(5): 1705-12. ISSN: 1073-449X.
Abstract: Despite recent investigations, the mechanisms responsible for intestinal epithelial injury during endotoxemia remain unclear. The present study tests the hypothesis that epithelial necrosis and/or apoptosis correlate with nitric oxide (NO) dysregulation in a nonischemic model of sepsis-induced ileal injury. To test this hypothesis, a well-established in situ, autoperfused, feline ileal preparation was employed. After endotoxin (lipopolysaccharide [LPS], 3 mg/ kg, intravenously; n = 9) or vehicle (control; n = 5) treatment, ileal segments were obtained at baseline, 2 and 4 h for simultaneous evaluations of cellular and mitochondrial ultrastructure, immunoprevalence of inducible nitric oxide synthase (iNOS) and 3-nitrotyrosine (a stable biomarker of peroxynitrite), and histochemical evidence of apoptosis. Epithelial necrosis was prominent by 2 h post-LPS, despite unaltered global ileal tissue oxygen content, blood volume, and blood flow. Significant evidence of apoptosis and increases in the immunoprevalence of iNOS and 3-nitrotyrosine were not evident until 4 h post-LPS. These results suggest that the early ileal mucosal necrosis may be due to LPS-induced activation of inflammatory pathways and/or microcirculatory disturbances, whereas NO dysregulation may participate in later events, including protein nitration and epithelial apoptosis.
Descriptors: ileum, intestinal mucosa, nitric oxide, sepsis, apoptosis, cats, ileum, ileum ultrastructure, immunohistochemistry, intestinal mucosa, lipopolysaccharides, mitochondria ultrastructure, multiple organ failure, multiple organ failure, multiple organ failure, necrosis, nitric oxide synthase analysis, oxygen consumption, sepsis, sepsis, tyrosine, tyrosine analysis.

Crouser, E.D., M.W. Julian, and P.M. Dorinsky (1999). Ileal vo2-do2 alterations induced by endotoxin correlate with severity of mitochondrial injury. American Journal of Respiratory and Critical Care Medicine 160(4): 1347-1353. ISSN: 1073-449X.
Descriptors: infection , respiratory system, respiration, mitochondrial injury, injury , sepsis , bacterial disease, endotoxin, in situ, feline ileum, cell injury.

Crowe, M.J., Z.P. Sun, J.H. Battocletti, M.Y. Macias, F.A. Pintar, and D.J. Maiman (2003). Exposure to pulsed magnetic fields enhances motor recovery in cats after spinal cord injury. Spine 28(24): 2660-6. ISSN: 0362-2436.
Abstract: STUDY DESIGN: Animal model study of eight healthy commercial cats was conducted. OBJECTIVE: To determine whether pulsed electromagnetic field (PMF) stimulation results in improvement of function after contusive spinal cord injury in cats. SUMMARY OF BACKGROUND DATA: PMF stimulation has been shown to enhance nerve growth, regeneration, and functional recovery of peripheral nerves. Little research has been performed examining the effects of PMF stimulation on the central nervous system and no studies of PMF effects on in vivo spinal cord injury (SCI) models have been reported. MATERIALS AND METHODS: PMF stimulation was noninvasively applied for up to 12 weeks to the midthoracic spine of cats with acute contusive spinal cord injury. The injury was produced using a weight-drop apparatus. Motor functions were evaluated with the modified Tarlov assessment scale. Morphologic analyses of the injury sites and somatosensory-evoked potential measurements were conducted to compare results between PMF-stimulated and control groups. RESULTS: There was a significant difference in locomotor recovery between the PMF-stimulated and control groups. Although not statistically significant, PMF-stimulated spinal cords demonstrated greater sparing of peripheral white matter and smaller lesion volumes compared to controls. Somatosensory-evoked potential measurements indicated that the PMF-stimulated group had better recovery of preinjury waveforms than the control group; however, this observation also was not statistically significant because of the small sample size. CONCLUSIONS: This preliminary study indicates that pulsed magnetic fields may have beneficial effects on motor function recovery and lesion volume size after acute spinal cord injury.
Descriptors: electromagnetic fields, spinal cord injuries therapy, acute disease, cats, evoked potentials, somatosensory, spinal cord injuries, spinal cord injuries, thoracic vertebrae, walking.

Curran, M.A., M.S. Ochoa, R.D. Molano, A. Pileggi, L. Inverardi, N.S. Kenyon, G.P. Nolan, C. Ricordi, and E.S. Fenjves (2002). Efficient transduction of pancreatic islets by feline immunodeficiency virus vectors. Transplantation 74(3): 299-306. ISSN: 0041-1337.
Descriptors: endocrine system, immune system, Diabetes Mellitus, pancreas, metabolic disease, feline immunodeficiency virus, immune system disease, islet cell survival, genetic engineering, transduction, green fluorescent protein.

D'Cruz, O.J., B. Waurzyniak, and F.M. Uckun (2004). Antiretroviral spermicide WHI-07 prevents vaginal and rectal transmission of feline immunodeficiency virus in domestic cats. Antimicrobial Agents and Chemotherapy 48(4): 1082-8. ISSN: 0066-4804.
Abstract: WHI-07 [5-bromo-6-methoxy-5,6-dihydro-3'-azidothymidine-5'-(p-bromophenyl)-methoxy alaninyl phosphate] is a novel dual-function aryl phosphate derivative of zidovudine with potent anti-human immunodeficiency virus (HIV) and spermicidal activities. WHI-07 was active against the feline immunodeficiency virus (FIV). This study evaluated whether topical application of WHI-07 as a single agent and in combination with an organometallic vanadium complex, vanadocene dithiocarbamate (VDDTC), via a nontoxic gel microemulsion can block vaginal as well as rectal transmission of feline AIDS (FAIDS) by chronically FIV-infected feline T cells in the natural host model. Genital transmission of FIV was monitored in recipient cats by the appearance of viral antibodies to FIV Gag proteins and by virus isolation of blood leukocytes as measured by FIV reverse transcriptase activity and FIV-specific PCR. Microbicidal activity was considered effective when the treated cats did not show evidence of FIV infection for up to 18 weeks postchallenge. An aggregate analysis of 46 specific-pathogen-free cats revealed that a single dose of the infected cell inoculum efficiently transmitted FIV infection when delivered into the vagina (100%) or rectum (66%). Pretreatment of the vagina or rectum with 2% WHI-07 alone or in combination with 0.25% VDDTC significantly (P = 0.004) protected cats from genital transmission by the highly infectious inoculum (7 million FIV(Bangston)-infected feline T cells). Collectively, using the vaginal and rectal transmucosal model for FAIDS, our studies demonstrated that WHI-07 either alone or in combination with a vanadocene has clinical potential for the development of a dual-function anti-HIV microbicide for sexually active women.
Descriptors: antiviral agents, feline acquired immunodeficiency syndrome, feline acquired immunodeficiency syndrome transmission, feline immunodeficiency virus, rectum, retroviridae, spermatocidal agents, thymidine monophosphate, thymidine monophosphate, vagina, zidovudine, zidovudine, cats, , combination, emulsions, gels, spermatocidal agents, thymidine monophosphate, vanadium compounds, zidovudine.

da Silva, M.C., J.M. Drake, C. Lemaire, A. Cross, and U.I. Tuor (1994). High-energy phosphate metabolism in a neonatal model of hydrocephalus before and after shunting. Journal of Neurosurgery 81(4): 544-53. ISSN: 0022-3085.
Abstract: The authors studied the effects of hydrocephalus on the high-energy phosphate metabolism of the brain and the impact of ventriculoperitoneal (VP) shunting on these changes in an experimental model of hydrocephalus. High-energy phosphate metabolism was analyzed using in vivo magnetic resonance (MR) imaging and 31P MR spectroscopy. Hydrocephalus was produced in 34 1-week-old kittens by cisternal injection of 0.05 ml of a 25% kaolin solution. Sixteen litter mates were used as controls. A VP shunt with a distal slit valve was implanted in 17 of the 34 hydrocephalic animals 10 days after induction of hydrocephalus. Both MR imaging and 31P MR spectroscopy were obtained 1 and 3 weeks after either kaolin or distilled water injection. Untreated hydrocephalic animals had marked dilatation of the lateral ventricles and periventricular edema. Magnetic resonance spectroscopy showed a significant decrease in the energy index ratio of phosphocreatine (PCR): inorganic phosphate (PI) and an increase in the PI:adenosine triphosphate (ATP) ratio. There was a direct correlation between the decrease in the energy index and ventricular size. Compared with preoperative scans, shunted animals showed no periventricular edema, and the ventricles decreased in size. Also, PCR:PI and PI:ATP ratios were within the levels of controls. This study suggests that neonatal hydrocephalus results in a mild hypoxic/ischemic insult that is treatable by VP shunting.
Descriptors: adenosine triphosphate, hydrocepHalus, hydrocepHalus surgery, phosphates, phosphocreatine, ventriculoperitoneal shunt, animals, newborn, cats, animal disease models, magnetic resonance spectroscopy.

Dahlem, M.A., R. Engelmann, S. Lowel, and S.C. Muller (2000). Does the migraine aura reflect cortical organization? European Journal of Neuroscience 12(2): 767-70. ISSN: 0953-816X.
Abstract: Individuals suffering from classical migraine report an astonishing diversity of migraine auras. A frequently reported symptom is a visual hallucination known as fortification illusion (FI). Here we demonstrate that the typical zig-zag pattern of the FI can be reproduced using experimental data of orientation maps of the primary visual cortex (V1) assuming that a continuous excitation front propagates across V1. We put forward a model in which the cortical neurons within this excitation wave are activated sufficiently to contribute to conscious perception. It is shown that the discontinuous repetitive nature of the zig-zag pattern of the FI can reflect the specific layout of visual cortical orientation maps. Additionally, dynamic features of the FI are predicted based on our model.
Descriptors: classic migraine, scotoma, spreading cortical depression, visual cortex, brain mapping, cats, electrophysiology, epilepsy, models, neurological.

Dawson, A.N., B. Walser, M. Jafarzadeh, and C.L. Stebbins (2004). Topical analgesics and blood pressure during static contraction in humans. Medicine and Science in Sports and Exercise 36(4): 632-638. ISSN: 0195-9131.
Descriptors: cardiovascular system, anlgesic balm, cats, pressure, brachial artery flow, heart rate, static contraction.

de Groot Mijnes, J.D., J.M. van Dun, R.G. van der Most, and R.J. de Groot (2005). Natural history of a recurrent feline coronavirus infection and the role of cellular immunity in survival and disease. Journal of Virology 79(2): 1036-44. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Abstract: We describe the natural history, viral dynamics, and immunobiology of feline infectious peritonitis (FIP), a highly lethal coronavirus infection. A severe recurrent infection developed, typified by viral persistence and acute lymphopenia, with waves of enhanced viral replication coinciding with fever, weight loss, and depletion of CD4+ and CD8+ T cells. Our combined observations suggest a model for FIP pathogenesis in which virus-induced T-cell depletion and the antiviral T-cell response are opposing forces and in which the efficacy of early T-cell responses critically determines the outcome of the infection. Rising amounts of viral RNA in the blood, consistently seen in animals with end-stage FIP, indicate that progression to fatal disease is the direct consequence of a loss of immune control, resulting in unchecked viral replication. The pathogenic phenomena described here likely bear relevance to other severe coronavirus infections, in particular severe acute respiratory syndrome, for which multiphasic disease progression and acute T-cell lymphopenia have also been reported. Experimental FIP presents a relevant, safe, and well-defined model to study coronavirus-mediated immunosuppression and should provide an attractive and convenient system for in vivo testing of anticoronaviral drugs.
Descriptors: feline infectious peritonitis, cd8 positive t lymphocytes, cats, coronavirus, feline, feline infectious peritonitis mortality, feline infectious peritonitis, cellular immunity, lymphopenia, virus replication, weight loss.

de Groote, D.H.F., R. Ducatelle, and L. Devriese (1997). Helicobacter spp. en gastro-intestinale problemen bij dieren [Helicobacter spp. and gastrointestinal diseases in animals]. Vlaams Diergeneeskundig Tijdschrift 66(1): 8-13. ISSN: 0303-9021.
NAL Call Number: 41.8 V84
Abstract: The genus Helicobacter is a relatively new genus that thanks his origin to the discovery of Helicobacter pylori in the human stomach in 1984 by Marshall and Warren. A world-wide scientific interest for H. pylori emerged when the relationship between the presence of this bacterium and the occurrence of peptic ulcers, chronic gastritis and gastric carcinoma was proven. In the search of a suitable animal model, several additional Helicobacter spp. were found in animals (f.i. in cats, dogs, pigs, cows, mice, rats, ferrets, cheetahs, monkeys and chickens). Recent publications have raised the possibility that these animal Helicobacter spp. could also have a pathogenic significance in the onset of gastro-intestinal diseases. Further research is needed to elucidate this issue.This article aims to give an overview on the literature about this subject.
Descriptors: omestic animals, pet animals, bacterioses, gastrointestinal agents, human diseases, zoonoses, Helicobacter.
Language of Text: Dutch with summaries in English and Dutch.

De Maria, R., M. Olivero, S. Iussich, M. Nakaichi, T. Murata, B. Biolatti, and M.F. Di Renzo (2005). Spontaneous feline mammary carcinoma is a model of HER2 overexpressing poor prognosis human breast cancer. Cancer Research 65(3): 907-12. ISSN: 0008-5472.
NAL Call Number: 448.8 C16
Abstract: Companion animal spontaneous tumors are suitable models for human cancer, primarily because both animal population and the tumors are genetically heterogeneous. Feline mammary carcinoma (FMC) is a highly aggressive, mainly hormone receptor-negative cancer, which has been proposed as a model for poor prognosis human breast cancer. We have identified and studied the feline orthologue of the HER2 gene, which is both an important prognostic marker and therapeutic target in human cancer. Feline HER2 (f-HER2) gene kinase domain is 92% similar to the human HER2 kinase. F-HER2-specific mRNA was found 3- to 18-fold increased in 3 of 3 FMC cell lines, in 1 of 4 mammary adenomas and 6 of 11 FMC samples using quantitative reverse transcription-PCR. Western blot showed that an anti-human HER2 antibody recognized a protein comigrating with the human p185HER2 in FMC cell lines. The same antibodies strongly stained 13 of 36 FMC archival samples. These data show that feline HER2 overexpression qualifies FMC as homologous to the subset of HER2 overexpressing, poor prognosis human breast carcinomas and as a suitable model to test innovative approaches to therapy of aggressive tumors.
Descriptors: breast neoplasms, breast neoplasms, genes, erbb 2, receptor, erbb 2 biosynthesis, breast neoplasms, breast neoplasms, cats, cell line, tumor, animal disease models, immunohistochemistry, mammary glands, animal, prognosis, RNA, messenger biosynthesis, RNA, messenger, receptor, erbb 2, reverse transcriptase polymerase chain reaction.

DeBoer, D.J. and K.A. Moriello (1994). Development of an experimental model of Microsporum canis infection in cats. Veterinary Microbiology 42(4): 289-295. ISSN: 0378-1135.
NAL Call Number: SF601. V44
Descriptors: cats, microsporum, ringworm, dermatomycoses , deuteromycotina , fungi , infectious diseases, mycoses , organic diseases, skin diseases.

Delgado Garcia, J.M., A. Gruart, and J.A. Trigo (2003). Physiology of the eyelid motor system. Annals of the New York Academy of Sciences 1004: 1-9. ISSN: 0077-8923.
NAL Call Number: 500 N484
Abstract: The eyelid motor system represents an excellent experimental model for the study of reflex and learned motor responses. Eyelid responses can be recorded quantitatively with the search coil in a magnetic-field technique. Stimuli able to evoke reflex blinks (air puffs, flashes of light, tones) can also be controlled quantitatively. Eyelid movements can be classified as spontaneous, passive (such as those following eye saccades), reflex, and acquired with classical conditioning procedures. Information is available regarding the firing activity of brainstem motoneuronal pools (abducens, accessory abducens, and facial motoneurons) involved in these types of eyelid response. In particular, facial motoneurons present different encoding properties for the generation of reflex against learned eyelid responses. In cats, accessory abducens motoneurons are involved only in reflex (but not in learned) blinks. The recent description of the complete organization of premotoneuronal pathways related to eyelid motorics opens new experimental possibilities for the study of this particular motor system.
Descriptors: eyelids, motor neurons, ocular, abducens nerve, blinking, conditioning, eyelid, eyelids innervation, oculomotor muscles innervation, oculomotor muscles, proprioception.

Destexhe, A., D. Contreras, T.J. Sejnowski, and M. Steriade (1994). A model of spindle rhythmicity in the isolated thalamic reticular nucleus. Journal of Neurophysiology 72(2): 803-18. ISSN: 0022-3077.
Abstract: 1. The oscillatory properties of the isolated reticular (RE) thalamus were modeled with the use of compartmental models of RE cells. Hodgkin-Huxley type kinetic models of ionic channels were derived from voltage- and current-clamp data from RE cells. Interactions between interconnected RE cells were simulated with the use of a kinetic model of gamma-aminobutyric acid (GABA) inhibitory synapses. 2. The intrinsic bursting properties of RE cells in the model were due to the presence of a low-threshold Ca2+ current and two Ca(2+)-activated currents. The properties of these model RE cells were compared with RE neurons recorded intracellularly in vivo in cats. 3. Model RE cells densely interconnected with GABAA synapses produced synchronous oscillations at a frequency close to that of spindles (7-14 Hz). Networks of RE neurons organized in a two-dimensional array with only proximal connectivity also exhibited synchronized oscillations in the spindle range. In addition, the proximally connected network showed periods of high and low synchronicity, giving rise to waxing and waning oscillations in the population of RE cells. 4. The spatiotemporal behavior of the network was investigated during waxing and waning oscillations. The waxing and waning emerged as an alternation between periods of desynchronized and synchronized activity, corresponding to periods of irregular and coherent spatial activity. During synchronized periods, the network displayed propagating coherent waves of synchronous activity that had a tendency to form spirals. 5. Networks of model RE neurons fully connected through GABAB synapses exhibited perfectly synchronous oscillations at lower frequencies (0.5-1 Hz), but two-dimensional networks with proximal GABAB connectivity failed to synchronize. 6. These simulations demonstrate that networks of model neurons that include the main intrinsic currents found in RE cells can generate waxing and waning oscillatory activity similar to the spindle rhythmicity observed in the isolated RE nucleus in vivo. The model reveals the interplay between the intrinsic rhythmic properties of RE cells and the fast synaptic interactions in organizing synchronized rhythmicity.
Descriptors: ion channels, neural networks computer, synaptic transmission, thalamic nuclei, afferent pathways, calcium channels, cats, cerebral cortex, electroencephalography, membrane potentials, nerve net, neural inhibition, potassium channels, receptors, gaba b, sleep stages, synapses, gamma aminobutyric acid.

Dithmar, S., D.M. Albert, and H.E. Grossniklaus (2000). Animal models of uveal melanoma. Melanoma Research 10(3): 195-211. ISSN: 0960-8931.
Abstract: Many attempts have been made to develop a suitable animal model to study more effectively the aetiology, pathogenesis, diagnosis and therapy of intraocular (uveal) melanoma. Uveal melanoma may spontaneously occur in some animals, including dogs, cats, horses, rats, mice, birds and fish. The histological features, metastatic behaviour and unpredictable nature of occurrence of these uncommon spontaneous tumours detract from their suitability as a model. Several methods have been developed to induce intraocular melanoma chemically or by radiation in laboratory animals. Some of these induced tumours resemble human uveal melanoma, although the majority originate from the retinal pigment epithelium. Uveal proliferations have been biologically induced by feline leukaemia/sarcoma virus and simian virus 40, although the presence of virus in tumour cells and extraocular tumours resulting from shed virus detract from the utility of this model. Inoculation of tissue culture hamster, murine or human melanoma cells into animal eyes has the advantage that the inoculation site and size of inoculum can be controlled. Disadvantages include the immune suppression necessary for tumour growth in some models as well as the fact that many of the melanoma cell lines are of cutaneous origin. Transgenic murine models have been developed using the promoter region of the tyrosinase gene to target expression of oncogenes in melanin-producing cells. Spontaneous intraocular pigmented tumours and distant metastases may occur, although many, if not all, of the intraocular tumours arise in the retinal pigment epithelium.
Descriptors: animal disease models, melanoma, uveal neoplasms, cats, chick embryo, hamsters, mice, transgenic, neoplasm transplantation, rabbits.

Dolgikh, V.G. and V.K. Reshetniak (1994). Povedencheskie priznaki neiropaticheskoi boli u koshek vsledstvie kompressii infraorbital'nogo nerva. [Behavioral signs of neuropathic pain in cats due to compression of the infraorbital nerve]. Patologicheskaia Fiziologiia i Eksperimental'Naia Terapiia(3): 13-4. ISSN: 0031-2991.
Abstract: The changes in behavioral reactions were studied in cats after incomplete compression of the infraorbital nerve by means of two ligatures as a model of trigeminal neuropathy. It was found that there appeared a behaviour protective the damaged side of the face, sudden standstills of the animals which threw their head back and raised their anterior paws to the face, as well as inhibition of motor activity. Decreases in the nociceptive threshold and the threshold of emotionally affective responses to lip electrostimulation as the sensory threshold increased. These behavioral changes are regarded as signs of spontaneous pain and hyperalgesia in animals with nerve compression, and the used model is considered to be adequate for studying the mechanisms of neuropathic pain.
Descriptors: animal behavior, nerve compression syndromes psychology, orbit innervation, pain psychology, cats.
Language of Text: Russian.

Dominy, B.N. and C.L.I. Brooks (1999). Methodology for protein-ligand binding studies: application to a model for drug resistance, the hiv/fiv protease system. Proteins 36(3): 318-331. ISSN: 0887-3585.
NAL Call Number: QP551.P698
Descriptors: enzymology, drug resistance, empirical free energy function, validation , protein ligand binding, human immunodeficiency virus feline immunodeficiency virus protease system, model system.

Doppenberg, E.M., J.C. Watson, R. Bullock, M.J. Gerber, A. Zauner, and D.J. Abraham (1997). The rationale for, and effects of oxygen delivery enhancement to ischemic brain in a feline model of human stroke. Annals of the New York Academy of Sciences 825: 241-57. ISSN: 0077-8923.
NAL Call Number: 500. N484
Abstract: Reduced brain tissue oxygenation is frequently seen in severe head injury and after subarachnoid hemorrhage, and this is considered a major cause of secondary ischemic brain injury. In fact, in a previous study, we found a tight correlation between low brain tissue oxygen tension and poor outcome. Therefore, we tested the hypothesis that an allosteric modifier of hemoglobin, which improves oxygen transport to tissue, could reduce the size of an acute infarct in a feline model of human stroke. This compound produces a shift in the hemoglobin dissociation curve to the right and therefore facilitates the unloading of oxygen during low oxygen tension. Seventeen adult cats were studied. Ischemic stroke was induced through a transorbital, permanent, middle cerebral artery occlusion. Seven animals received saline, and 10 received the allosteric Hb modifier RSR-13. Three different endpoints were used to determine the effect of the allosteric modifier. Delta p50 values were measured in the arterial blood; the intra-infarct oxygen tension was measured, and finally, the volume of the infarct was assessed using TTC staining. Mean delta p50 changes varied from 10.4 +/- 9.2 mmHg up to 15.0 +/- 6.8 mmHg. Mean intra-infarct oxygen tension was 27 +/- 6 mmHg for the control group and 33 +/- 7 mmHg for the drug-treated animals. The mean infarct size (measured as percentage of hemisphere volume) in the control group was 32 +/- 9% and for the RSR-13 animals 22 +/- 10% (p < 0.05). A definitive trend towards improvement in brain oxygen tension was seen, such that animals pretreated with RSR-13 showed a higher infarct oxygen tension. Infarct size was significantly reduced in the drug group. Therefore, RSR-13 is potentially beneficial in the treatment of brain ischemia. Since human studies with this compound are already completed, and other compounds which increase oxygen delivery, such as perfluorocarbons, are already being evaluated, it is likely that oxygen delivery enhancement will rapidly become the first 'neuroprotective' modality, employed in patients with severe brain injury, stroke and subarachnoid hemorrhage.
Descriptors: aniline compounds, brain, brain ischemia, cerebral hemorrhage, oxygen, oxygen consumption, propionic acids, adult, aged, brain, brain injuries, brain injuries radiography, brain injuries surgery, brain ischemia, cats, cerebral hemorrhage radiography, cerebral hemorrhage surgery, cerebral infarction, cerebral infarction, clofibrate, animal disease models, hematoma, subdural, hematoma, subdural radiography, hematoma, subdural surgery, oxyhemoglobins, tomography, x ray computed.

Drici, M.D., W.X. Wang, X.K. Liu, R.L. Woosley, and D.A. Flockhart (1998). Prolongation of QT interval in isolated feline hearts by antipsychotic drugs. Journal of Clinical Psychopharmacology 18(6): 477-81. ISSN: 0271-0749.
Abstract: Some antipsychotic drugs have been found to prolong the QT interval on electrocardiographic (ECG) recordings, a phenomenon which, when severe, may facilitate the occurrence of complex ventricular arrhythmias such as torsade de pointes. However, the effects of these drugs on the cardiac repolarization process have not been evaluated extensively. This study was designed to examine the potency of five antipsychotic drugs in lengthening the QT interval of the perfused feline heart: haloperidol, risperidone, sertindole, clozapine, and olanzapine. The hearts were infused with increasing concentrations of drugs (0.1-20 micromol/L) for 40-minute intervals at each concentration. ECG recordings were made, with signals amplified and data recorded on a strip chart recorder. Four representative beats from each set of three signal recordings were chosen for QT interval measurement. Our data indicated that all tested drugs prolonged the QT interval in a concentration-dependent manner (p < 0.01). Haloperidol and risperidone were significantly more potent than sertindole, clozapine, and olanzapine (p < 0.001). At a concentration of 0.5 micromol/L over a 40-minute infusion interval, haloperidol lengthened the interval by 26.2+/-0.7%, risperidone by 19.4+/-2.2%, and sertindole by 8.9+/-3.5% (p < 0.05 compared with baseline); clozapine and olanzapine were less potent. Although species differences may limit extrapolation of our findings to humans, the cardiac potassium channels of felines clearly resemble those of humans. This model may serve as the basis for further studies of drug-induced prolongation of the QT interval and precipitation of ventricular arrhythmias.
Descriptors: antipsychotic agents, electorcardiography, heart, analysis of variance, antipsychotic agents, antipsychotic agents, cats, clozapine, haloperidol, heart, imidazoles, indoles, risperidone.

Eckhorn, R., A. Stett, T. Schanze, F. Gekeler, H. Schwahn, E. Zrenner, M. Wilms, M. Eger, and L. Hesse (2001). Physiologische Funktionsprufungen von Retinaimplantaten an Tiermodellen [Physiological functional evaluation of retinal implants in animal models]. Der Ophthalmologe Zeitschrift Der Deutschen Ophthalmologischen Gesellschaft 98(4): 369-375. ISSN: 0941-293X.
Abstract: Retinal implants can--by electrical stimulation--create visual impressions in people with certain kinds of degenerative retinal diseases (e.g. Retinitis Pigmentosa). Electrically evoked potentials in the retina must be transferred into the visual cortex in an orderly manner, a prerequisite for any kind of form- and movement-perception. In the current developmental stage the difficult investigations are performed in various animal models: isolated retinae of intact chicken and of RCS-rats (a model for Retinitis Pigmentosa), as well as in anesthetised rabbits, pigs and cats with intact retinae. Our investigations show that spatially selective ganglion-cell responses can be recorded following focal electrical stimulation, in healthy and as well in degenerated retinae. Registration of activities in area 17 of the visual cortex demonstrate that electrical retinal stimulation can indeed activate it.
Descriptors: animal disease models, implants, microcomputers, microelectrodes, prosthesis implantation, retina surgery, retinal degeneration rehabilitation, visual cortex, chickens, evoked potentials, visual, prosthesis design, rabbits, rats, retina, retinal degeneration, swine, synaptic transmission, visual pathways.
Language of Text: German.

Elder, J.H. and T.R. Phillips (1995). Feline immunodeficiency virus as a model for development of molecular approaches to intervention strategies against lentivirus infections. Advances In Virus Research 45: 225-247. ISSN: 0065-3527.
NAL Call Number: 448.8 Ad9
Descriptors: lentivirinae, mankind, herpetoviridae, models, genomes, animal viruses, proteins, nucleotide sequence, chemical composition, genomes , retroviridae , viruses , long term repeats, open reading frames, human immunodeficiency virus, disease models, amino acid sequences, comparisons .

English, R.V., P. Nelson, C.M. Johnson, M. Nasisse, W.A. Tompkins, and M.B. Tompkins (1994). Development of clinical disease in cats experimentally infected with feline immunodeficiency virus. The Journal of Infectious Diseases 170(3): 543-52. ISSN: 0022-1899.
NAL Call Number: 448.8 J821
Abstract: Cats naturally infected with feline immunodeficiency virus (FIV) develop an AIDS-like syndrome whereas experimentally infected cats do not. To investigate the role of cofactors in the development of this disease in cats, 7 specific pathogen-free (SPF) and 12 random-source (RS) cats were infected with FIV. Over 4 years, infected cats developed similar phenotypic and functional immune abnormalities characterized by early and chronic inversion of CD4+:CD8+ cell ratios and significantly decreased mitogen responses compared with controls. Beginning 18-24 months after infection, 10 RS cats developed chronic clinical disease typical of feline AIDS, including stomatitis and recurrent upper respiratory disease; 4 SPF cats also developed chronic clinical disease, 2 with neurologic disease and 2 with B cell lymphomas. Thus, immunologic background is important in the type of disease that develops in cats infected with FIV, and FIV represents a promising animal model for studying the immunopathogenesis of AIDS in humans.
Descriptors: feline acquired immunodeficiency syndrome, feline immunodeficiency virus pathogenicity, lymphocyte activation, lymphocyte subsets, antibody formation, b lymphocytes, Southern blot, cd4 cd8 ratio, cats, feline acquired immunodeficiency syndrome, feline acquired immunodeficiency syndrome, feline immunodeficiency virus, polymerase chain reaction, time factors.

Eppihimer, M.J. and R.G. Schaub (2001). Soluble P-selectin antagonist mediates rolling velocity and adhesion of leukocytes in acutely inflamed venules. Microcirculation 8(1): 15-24. ISSN: 1073-9688.
Abstract: OBJECTIVE: Leukocyte rolling is recognized as an important event in facilitating the extravasation of leukocytes from the vascular to the interstitial compartment, and is mediated by the selectin family of cell adhesion molecules. The aim of this study was to evaluate and characterize the rolling behavior of leukocytes in a model of acute inflammation using a novel soluble selectin ligand directed against P-selectin. METHODS: Feline mesenteric postcapillary venules were visualized using intravital microscopy prior to and following exposure to leukotriene C4 (LTC4) in animals pretreated with vehicle (saline) and the P-selectin antagonist rPSGL-Ig. RESULTS: A concentration of 500 pM LTC4 induced a threefold and sixfold elevation in leukocyte rolling flux and adhesion, respectively, compared to baseline values (p < 0.05). Administration of rPSGL-Ig had no effect on LTC4-induced leukocyte rolling flux but significantly attenuated the increase in the fraction of rolling leukocytes (p < 0.05). In addition, rPSGL-Ig inhibited the LTC4-induced reductions in leukocyte rolling velocity (p < 0.001). Finally, LTC4-induced leukocyte adhesion in animals pretreated with rPSGL-Ig was reduced by 60%, compared to vehicle-treated animals (p < 0.05). CONCLUSIONS: LTC4 induces leukocyte rolling and adhesion in feline mesenteric venules in a dose-dependent manner. Administration of rPSGL-Ig inhibits LTC4-induced reductions in leukocyte rolling velocity and attenuates the elevation in the fraction of rolling leukocytes produced by LTC4 stimulation. This suggests that rPSGL-Ig may be used to reduce leukocyte rolling and adhesion, and subsequently attenuate tissue injury during inflammation.
Descriptors: inflammation, leukocytes, p selectin, amino acid sequence, cats, cell adhesion, cell movement, animal disease models, ileukotriene c4, membrane glycoproteins, mesenteric veins, molecular sequence data, phlebitis, recombinant proteins, solubility, venules.

Erickson, C.H., R.L. McLeod, G.G. Mingo, R.W. Egan, O.F. Pedersen, and J.A. Hey (2001). Comparative oral and topical decongestant effects of phenylpropanolamine and d-pseudoephedrine. American Journal of Rhinology 15(2): 83-90. ISSN: 1050-6586.
Abstract: Nonselective adrenergic alpha-agonists such as phenylpropanolamine and d-pseudoephedrine are widely used as decongestants to treat nasal congestion associated with a variety of nasal diseases. Although the activity of these drugs is well established in clinical studies, a direct comparison of their nasal decongestant effect as determined by changes in nasal cavity dimensions and nasal architecture has not been studied. Using acoustic rhinometry, we evaluated the effects of these drugs on nasal cavity volume, minimum cross-sectional area (Amin), and the distance from the nosepiece to the Amin (Dmin) in a feline, pharmacological model of nasal congestion. Administration of topical compound 48/80 (1%), a mast cell histamine liberator, into the left nasal passageway decreased nasal volume by 66%, reduced Amin by 51%, and increased Dmin by 116%. The congestive responses to compound 48/80 (1%) were reproducible through six weeks. In a subset of cats, the nasal cavity volume effect of repetitive exposure to compound 48/80, given once every two weeks for six weeks, was not different from the nasal responses after the initial exposure to compound 48/80. Pretreatment with oral phenylpropanolamine (10 mg/kg) or oral d-pseudoephedrine (10 mg/kg) attenuated the nasal effects of compound 48/80, but were associated with a pronounced increase in systolic blood pressure of +51 and +82 mmHg, respectively. A similar decongestant profile was observed with phenylpropanolamine (1%) and d-pseudoephedrine (1%) when given topically. Topical phenylpropanolamine (1%) and d-pseudoephedrine (1%) 45 minutes after dosing increased blood pressure +44 and +17 mmHg, respectively, over control animals. We conclude that oral and topical phenylpropanolamine and d-pseudoephedrine display equieffective nasal decongestant activity and produce similar cardiovascular profiles characterized by significant increases in blood pressure.
Descriptors: adrenergic alpha agonists, epHedrine, nasal decongestants, nasal obstruction, pHenylpropanolamine, oral administration, topical administration, pressure, cats, animal disease models, histamine release, nasal cavity, nasal obstruction.

Esteves, M.I., M.D. Schrenzel, R.P. Marini, N.S. Taylor, S. Xu, S. Hagen, Y. Feng, Z. Shen, and J.G. Fox (2000). Helicobacter pylori gastritis in cats with long-term natural infection as a model of human disease. American Journal of Pathology 156(2): 709-721. ISSN: 0002-9440.
NAL Call Number: 448.8
Descriptors: Helicobacter pylori infection, bacterial disease, lymphofollicular atropHic gastritis, digestive system disease, mucosal dysplasia.

Evans, M.D.M., R.Z. Xie, M. Fabbri, M.C. Madigan, H. Chaouk, G.J. Beumer, G.F. Meijs, H.J. Griesser, J.G. Steele, and D.F. Sweeney (2000). Epithelialization of a synthetic polymer in the feline cornea: a preliminary study. Investigative Ophthalmology and Visual Science 41(7): 1674-1680. ISSN: 0146-0404.
Descriptors: biomaterials, feline corneas, corneal transplant model, eye research, perfluoropolyether polymer, sense organs, implant, sensory reception, lenticules, epithelial growth, adhesion, collagen I, ultrastructure .

Fan, L.L., J. Ma, Y.F. Wang, Y.M. Ruan, and X.K. Zeng (2005). Effects of oxyphenamone on myocardial ischemia in cats and rats. Yao Xue Xue Bao [Acta Pharmaceutica] 40(2): 122-126. ISSN: 0513-4870.
Abstract: AIM: To study the therapeutic effects of oxyphenamone, a novel inodilator, on myocardial ischemia. METHODS: The cardiac hemodynamic variables in cats with acute myocardial infarction induced by occlusion of the left anterior descending coronary artery (LAD) were recorded with a physiological polygraph and electromagnetic flowmeter. A model of myocardial necrosis induced by subcutaneous injection of isoproterenol was used for evaluating the effects of drugs on myocardial enzymes and morphological change. RESULTS: Intravenous injection of oxyphenamone (2 - 8 mg x kg(-1)) dose-dependently decreased heart rate, mean arterial pressure, vascular resistance and the parameters of myocardial oxygen consumption (tension time index, TTI) in cats with myocardial infarction. It increased myocardial contractile force and cardiac output transiently but showed no influence on the left ventricular pressure and cardiac work. The changes of myocardial morphology, creatine phosphate kinase (CPK), malodialdehyde (MDA) and serum glutamic-oxaloacetic transaminase (GOT) induced by isoproterenol in rats were diminished by intraperitoneal injection of oxyphenamone (4 - 8 mg x kg(-1)). CONCLUSION: By the examination of the cardiac hemodynamics, myocardial enzymes and morphology, it showed that the myocardial damage induced by ischemia or beta-agonist can be antagonized markedly by oxyphenamone, indicating that oxyphenamone may be beneficial for the treatment of myocardial infarction.
Descriptors: oxyphenamone, inodilator, heart, infarction, model, myocardial necrosis, enzymes, malondialdehyde, GOT, CPK, cats.
Language of Text: Chinese.

Federico, S., G. La Rosa, W. Herzog, and J.Z. Wu (2004). Effect of fluid boundary conditions on joint contact mechanics and applications to the modeling of osteoarthritic joints. Journal of Biomechanical Engineering 126(2): 220-5. ISSN: 0148-0731.
Abstract: The long-term goal of our research is to understand the mechanism of osteoarthritis (OA) initiation and progress through experimental and theoretical approaches. In previous theoretical models, joint contact mechanics was implemented without consideration of the fluid boundary conditions and with constant permeability. The primary purpose of this study was to investigate the effect of fluid boundary conditions at the articular surfaces on the contact mechanics, in terms of load sharing and fluid flow properties using variable permeability. The tested conditions included totally sealed surfaces, open surfaces, and open surfaces with variable permeability. While the sealed surface model failed to predict relaxation times and load sharing properly, the class of open surface models (open surfaces with constant permeability, and surfaces with variable permeability) gave good agreement with experiments, in terms of relaxation time and load sharing between the solid and the fluid phase. In particular, the variable permeability model was judged to be the most realistic of the three models, from a biological and physical point of view. This model was then used to simulate joint contact in the early and late stages of OA. In the early stages of OA, the model predicted a decrease in peak contact pressure and an increase in contact area, while in the late stages of OA, peak pressures were increased and contact areas were decreased compared to normal. These findings agree well with experimental observations.
Descriptors: cartilage, articular, joints, osteoarthritis, synovial fluid, weight bearing, biomechanics, cats, computer simulation, elasticity, biological models, porosity, pressure, surface properties.

Fernandez Guardiola, A., A. Martinez, and R. Fernandez Mas (1995). Repeated penicillin-induced amygdala epileptic focus in freely moving cats. EEG, polysomnographic (23-h recording), and brain mapping study. Epilepsy Research 22(2): 127-36. ISSN: 0920-1211.
Abstract: The effect of repeated Na-penicillin (PCN) microinjections in the temporal lobe amygdala (AM) of free-moving cats was investigated in order to establish if kindling epileptogenesis is possible with this procedure. The cortical propagation of the PCN-induced post-discharge in AM and the sequence of behavioral changes induced by PCN were similar to those of AM electrical kindling. Nevertheless, the epileptogenic effect of PCN had a different evolution from that of electrical kindling, since some PCN habituation was observed after several doses. Repeated microinjections of PCN did not produce lasting alterations in sleep onset and organization. The only mild changes recorded in the 23 h following PCN microinjections were an increased latency of the first rapid eye movement (REM) sleep episode, a SWS II total time and percentage increase, and, with the highest PCN doses, a not very significant diminution of REM sleep total time. Another finding was the occurrence of REM sleep ponto-geniculo-occipital (PGO) waves, coinciding with a depression of the frequency and amplitude of interictal amygdaloid and cortical spikes. The results showed that a microinjection of PCN in the AM produced a reliable model of interictal spikes, paroxysms and generalized convulsive seizures. Nevertheless, long lasting kindling effect was not observed.
Descriptors: amygdala, brain mapping, electroencephalography, epilepsy, penicillins, polysomnography, amygdala, animal behavior, cats, drug administration schedule, epilepsy psychology, microinjections, penicillins, sleep, sleep.

Fletcher, N.F., D.J. Brayden, B. Brankin, S. Worrall, and J.J. Callanan (2004). Growth and characterization of a feline in vitro blood-brain barrier. Journal of Anatomy 205(6): 537. ISSN: 0021-8782.
Descriptors: infection, nervous system, HIV 1 infection, immune system disease, nervous system disease, FD4 permeability assay, laboratory techniques, feline in vitro brain barrier model, transendothelial electrical resistance measurement, transmission electron microscopy.

Flynn, J.N., C.A. Cannon, J.A. Beatty, M. Mackett, M.A. Rigby, J.C. Neil, and O. Jarrett (1994). Induction of feline immunodeficiency virus-specific cytotoxic t cells in vivo with carrier-free synthetic peptide. Journal of Virology 68(9): 5835-5844. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Descriptors: immune system, lentivirus, model system, infection, T cell proliferation in vitro, env gene product gp120, gag capsid protein p24, pathologic response, protection, cats, lymphocytotoxicity .

Foley, J.E., C.M. Leutenegger, J. Stephen Dumler, N.C. Pedersen, and J.E. Madigan (2003). Evidence for modulated immune response to Anaplasma phagocytophila sensu lato in cats with FIV-induced immunosuppression. Comparative Immunology, Microbiology and Infectious Diseases 26(2): 103-13. ISSN: 0147-9571.
NAL Call Number: QR180. C62
Abstract: Human granulocytic ehrlichiosis (HGE) is an emerging infectious disease in which some patients experience unusual opportunistic infections. In this study, cats infected with the HGE agent, Anaplasma phagocytophila s.l., had clinical granulocytic ehrlichiosis (GE), anti-nuclear antibodies and increased IFN-gamma mRNA. In FIV-immunosuppressed cats with GE, there was upregulated IL-10 transcription but not IFN-gamma. Cats with FIV had poor response to vaccines, regardless of GE status. This preliminary report demonstrates that cats with FIV-infection make a good model of ehrlichiosis in an immunocompromised host, and that viral immunosuppression may not increase the severity of ehrlichiosis but may attenuate immune responses to the pathogen.
Descriptors: anaplasma pHagocytopHilum, ehrlichiosis, feline acquired immunodeficiency syndrome, feline immunodeficiency virus, anaplasma pHagocytopHilum, antibodies, bacterial, cd4 positive t lymphocytes, cd8 positive t lymphocytes, cats, DNA, bacterial, DNA, bacterial, ehrlichiosis, ehrlichiosis, ehrlichiosis microbiology, feline acquired immunodeficiency syndrome, feline acquired immunodeficiency syndrome, flow cytometry, fluorescent antibody technique, immunocompromised host, interferon type ii biosynthesis, interleukin 10 biosynthesis, polymerase chain reaction, specific pathogen free organisms.

Forslund, K. (1997). Similarities and differences between animal species and man, with special reference to rheumatoid arthritis and diabetes mellitus. Alternatives to Laboratory Animals 25(2): 183-185. ISSN: 0261-1929.
NAL Call Number: Z7994L3A5
Descriptors: arthritis, diabetes, mankind, dogs, cats, rats, mice, cattle, animal models, experimentation, laboratory animals, legislation, bovidae , bovinae , disorders , domestic animals, joint diseases, livestock , metabolic disorders, organic diseases, rodentia , ruminants , useful animals, rheumatoid arthritis.

Fox, P.R., S.K. Liu, and B.J. Maron (1995). Echocardiographic assessment of spontaneously occurring feline hypertrophic cardiomyopathy. An animal model of human disease. Circulation 92(9): 2645-2651. ISSN: 0009-7322.
NAL Call Number: RC681 .A1C8
Abstract: BACKGROUND: Necropsy studies in domestic cats have suggested the occurrence of a primary cardiac disease resembling hypertrophic cardiomyopathy (HCM) in humans. We used two-dimensional echocardiography to define morphological and functional features of HCM during life in 46 domestic cats evaluated in a subspecialty veterinary clinic. Cats were 8 months to 14 years old (mean, 6 years). METHODS AND RESULTS: During the follow-up period of as long as 49 months, 18 cats died (or were euthanatized) due to congestive heart failure, peripheral embolization, or both, and 3 other cats experienced out-of-hospital sudden, unexpected death. Echocardiography showed a small left ventricular cavity, associated with a variety of patterns of hypertrophy. Wall thickening was most often diffuse (involving ventricular septum and free wall) in 31 cats (67%) and segmental in 15 (33%), including 12 with thickening confined to anterior septum; wall thickening was judged to be asymmetrical in 42 and symmetrical (concentric) in 4. In 30 cats (65%), marked mitral valve systolic anterior motion produced dynamic obstruction to left ventricular outflow (Doppler estimated gradients, 25 to 110 mm Hg). Compared with survivors, cats with HCM that died with heart failure had greater left ventricular thickness (8.1 +/- 1.5 versus 7.3 +/- 0.9 mm; P < .05) and larger left atria (20.1 +/- 4.6 versus 16.8 +/- 3.4 mm; P = .01) and more often had the nonobstructive form (89% versus 48%; P < .01). CONCLUSIONS: A spontaneously occurring disease of domestic cats was identified by echocardiography and was similar in its phenotypic expression to HCM in humans; it was characterized by unexplained left ventricular hypertrophy in a variety of patterns with or without evidence of outflow obstruction. Unfavorable prognosis was associated with greater magnitude of hypertrophy and absence of outflow obstruction. Feline HCM may prove to be a valuable animal model of the human disease.
Descriptors: cardiomyopathy, echocardiograpHy, hypertrophic cardiomyopathy, cats, animal disease models.

Foxd, P.R. and B.J. Maron (1994). Echocardiographic identification of spontaneously occurring feline hypertrophic cardiomyopathy: a potential animal model of human disease. Journal of the American College of Cardiology 0(SPEC. ISSUE): 26A. ISSN: 0735-1097.
Descriptors: cardiovascular system, diagnostic model , feline hypertrophic cardiomyopathy, echocardiogram.

Fukuhara, T., M. Gotoh, M. Kawauchi, S. Asari, and T. Ohmoto (1994). Superoxide scavenging activity in the extracellular space of the brain in forming edema. Neurosurgery 35(5): 924-8. ISSN: 0147-396X.
Abstract: We carried out a time course study of cerebral superoxide scavenging activity using a modified microdialysis technique. Twelve cats were divided into two groups; six were the reperfusion injury models, and six were cold injury models. In the reperfusion injury model, dialysates were collected during 60 minutes of middle cerebral artery occlusion and at 300 minutes during reperfusion. In the cold injury model, dialysates were collected 240 minutes after the injury. Regional cerebral blood flow on the injured side decreased during occlusion in the reperfusion injury model and 60 minutes after injury in the cold injury model. In the reperfusion model, superoxide scavenging activity, as determined with electron spin resonance, increased in the first 30 minutes and decreased 300 and 330 minutes after occlusion. In the dialysate, albumin increased 180 minutes after cold injury, which may show the progress of vasogenic edema. An increase in water content was observed on the injured side of both models, and a correlation between water content and superoxide scavenging activity was found in the reperfusion injury model. By this technique, a method of detecting the alteration of superoxide scavenging activity in the extracellular space of the brain was established.
Descriptors: blood brain barrier, brain, brain edema, superoxide dismutase, superoxides, cats, extracellular space, serum albumin, water electrolyte balance.

Fyfe, J.C., R.L. Kurzhals, M.E. Lassaline, P.S. Henthorn, P.R.K. Alur, P. Wang, J.H. Wolfe, U. Giger, M.E. Haskins, and D.F. Patterson (1999). Molecular basis of feline beta-glucuronidase deficiency: an animal model of mucopolysaccharidosis VII. Genomics 58(2): 121-128. ISSN: 0888-7543.
NAL Call Number: QH445.2 .G45
Descriptors: cats, enzyme deficiencies, beta glucuronidase, mucopolysaccharidosis, animal models, complementary DNA, nucleotide sequences, amino acid sequences, mutations, symptoms, gene expression, messenger RNA, segregation, molecular sequence data, genbank, af012423 , genbank, af012424 , missense mutations.

Garg, H., A. Joshi, and W.A. Tompkins (2004). Feline immunodeficiency virus envelope glycoprotein mediates apoptosis in activated PBMC by a mechanism dependent on gp41 function. Virology 330(2): 424-436. ISSN: 0042-6822.
NAL Call Number: 448.8 V81
Abstract: Feline Immunodeficiency Virus (FIV) is a lentivirus that causes immunodeficiency in cats, which parallels HIV-1-induced immunodeficiency in humans. It has been established that HIV envelope (Env) glycoprotein mediates T cell loss via a mechanism that requires CXCR4 binding. The Env glycoprotein of FIV, similar to HIV, requires CXCR4 binding for viral entry, as well as inducing membrane fusion leading to syncytia formation. However, the role of FIV Env in T cell loss and the molecular mechanisms governing this process have not been elucidated. We studied the role of Env glycoprotein in FIV-mediated T cell apoptosis in an in vitro model. Our studies demonstrate that membrane-expressed FIV Env induces apoptosis in activated feline peripheral blood mononuclear cells (PBMC) by a mechanism that requires CXCR4 binding, as the process was inhibited by CXCR4 antagonist AMD3100 in a dose-dependent manner. Interestingly, studies regarding the role of CD134, the recently identified primary receptor of FIV, suggest that binding to CD134 may not be important for induction of apoptosis in PBMC. However, inhibiting Env-mediated fusion post CXCR4 binding by FIV gp41-specific fusion inhibitor also inhibited apoptosis. Under similar conditions, a fusion-defective gp41 mutant was unable to induce apoptosis in activated PBMC. Our findings are the first report suggesting the potential of FIV Env to mediate apoptosis in bystander cells by a process that is dependent on gp41 function.
Descriptors: apoptosis, glycoproteins, feline immunodeficiency virus, viral envelope proteins, viral fusion proteins, anti HIV agents, cats, cell fusion, cell survival, glycoproteins, heterocyclic compounds, membrane fusion, tumor necrosis factor.

Gaschen, F. and J.M. Burgunder (2001). Changes of skeletal muscle in young dystrophin-deficient cats: a morphological and morphometric study. Acta Neuropathologica 101(6): 591-600. ISSN: 0001-6322.
Abstract: Dystrophin deficiency causes Duchenne muscular dystrophy (DMD). Hypertrophic feline muscular dystrophy (HFMD) is a homologous animal model of DMD. Our objective was to investigate the early changes caused by dystrophin deficiency in skeletal muscle of cats of 3-4 and 6-9 months. Obvious histological lesions were already present in the younger cats, and they increased in magnitude over time. They consisted of multifocal areas of degeneration and regeneration with mononuclear infiltration, and a wide variation in myofiber diameter, as evidenced by significantly increased variability coefficients in muscle fiber size, myofiber splitting, central nuclei, and hypercontracted myofibers. Widespread multifocal mineralizations were frequently observed. Endomysial and perimysial fibrosis was not a feature observed in axial or appendicular muscles, but was present in the diaphragm of two cats at necropsy. There was a significant decrease in the number of type 2A myofibers in dystrophin-deficient cats at both ages. Sarcolemmal dystrophin was mostly absent in all dystrophin-deficient cats; however, a small percentage of fibers stained positive, accounting for a faint residual band in the immunoblot. Carrier females had a mosaic staining pattern with irregular staining in most fibers, or even absent staining in rare fibers. However, no histological lesions were seen. Taken together, these data provide significant baseline information for further studies on the early changes associated with dystrophin deficiency in cats, or use of young dystrophin-deficient cats in therapeutic trials.
Descriptors: dystropHin deficiency, muscle, skeletal, muscular dystrophy, animal, adenosinetriphosphatase, cats, dyes, dystropHin, immunohistochemistry, muscle fibers, muscular dystrophy, animal, sarcolemma.

Gehlbach, P.L. and R.L. Purple (1994). A paired comparison of two models of experimental retinal ischemia. Current Eye Research 13(8): 597-602. ISSN: 0271-3683.
Abstract: Increased intraocular pressure and vascular ligation models are often used in studies of global ocular ischemia. The purpose of this study is to perform a paired comparison of retinal recovery in these paradigms. Our data indicate that ERG b-wave recovery profiles, following identical periods of ischemia, differ significantly between models. We propose that increased intraocular pressure models induce greater retinal injury than vascular ligation models. We suggest that pressure or another aspect of the increased intraocular pressure model induces injury beyond that caused by ischemia alone and caution against direct comparison of results obtained using these two models.
Descriptors: animal disease models, ischemia, retina, retinal vessels, cats, constriction, pathologic, electroretinograpHy, fluorescein angiograpHy, intraocular pressure, perfusion, reperfusion injury.

Giannecchini, S., P. Isola, O. Sichi, D. Matteucci, M. Pistello, L. Zaccaro, D.d. Mauro, and M. Bendinelli (2002). AIDS vaccination studies using an ex vivo feline immunodeficiency virus model: failure to protect and possible enhancement of challenge infection by four cell-based vaccines prepared with autologous lymphoblasts. Journal of Virology 76(14): 6882-6892. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Descriptors: antibodies, epitopes, immune response, immunity, immunization, lymphocyte transformation, potency, vaccination, vaccine development, vaccines, cats, feline immunodeficiency virus.

Giannecchini, S., D.d. Mauro, D. Matteucci, and M. Bendinelli (2001). AIDS vaccination studies using an ex vivo feline immunodeficiency virus model: reevaluation of neutralizing antibody levels elicited by a protective and a nonprotective vaccine after removal of antisubstrate cell antibodies. Journal of Virology 75(9): 4424-4429. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Descriptors: acquired immune deficiency syndrome, antibodies, immunization, serum, vaccination, vaccines, virulence, cats, feline immunodeficiency virus.

Giannecchini, S., A. Di Fenza, A.M. D'ursi, D. Matteucci, P. Rovero, and M. Bendinelli (2003). Antiviral activity and conformational features of an octapeptide derived from the membrane-proximal ectodomain of the feline immunodeficiency virus transmembrane glycoprotein. Journal of Virology 77(6): 3724-3733. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Descriptors: feline immunodefieciency virus, cell biology, antiviral activity, peptides, tryptophan residues, feline fibroblastoid kidney cells.

Gibson, M.D., M.T. Omran, and C.R. Young (1995). Experimental feline Lyme borreliosis as a model for testing Borrelia burgdorferi vaccines. Advances in Experimental Medicine and Biology 383: 73-82. ISSN: 0065-2598.
NAL Call Number: QP901 A33
Abstract: The feline model investigated establishes that domestic cats may act as an animal model for evaluating the pathogenesis of Lyme borreliosis. Specifically this feline model demonstrates: First, that animals seroconvert following either needle injection of, or arthropod delivery of, Borrelia burgdorferi. Clinical findings obtained are consistent with those observed in human Lyme disease; histopathological observations are also consistent with those observed in human Lyme disease. Therefore, cats may also be used as a representative animal model for measuring immune protection against Lyme borreliosis. Specifically we are exploring the protective capacity of Borrelia burgdorferi antigenic compounds in cats, namely OspA, OspB, OspC, heat shock proteins, flagellar antigens and various protective immunological combinations.
Descriptors: bacterial vaccines, borrelia burgdorferi group, animal disease models, lyme disease, cats.

Haghighi, S.S., D.H. York, L. Spollen, J.J. Oro, and M.A. Perez Espejo (1996). Neurophysiological evidence of spared upper motor neurons after spinal cord injury. Paraplegia 34(1): 39-45. ISSN: 0031-1758.
Abstract: Fourteen cats were subjected to a moderate (100 gm-cm; n = 7) or a severe (600 gm-cm; n = 7) spinal cord injury at the C4-C5 level using a weight drop technique. Somatosensory evoked potentials (SSEPs) were recorded after stimulation of the median nerve in the forearm. The SSEPs were measured in each animal before and after the injury. Motor evoked potentials (MEPs) were recorded from forearm extensor muscles after transcranial magnetic stimulation of the motor cortex. The SSEPs and The MEPs were measured in each animal before and after the injury under ketamine-based anesthesia. After the moderate injury (n = 7), 83% of the animals (6/7) maintained the SSEPs and 100% (7/7) maintained the MEPs. Postoperatively, only one animal who lost the SSEPs post-injury became tetraplegic. The remainder were neurologically intact. In the severely injured animals (n = 7), 5/7 of animals lost SSEPs and subsequently became tetraplegic. The MEPS were maintained in 3/5 (60%) of these tetraplegic animals. Two of seven animals (40%) in this group did not lose SSEPs or MEPs and recovered with no clinical deficit. Our data show a good correlation between the presence of SSEPs and functional recovery in the injured groups. The presence of MEPs in 3/5 (60%) of the tetraplegic animals may imply the existence of functionally active motor fibers after severe spinal trauma.
Descriptors: motor neurons, spinal cord injuries, cats, electric stimulation, evoked potentials, motor, evoked potentials, somatosensory, magnetics, median nerve, muscle, skeletal innervation, muscle, skeletal, neural conduction.

Halstead, S.B., N.T. Lan, T.T. Myint, T.N. Shwe, A. Nisalak, S. Kalyanarooj, S. Nimmannitya, S. Soegijanto, D.W. Vaughn, and T.P. Endy (2002). Dengue hemorrhagic fever in infants: research opportunities ignored. Emerging Infectious Diseases 8(12): 1474-9. ISSN: 1080-6059.
NAL Call Number: RA648.5.E46
Abstract: The age distribution of cases of dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS) in infants under the age of 1 year are reported from Bangkok, Thailand, and for the first time for Ho Chi Minh City, Vietnam; Yangon, Myanmar; and Surabaya, Indonesia. The four dengue viruses were isolated from Thai infants, all of whom were having a primary dengue infection. Progress studying the immunologically distinct infant DHF/DSS has been limited; most contemporary research has centered on DHF/DSS accompanying secondary dengue infections. In designing research results obtained in studies on a congruent animal model, feline infectious peritonitis virus (FIPV) infections of kittens born to FIPV-immune queens should be considered. Research challenges presented by infant DHF/DSS are discussed.
Descriptors: dengue hemorrhagic fever epidemiology, dengue virus, age distribution, child, child, preschool, dengue virus classification, hospitalization statistics and numerical data, indonesia epidemiology, infant, myanmar epidemiology, research, thailand epidemiology, vietnam epidemiology.

Harrison, J.D., H.M. Fouad, and J.R. Garrett (2001). Variation in the response to ductal obstruction of feline submandibular and sublingual salivary glands and the importance of the innervation. Journal of Oral Pathology and Medicine 30(1): 29-34. ISSN: 0904-2512.
Abstract: A variable response following ductal ligation of feline salivary glands corresponds to the human condition but contrasts with a predictable atrophy in obstructed salivary glands of rodents popularly used as a model for human salivary problems. The present investigation is concerned with a possible reason for the variable response, namely the preservation of the innervation. Ducts of feline submandibular and sublingual salivary glands were ligated with or without the inclusion of the chorda tympani. Inclusion led to a delayed initial response followed by progressive atrophy until the parenchyma was extremely atrophic, whereas avoidance of the chorda led to the variable response in which variable numbers of acini of a similar form to normal persisted. The results establish the atrophic effect of inclusion of the chorda tympani in ductal ligation and indicate the caution that should be exercised in the extrapolation of the rodent model to the human condition.
Descriptors: chorda tympani nerve, animal disease models, salivary gland diseases, salivary glands innervation, atrophy, cats, chorda tympani nerve surgery, denervation, ligation, electron microscopy, organ size, rodentia, salivary ducts, salivary glands, sublingual gland innervation, sublingual gland, submandibular gland innervation, submandibular gland.

Hasenfuss, G. (1998). Animal models of human cardiovascular disease, heart failure and hypertrophy. Cardiovascular Research 39(1): 60-76. ISSN: 0008-6363.
Abstract: The progress made in our understanding of the pathophysiology and treatment of congestive heart failure (CHF) would not have been possible without a number of animal models of heart failure and hypertrophy, each one having unique advantages as well as disadvantages. The species and interventions used to create CHF depends on the scientific question as well as on factors such as ethical and economical considerations, accessibility and reproducibility or the model. How closely the model should mimic the human syndrome of CHF depends on the scientific question under investigation. If the goal is to study pathophysiological processes like remodeling or the function of subcellular systems such as excitation contraction-coupling processes, contractile protein function or energetics, the model of heart failure should mimic the clinical setting as closely as possible. However, if defined causal connections are under investigation such as structure-function analyses or regulation of gene expression, exact reflection of the clinical setting by the animal model may be less important. In this review, animal models of heart failure are discussed with particular focus on similarities between the animal model and the failing human heart regarding myocardial function as well as molecular and subcellular mechanisms. In addition, new models of heart failure and hypertrophy, and finally some recent animal models of myocarditis are reviewed.
Descriptors: cardiovascular diseases, animal disease models, cardiomegaly, cats, cattle, dogs, guinea pigs, hamsters, heart failure, congestive, mesocricetus, rabbits, rats, rats, sprague dawley, sheep, swine, turkeys.

Hayes, K.A., A.J. Phipps, S. Francke, and L.E. Mathes (2000). Antiviral therapy reduces viral burden but does not prevent thymic involution in young cats infected with feline immunodeficiency virus. Antimicrobial Agents and Chemotherapy 44(9): 2399-405. ISSN: 0066-4804.
Abstract: The thymus is a major target organ in human immunodeficiency virus type 1 (HIV-1)-infected children and feline immunodeficiency virus (FIV)-infected young cats (G. A. Dean and N. C. Pedersen, J. Virol. 72:9436-9440, 1998; J. L. Heeney, Immunol. Today 16:515-520, 1995; S. M. Schnittman et al., Proc. Natl. Acad. Sci. USA 87:7727-7731, 1990; T. A. Seemayer et al., Hum. Pathol. 15:469-474, 1984; H.-J. Shuurn et al., Am. J. Pathol. 134:1329-1338, 1989; J. C. Woo et al., J. Virol. 71:8632-8641, 1997; J. C. Woo et al., AIDS Res. Hum. Retrovir. 15:1377-1388, 1999). It is likely that the accelerated disease process in children and cats is due to infection of the thymus during the time when generation of naive T lymphocytes is needed for development of the mature immune system. Zidovudine (ZDV) monotherapy, which is used to prevent and treat perinatal HIV-1 infection (R. Sperling, Infect. Dis. Obstet. Gynecol. 6:197-203, 1998), previously had been shown to reduce viral burden in FIV-infected young cats (K. A. Hayes et al., J. Acquir. Immune Defic. Syndr. 6:127-134, 1993). The purpose of this study was to evaluate the effect of drug-induced reduction of viral burden in the thymus on virus-mediated thymic involution and peripheral blood CD4 decline using FIV-infected cats as a model for pediatric HIV-1 infection. Eight-week-old cats were randomly assigned to uninfected, saline-treated; uninfected, ZDV-treated; FIV-infected, saline-treated; and FIV-infected, ZDV-treated groups. Parameters measured included blood lymphocyte numbers, viral load in blood and thymic tissue, and thymic histopathology. While the viral burden was significantly reduced by ZDV monotherapy in peripheral blood lymphocytes, plasma, and thymus, thymic lesions were similar for the treated and untreated FIV-infected cats. Further, markedly lowering the viral burden did not increase blood CD4 lymphocyte numbers or prevent their decline. The data suggest that an inflammatory process continued in spite of reduced virus replication. These observations imply that reducing virus load and limiting thymic inflammation are separate factors that must be addressed when considering therapeutic strategies aimed at preserving thymic function.
Descriptors: anti HIV agents, feline acquired immunodeficiency syndrome, HIV infections, feline immunodeficiency virus, thymus gland, zidovudine, anti HIV agents, cats, animal disease models, feline acquired immunodeficiency syndrome, feline acquired immunodeficiency syndrome, feline immunodeficiency virus, lymphocyte count, lymphocytes, lymphocytes, lymphocytes, phenotype, plasma, plasma, thymus gland, thymus gland, thymus gland, viral load, zidovudine.

He, Q., C. Lowrie, G.D. Shelton, R.J. Castellani, M. Menotti Raymond, W. Murphy, S.J. O'Brien, W.F. Swanson, and J.C. Fyfe (2005). Inherited motor neuron disease in domestic cats: a model of spinal muscular atrophy. Pediatric Research 57(3): 324-30. ISSN: 0031-3998.
Abstract: Juvenile-onset spinal muscular atrophy was observed in an extended family of purebred domestic cats as a fully penetrant, simple autosomal recessive trait. Affected kittens exhibited tremor, proximal muscle weakness, and muscle atrophy beginning at ~4 mo of age. Apparent loss of function was rapid initially but progressed slowly after 7-8 mo of age, and variably disabled cats lived for at least 8 y. Electromyography and microscopic examination of muscle and nerve biopsies were consistent with denervation atrophy as a result of a central lesion. There was astrogliosis and dramatic loss of motor neurons in ventral but not dorsal horn gray matter of spinal cord and loss of axons in ventral horn nerve roots. These phenotypic findings were similar to mild forms (type III) of spinal muscular atrophy in humans caused by survival of motor neuron mutations, but molecular analysis excluded feline survival of motor neuron as the disease gene in this family. A breeding colony has been established for further investigation of this naturally occurring large-animal model of inherited motor neuron disease.
Descriptors: models, spinal muscular atrophy, biopsies, juvenile-onset, kittens.

He, Q.C., C. Lowrie, G.D. Shelton, R.J. Castellani, M. Menotti Raymond, W. Murphy, S.J. O' Brien, W.F. Swanson, and J.C. Fyfe (2005). Inherited motor neuron disease in domestic cats: a model of spinal muscular atrophy. Pediatric Research 57(3): 324-330. ISSN: 0031-3998.
Descriptors: animal models, atrophy, clinical aspects, DNA, hereditary diseases, histopathology, inheritance, molecular, nervous system diseases, neurons, nucleotide sequences, skeletal muscle, spinal cord, spinal diseases, spine, cats.

Hebben, M., V. Duquesne, J. Cronier, B. Rossi, and A. Aubert (2004). Modified vaccinia virus Ankara as a vaccine against feline coronavirus: immunogenicity and efficacy. Journal of Feline Medicine and Surgery 6(2): 111-8. ISSN: 1098-612X.
NAL Call Number: SF985 .J68
Abstract: Feline infectious peritonitis virus (FIPV) is a coronavirus that induces a fatal systemic disease mediated by an inappropriate immune response. Most previous vaccination attempts against FIPV were unsuccessful because IgG antibodies against the surface protein enhance the infection. However, two studies have shown that poxvirus vectors (vaccinia WR and canarypox) expressing only the FIPV membrane (M) protein can elicit a partially protective immunity which is supposed to be cell-mediated (Virology 181 (1991) 327; International patent WO 97/20054 (1997)). In our study, we report the construction of another poxvirus, the modified vaccinia virus Ankara (MVA), as an expression vector for the FIPV M protein. In this vector, the M gene has been inserted downstream a strong early/late promoter, whereas the two previously described poxviruses expressed the M protein during their early stage only. The immunogenicity of the recombinant MVA-M was evaluated in the murine model which revealed an effect of the vector on the Th1/Th2 balance. The vaccine was then tested in cats to evaluate its efficacy in an FIPV 79-1146 challenge. Vaccinated kittens developed FIPV-specific antibodies after immunization, however, none of them was protected against FIPV. Our results suggest a crucial role for the type of poxviral promoter that must be used to induce an effective immune response against FIPV.
Descriptors: coronavirus, feline, feline infectious peritonitis, vaccinia virus, viral vaccines, cats, mice, mice, inbred balb c, specific pathogen free organisms, treatment outcome, vaccination.

Hein, A., J.P. Martin, and R. Dorries (2001). In vitro activation of feline immunodeficiency virus in ramified microglial cells from asymptomatically infected cats. Journal of Virology 75(17): 8090-5. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Abstract: Intravenous infection of cats with feline immunodeficiency virus was used as a model system to study activation of virus replication in brain-resident microglial cells in vitro. Virus release by ramified microglial cells isolated from subclinically infected animals was detectable in cell-free tissue culture supernatant only by reverse transcription and nested PCR of gag-specific RNA sequences and not by virion-associated reverse transcriptase activity. In contrast, cocultivation of in vivo-infected microglial cells with mitogen-activated peripheral blood mononuclear cells (PBMC) regularly allows detection of high virus yields in cell-free tissue culture fluid. Besides uptake and multiplication of microglia-derived virus in PBMC, release of virus from microglia is stimulated by cell contact with PBMC. The data suggest that T lymphocytes patrolling the central nervous system could reactivate the semilatent state of lentiviruses in microglial cells in the course of clinically silent central nervous system infection.
Descriptors: feline immunodeficiency virus growth and development, lentivirus infections, microglia, cats, cell line, coculture techniques, leukocytes, mononuclear, leukocytes, mononuclear, lymphocyte activation, microglia, virion, virus activation, virus replication.

Hein, A., H. Schuh, S. Thiel, J.P. Martin, and R. Dorries (2003). Ramified feline microglia selects for distinct variants of feline immunodeficiency virus during early central nervous system infection. Journal of Neurovirology 9(4): 465-76. ISSN: 1355-0284.
Abstract: It is widely accepted that human immunodeficiency virus (HIV) invades the central nervous system (CNS) shortly after peripheral infection to establish a persistent infection of tissue-resident microglial cells. To what extent this early CNS infection is of pathogenic relevance is a matter of discussion. It is conceivable, however, that infected microglia releases virus variants of enhanced neurotropism and/or neurovirulence compared to peripheral isolates. Moreover, microglial variants may exhibit high resistance to antiviral therapeutics that poorly penetrate into brain tissue. The molecular basis of these biological properties is suspected to be associated with specific sequences in the viral env gene, particularly within the V3 loop. Therefore, we analyzed in the animal model of feline immunodeficiency virus (FIV) infection of cats lentiviral V3 sequences in highly purified microglial cells and blood from acutely infected animals. Compared to the inoculated virus, nucleotide sequence alterations in serum samples were rarely detectable, if at all. In contrast, up to 19 nucleotide exchanges could be identified within FIV V3 from microglia, resulting in a mutation frequency of up to 14.5% with respect to the deduced amino acid sequence. These findings suggest selection of specific virus variants by brain-resident target cells that might have implications for antiretroviral drug design.
Descriptors: brain diseases, feline acquired immunodeficiency syndrome, feline immunodeficiency virus, feline immunodeficiency virus growth and development, microglia, amino acid sequence, base sequence, brain diseases, cats, feline acquired immunodeficiency syndrome, glycoproteins, feline immunodeficiency virus pathogenicity, molecular sequence data, pHylogeny, polymorpHism, single stranded conformational, viral envelope proteins, virulence.

Heiss, W.D., C. Dohmen, J. Sobesky, L. Kracht, B. Bosche, F. Staub, S. Toyota, M. Valentino, and R. Graf (2003). Identification of malignant brain edema after hemispheric stroke by PET-imaging and microdialysis. Acta Neurochirurgica/ Supplementum 86: 237-40. ISSN: 0065-1419.
Abstract: Cerebral blood flow (CBF) and extent of irreversible tissue damage as well as the time course of extracellular concentration of amino acids, substrates of energy metabolism, and purine metabolites, intracranial pressure and tissue oxygen tension were assessed in 34 patients with large strokes covering more than 50% of the MCA territory. The results were compared to findings in the experimental model of transient (for 3 hours) MCA occlusion in cats. In the experimental model as well as in the clinical setting development of malignant brain infarcts (due to formation of space occupying brain edema) was predicted by the size of critically hypoperfused tissue and the volume of irreversibly damaged tissue. The course of malignant infarcts was characterized by progressive increase in concentrations of excitatory amino acids, lactate, pyruvate, glycerol, hypoxanthine and in intracranial pressure, while cerebral perfusion pressure and tissue oxygen tension decreased. These results clearly differentiate a malignant from a benign course of large hemispheric infarction. The methods can be used to identify patients at risk for formation of space occupying edema and to select patients who could benefit from invasive therapeutic strategies.
Descriptors: brain edema diagnosis, brain edema, cerebrovascular accident, microdialysis, tomography, emission computed, amino acids, brain edema mortality, brain edema, cats, cerebral infarction, cerebrovascular circulation, flumazenil diagnostic use, flumazenil, infarction, middle cerebral artery, intracranial pressure, prognosis.

Henckaerts, E., H. Geiger, J.C. Langer, P. Rebollo, G. Van Zant, and H.W. Snoeck (2002). Genetically determined variation in the number of phenotypically defined hematopoietic progenitor and stem cells and in their response to early-acting cytokines. Blood 99(11): 3947-3954. ISSN: 0006-4971.
NAL Call Number: RB145.A1B57
Descriptors: hematopoietic progenitor, stem cells, cytokines, cats, inbred mice, thrombopoietin, epistasis.

Ho, C.M., S.T. Ho, J.J. Wang, S.K. Tsai, and C.Y. Chai (2004). Dexamethasone has a central antiemetic mechanism in decerebrated cats. Anesthesia and Analgesia 99(3): 734-9. ISSN: 0003-2999.
Abstract: Dexamethasone is an effective antiemetic drug, but its mechanism of action is unclear. We designed this study to investigate the direct antiemetic action of dexamethasone in the medulla of cats. By using an oscillographic vomiting model, decerebrated cats received microinjections of dexamethasone 100 nL (1 microg, n = 7; 0.1 microg, n = 7) into the bilateral nuclei tractus solitarii, which led to a significant prolongation of the latency (1 microg, 6.4 +/- 1.1 min versus 28.2 +/- 4.9 min, P < 0.05; 0.1 microg, 6.7 +/- 1.1 min versus 27.1 +/- 5.0 min, P < 0.05) of the first emetic episode and significantly decreased the frequency of emetic episodes (1 microg, 2.7 +/- 0.8 versus 0.1 +/- 0.4, P < 0.05; 0.1 microg, 2.9 +/- 0.9 versus 0.3 +/- 0.5, P < 0.05) induced by xylazine. Pretreatment with mifepristone, a glucocorticoid receptor antagonist, blocked the antiemetic effect of dexamethasone in the bilateral nuclei tractus solitarii. However, microinjection of dexamethasone into the unilateral nucleus tractus solitarius alone did not alter the latency of the first emetic episode or the frequency of emetic episodes induced by xylazine. Local application of dexamethasone into the area postrema had no effect on the latency of the first emetic episode or the frequency of emetic episodes induced by xylazine. These results suggest that dexamethasone exerts its central antiemetic action through an activation of the glucocorticoid receptors in the bilateral nuclei tractus solitarii in the medulla.
Descriptors: antiemetics, dexamethasone, solitary nucleus, cats, decerebrate state, microinjections, mifepristone, receptors, glucocorticoid, solitary nucleus.

Hope, J. (1999). Animal models of prion diseases: the old and the new. Clinical Chemistry and Laboratory Medicine 37: S25. ISSN: 1434-6621.
Descriptors: infection, neurology, animal model, bovine spongiform encephalopathy, prion disease, feline spongiform encephalopathy, nervous system disease, scrapie, transmissible mink encephalopathy, Gerstmann Straussler Sheinker syndrome.
Notes: Meeting Information: IFC-WorldLab, International Federation of Clinical and Laboratory Medicine (17th International and 13th European Congress of Clinical Chemistry and Laboratory Medicine, 1st International Congress of Clinical Molecular Biology, 31st National Congress of the Italian Society of Clinical Biochemistry and Clinical Molecular Biology), Florence, Italy; June 6-11, 1999.

Hosie, M.J. (1994). The development of a vaccine against feline immunodeficiency virus. The British Veterinary Journal 150(1): 25-39. ISSN: 0007-1935.
NAL Call Number: 41.8 V643
Abstract: Feline immunodeficiency virus (FIV) is a retrovirus causing significant disease in cats. The virus has been shown to be similar biologically to the human immunodeficiency virus (HIV), the cause of acquired immunodeficiency syndrome (AIDS) in humans. Much interest has been expressed in the use of FIV as an animal model for HIV vaccination studies. Both FIV and HIV belong to the lentivirus group of retroviruses. While there are several effective vaccines against feline leukaemia virus (FeLV), a mammalian type C retrovirus, at present there are no effective vaccines against lentiviruses. This review illustrates the obstacles to the production of vaccines against FIV or HIV. FIV vaccine studies conducted in several laboratories are reviewed, the results are compared and factors important for inducing protection from FIV infection are discussed.
Descriptors: feline acquired immunodeficiency syndrome, feline immunodeficiency virus, viral vaccines, cats.

Hosie, M.J. and O. Jarrett (1995). Feline immunodeficiency virus as a vaccine model. North Atlantic Treaty Organization Advanced Study Institute Series 282(Series A, Life sciences (USA)): 85-95. ISSN: 0258-1213.
NAL Call Number: QH301.N32
Descriptors: cats, lentivirinae, vaccines, vaccination, antigens, antigen antibody reactions, immune response, antibodies, disease control, immune response, immunity , immunization , immunological factors, immunostimulation , immunotherapy , retroviridae , therapy , viruses , alloantigens , neutralizing antibodies, viral antigens, protective antigens, virus neutralization.

Houweling, A.R., M. Bazhenov, I. Timofeev, M. Steriade, and T.J. Sejnowski (2005). Homeostatic synaptic plasticity can explain post-traumatic epileptogenesis in chronically isolated neocortex. Cerebral Cortex 15(6): 834-45. ISSN: 1047-3211.
Abstract: Chronically isolated neocortex develops chronic hyperexcitability and focal epileptogenesis in a period of days to weeks. The mechanisms operating in this model of post-traumatic epileptogenesis are not well understood. We hypothesized that the spontaneous burst discharges recorded in chronically isolated neocortex result from homeostatic plasticity (a mechanism generally assumed to stabilize neuronal activity) induced by low neuronal activity after deafferentation. To test this hypothesis we constructed computer models of neocortex incorporating a biologically based homeostatic plasticity rule that operates to maintain firing rates. After deafferentation, homeostatic upregulation of excitatory synapses on pyramidal cells, either with or without concurrent downregulation of inhibitory synapses or upregulation of intrinsic excitability, initiated slowly repeating burst discharges that closely resembled the epileptiform burst discharges recorded in chronically isolated neocortex. These burst discharges lasted a few hundred ms, propagated at 1-3 cm/s and consisted of large (10-15 mV) intracellular depolarizations topped by a small number of action potentials. Our results support a role for homeostatic synaptic plasticity as a novel mechanism of post-traumatic epileptogenesis.
Descriptors: brain injuries, epilepsy, models, neurological, neocortex, neuronal plasticity, action potentials, acute disease, brain injuries, cats, chronic disease, denervation, electrodes, implanted, epilepsy, homeostasis, periodicity, research support, n, i, h, , extramural.

Ingles, A.C., D.J. Legare, and W.W. Lautt (1994). Evaluation of vascular tone in portacaval shunts comparing the index of contractility and resistance in cats. Hepatology 20(5): 1242-6. ISSN: 0270-9139.
Abstract: A model of prehepatic chronic portal hypertension in cats was used to determine portacaval shunt responses to infused norepinephrine and to possible transmitter overflow into portal blood from nerves supplying the gut. Responses are compared using a new index of contractility. Four weeks after application of a slowly constricting occluder, the portal vein was completely occluded and acute experiments were carried out under pentobarbital anesthesia. Portal pressure was elevated to 15.0 +/- 0.9 mmHg and all portal flow passed through the shunts. In response to intraportal norepinephrine (0.25, 0.5 and 1.25 micrograms.min-1.kg-1) shunt resistance rose by 6% +/- 3%, 19% +/- 4% and 26% +/- 5%, respectively, whereas the index of contractility rose (by 22% +/- 8%, 46% +/- 10% and 89% +/- 20%, respectively), the distending blood pressure also rose (5% +/- 1%, 7% +/- 1% and 14% +/- 3%, respectively). The difference in percentage increase of resistance and the index of contractility is a result of the passive dilator effect of the elevated distending pressure acting on the distensible shunt vessels. Stimulation of mesenteric nerves caused the mesenteric artery to constrict, but the shunt vessels showed no effect. In conclusion, the shunt vessels respond actively to norepinephrine and passively to altered distending pressure. However, transmitter overflow from nerves supplying the intestines is unlikely to play a role in determining resistance in the shunts. Vascular resistance is affected by both active and passive effects, so that the active contractile responses are best evaluated using the index of contractility, which is not altered passively.
Descriptors: portacaval shunt, surgical, vasoconstriction, vasodilation, vasomotor system, cats, dose response relationship, drug, electric stimulation, injections, intra arterial, injections, intravenous, mesenteric arteries innervation, nervous system, norepinephrine.

Ingles, A.C., D.J. Legare, and W.W. Lautt (1994). Distensibility of portacaval shunts in portal hypertensive cats: index of contractility model. Canadian Journal of Physiology and Pharmacology 72(6): 687-92. ISSN: 1205-7541.
NAL Call Number: 444.8 C16
Abstract: Complete shunting of portal blood flow through portacaval shunts was obtained using a constrictor around the portal vein to gradually produce a total occlusion. After 4 weeks, acute experiments were conducted in anesthetized cats. Blood from the femoral artery was shunted through a pump to supply and control the entire portal blood flow. As shunted portal blood flow was varied over a wide range, the portal shunt resistance showed distensibility. Decreasing portal venous pressure from 15.0 +/- 0.9 to 11.1 +/- 0.6 mmHg (1 mmHg = 133.3 Pa) resulted in elevations of resistance of 58%. The relation between the resistance (R) and the distending pressure (Pd) was a constant, the index of contractility (IC), where IC = R.Pd3. In steady state, the IC was 485 +/- 55 mmHg4.mL-1.min.kg and did not change passively in response to changes in portal blood flow. In conclusion, portacaval shunts are passively distensible, and resistance is altered as a cubic function of the distending pressure. Because resistance is altered both actively and passively, the IC should prove useful to differentiate these alternatives for evaluation of changes in portal hypertensive therapy.
Descriptors: hypertension, portal, muscle, smooth, vascular, portacaval shunt, surgical, pressure, cats, hemodynamic processes, biological models, muscle contraction, perfusion, portal vein, vascular resistance.

Inoue, S., M. Kawaguchi, K. Kurehara, T. Sakamoto, K. Kitaguchi, and H. Furuya (2001). Effect of mild hypothermia on nicorandil-induced vasodilation of pial arterioles in cats. Critical Care Medicine 29(11): 2162-8. ISSN: 0090-3493.
Abstract: OBJECTIVE: Nicorandil is characterized as hybrid between nitrates and potassium channel activators. Recent evidence suggested that mild hypothermia may alter cerebral vasodilation induced by a nitrate agent and potassium channel opener. However, the effect of mild hypothermia on nicorandil-induced vasodilation is not known. The present study was conducted to investigate whether mild hypothermia could alter nicorandil-induced cerebral vasodilation. In addition, the effects of mild hypothermia on cerebral vasodilation induced by nitroglycerin, a nitrate agent, and cromakalim, a selective adenosine 5'-triphosphate-sensitive potassium channel opener, were assessed in the same model. DESIGN: Prospective, randomized, experimental study with repeated measures. SETTING: Investigational animal laboratory. SUBJECTS: Twenty-four cats. INTERVENTIONS: Animals were anesthetized with pentobarbital. The cranial window technique, combined with microscopic video recording, was used to measure small (50-100 microm) and large (100-200 microm) pial arteriolar diameter in an experiment. Animals were assigned randomly to either a normothermic (37 degrees C) or a hypothermic (33 degrees C) group. Nicorandil, nitroglycerin, or cromakalim at concentrations of 10(-8), 10(-6), or 10(-4) mol/L was applied topically in the cranial window, and the diameter of pial arterioles was measured. MEASUREMENTS AND MAIN RESULTS: Topical administration of nicorandil, nitroglycerin, and cromakalim significantly dilated both small and large pial arterioles in a dose-dependent manner during normothermia. Nicorandil-induced vasodilation of either large or small pial arterioles was not affected by hypothermia. However, hypothermia significantly attenuated nitroglycerine-induced vasodilation in both large and small pial arterioles and enhanced cromakalim-induced vasodilation in both large and small pial arterioles. CONCLUSIONS: Nicorandil-induced vasodilation of cerebral pial arterioles was not affected by mild hypothermia. By contrast, mild hypothermia significantly attenuated nitroglycerin-induced vasodilation and enhanced cromakalim-induced vasodilation.
Descriptors: cerebral arteries, hemodynamic processes, hypothermia, nicorandil, vasodilation, vasodilator agents, topical administration, cats, cromakalim, cromakalim, dose response relationship, drug, nicorandil, nitroglycerin, nitroglycerin, vasodilator agents.

Jackson, M., M. Solomonow, B. Zhou, R.V. Baratta, and M. Harris (2001). Multifidus EMG and tension-relaxation recovery after prolonged static lumbar flexion. Spine 26(7): 715-23. ISSN: 0362-2436.
Abstract: STUDY DESIGN: The electromyogram (EMG) from the in vivo feline L1 to the L7 multifidus was recorded during the application of a 20-minute static lumbar flexion and after 7 hours of rest. OBJECTIVE: To determine the recovery of tension-relaxation and laxity in the lumbar viscoelastic structures as well as the recovery of reflexive EMG activity in the multifidus after prolonged static flexion. SUMMARY OF BACKGROUND: It has been established that prolonged static flexion of the spine induces creep or tension-relaxation in its viscoelastic structures as well as a sharp decrease in the reflexive activity of the dorsal musculature and initiation of spasms. Epidemiologic studies have pointed out that such static flexion is associated with unusually high rates of low back disorders. The rate and pattern of recovery of reflexive muscular activity with rest after static flexion is still unknown. METHODS: The lumbar spines of seven in vivo feline preparations were subjected to 20 minutes of passive anterior flexion followed by 7 hours of rest while monitoring flexion tension, EMG from the L1-L7 multifidus muscles, and the strain of the L4/L5 supraspinal ligament. A model describing the pattern of recovery of muscular activity and viscoelastic tension was developed. RESULTS: Twenty minutes of lumbar flexion was associated with an initial sharp decrease of multifidus EMG activity followed by spasms. During rest, EMG activity demonstrated an initial hyperexcitability on flexion, followed by an exponential recovery of muscle activity. Full recovery of residual strain in the L4/L5 supraspinous ligament and multifidus activity was not obtained after 7 hours of rest. CONCLUSIONS: Static flexion of the lumbar spine is an extremely imposing function on its viscoelastic tissues, resulting in spasms and requiring long periods of rest before normal functions are re-established.
Descriptors: muscle contraction, muscle relaxation, muscle, skeletal, recovery of function, cats, electromyogrphy, lumbar vertebrae, lumbar vertebrae, models, animal.

Jergens, A.E. (2002). Understanding gastrointestinal inflammation--implications for therapy. Journal of Feline Medicine and Surgery 4(3): 179-182. ISSN: 1098-612X.
NAL Call Number: SF985 .J68
Descriptors: cats, dogs, gastrointestinal diseases, inflammation, pathogenesis, intestinal mucosa, immune system, therapeutic diets.

Johnson, C., P.A. Lobelle Rich, A. Puetter, and L.S. Levy (2005). Substitution of feline leukemia virus long terminal repeat sequences into murine leukemia virus alters the pattern of insertional activation and identifies new common insertion sites. Journal of Virology 79(1): 57-66. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Abstract: The recombinant retrovirus, MoFe2-MuLV (MoFe2), was constructed by replacing the U3 region of Moloney murine leukemia virus (M-MuLV) with homologous sequences from the FeLV-945 LTR. NIH/Swiss mice neonatally inoculated with MoFe2 developed T-cell lymphomas of immature thymocyte surface phenotype. MoFe2 integrated infrequently (0 to 9%) near common insertion sites (CISs) previously identified for either parent virus. Using three different strategies, CISs in MoFe2-induced tumors were identified at six loci, none of which had been previously reported as CISs in tumors induced by either parent virus in wild-type animals. Two of the newly identified CISs had not previously been implicated in lymphoma in any retrovirus model. One of these, designated 3-19, encodes the p101 regulatory subunit of phosphoinositide-3-kinase-gamma. The other, designated Rw1, is predicted to encode a protein that functions in the immune response to virus infection. Thus, substitution of FeLV-945 U3 sequences into the M-MuLV long terminal repeat (LTR) did not alter the target tissue for M-MuLV transformation but significantly altered the pattern of CIS utilization in the induction of T-cell lymphoma. These observations support a growing body of evidence that the distinctive sequence and/or structure of the retroviral LTR determines its pattern of insertional activation. The findings also demonstrate the oligoclonal nature of retrovirus-induced lymphomas by demonstrating proviral insertions at CISs in subdominant populations in the tumor mass. Finally, the findings demonstrate the utility of novel recombinant retroviruses such as MoFe2 to contribute new genes potentially relevant to the induction of lymphoid malignancy.
Descriptors: leukemia virus, feline, lymphoma, t cell, moloney murine leukemia virus, moloney murine leukemia virus pathogenicity, recombination, genetic, terminal repeat sequences, animals, newborn, cats, DNA, viral, leukemia, leukemia, lymphoma, t cell, mice, oncogenes, proto oncogene proteins, proviruses, retroviridae infections, retroviridae infections, tumor virus infections, tumor virus infections, virus integration.

Johnson, C.M., S.J. Bortnick, P.C. Crawford, and G.P. Papadi (2001). Unique susceptibility of the fetal thymus to feline immunodeficiency virus infection: an animal model for HIV infection in utero. American Journal of Reproductive Immunology 45(5): 273-88. ISSN: 1046-7408.
Abstract: Human infants infected in utero with HIV develop thymus insufficiency and progress to AIDS sooner than infants infected peripartum. However, direct analysis of the thymus is difficult due to limited tissue access and variable timing of vertical transmission. METHOD OF STUDY: Fetal and neonatal cats were inoculated with feline immunodeficiency virus (FIV) at an equivalent infectious dose. The thymus, blood, and lymph nodes were harvested and compared at 23 and 46 days post-inoculation (p.i.) and also compared to sham-inoculated, age-matched controls. Lymphocyte phenotypes were analyzed by flow cytometry and virus burden was quantified in histologic sections and by virus isolation from plasma. RESULTS: Fetal cats inoculated with FIV had acute thymus atrophy at birth, which coincided with peak viremia. At 46 days p.i., thymus size and cell composition rebounded and supported increased productive infection. In contrast, neonatal cats inoculated with FIV developed chronic thymus atrophy and degeneration, which was associated with decreasing productive infection and low-level viremia. CONCLUSIONS: The fetal thymus is uniquely vulnerable to acute, transient depletion and high-level productive infection. The neonatal thymus is less vulnerable to acute changes, and responds through progressive atrophy and declining productive infection. Reduced immune competence, as reflected by the failure to control virus replication, may contribute to the accelerated progression of FIV and HIV infections in utero.
Descriptors: feline acquired immunodeficiency syndrome, fetus, HIV infections, feline immunodeficiency virus, thymus gland, animals, newborn, atrophy, cats, disease models, animal, feline acquired immunodeficiency syndrome, feline acquired immunodeficiency syndrome, feline acquired immunodeficiency syndrome, fetus, HIV infections, homeostasis, infant, newborn, biological models, pregnancy, infectious, pregnancy, infectious, t lymphocytes, thymus gland, thymus gland, viremia, virus replication.

Johnson, C.M., B.A. Torres, H. Koyama, and J.K. Yamamoto (1994). Tenth anniversary perspectives on aids: fiv as a model for aids vaccination. AIDS Research and Human Retroviruses 10(3): 225-228. ISSN: 0889-2229.
Descriptors: feline immunodeficiency virus, AIDS model, infection, microbiology, acquired immunodeficiency syndrome, antibody titer, challenge protection.

Jones, S.R., D.J. Pinto, T.J. Kaper, and N. Kopell (2000). Alpha-frequency rhythms desynchronize over long cortical distances: a modeling study. Journal of Computational Neuroscience 9(3): 271-291. ISSN: 0929-5313.
Descriptors: nervous system, cats, neural coordination, neocortex, alpha frequency rhythms, desynchronization, cortical distance, local rhythms, modeling study, synchrony .

Joshi, M.S., J.A. Bauer, M.W. Julian, and E.D. Crouser (2004). Cyclosporin a attenuates left ventricular dysfunction in a feline model of acute sepsis: relation to tlr4 induction, nos2 induction and protein nitration. Journal of the Federation of American Societies for Experimental Biology 18(4-5): Abst. 401.5. ISSN: 0892-6638.
Online: http://www.fasebj.org/
NAL Call Number: QH301. F3
Descriptors: infection, feline model, acute sepsis, bacterial disease, cardiac dysfunction, heart disease, immunohistochemistry, left ventricular dysfunction attenuation, myocardial function.

Judy, K.D., G.B. Bulkley, B.E. Hedlund, and D.M. Long (1994). Proposed toxic oxidant inhibitors fail to reduce brain edema. Acta Neurochirurgica/ Supplementum 60: 89-93. ISSN: 0065-1419.
Abstract: Toxic oxidants (oxygen free radicals) have been implicated in the formation of brain edema from ischemia-reperfusion injury or tumor growth. We investigated the ability of an iron chelator, a calcium channel blocker, and a xanthine oxidase inhibitor to reduce formation of brain edema following a cold lesion in cats. The agents were given independently of each other in an attempt to inhibit the Haber-Weiss reaction, prevent Ca++ modulated uncoupling of oxidative phosphorylation, and inhibit the generation of toxic oxidants via xanthine oxidase, respectively. Pentastarch-deferoxamine conjugate at a dose of 50 mg/kg was given 15 minutes before and 60 minutes after the cold lesion. Nimodipine was given at a dose of 1 mg/kg 1 hour before and 2 hours after the cold lesion. Allopurinol was given at a dose of 50 mg/kg 24 hours before, at the time of the lesion and, 24 and 48 hours after the lesion. Gravimetric measurements of multiple brain areas were performed at 24 hours post-lesion in the pentastarch-deferoxamine and nimodipine groups and at 72 hours post-lesion in the allopurinol group. None of these agents led to significant reduction in brain edema formation as measured with a gravimetric column of kerosene and bromobenzene. Pentastarch-deferoxamine conjugate was utilized to avoid the confounding effects of arterial hypotension which is seen with intravenous deferoxamine. There was even a suggestion of increased edema in the periventricular white matter in animals treated with nimodipine. Taken together, independent inhibition of the Haber-Weiss reaction, of calcium channels, or of xanthine oxidase does not reduce formation of brain edema in the cold lesion model.
Descriptors: allopurinol, brain edema, brain injuries, calcium, cerebral infarction, deferoxamine, nimodipine, reactive oxygen species, cats, cerebral cortex, cerebral cortex injuries, cerebral cortex, dose response relationship, drug, freezing, water electrolyte balance.

Justus, C. and J.F. Quirke (1995). Dose-response relationship for the antipyretic effect of meloxicam in an endotoxin model in cats. Veterinary Research Communications 19(4): 321-330. ISSN: 0165-7380.
NAL Call Number: SF601. V38
Descriptors: cats, antipyretics, endotoxins, drugs , toxic substances, toxins .

Kadoi, K., H. Kamata, S. Ohba, T. Satoh, and Y. Inaba (1998). Experimental infection in spf kittens with a particular calicivirus strain originally isolated from lion. Microbiologica 21(3): 255-258. ISSN: 1121-7138.
NAL Call Number: QR1. M57
Descriptors: infection , kittens, calicivirus, intranasal, lion, vesicular disease, viral infection, viral disease.

Kamata, I., Y. Terai, and T. Ohmoto (2003). Attempt to establish an experimental animal model of moyamoya disease using immuno-embolic material--histological changes of the arterial wall resulting from immunological reaction in cats. Acta Medica Okayama 57(3): 143-150. ISSN: 0386-300X.
Abstract: In this study, we investigated the relationship between intimal thickening of the internal carotid artery (ICA) and immunological reaction, and between occlusion of the ICA and development of basal collateral vessels in moyamoya disease. Rod-shaped lactic acid-glycolic acid copolymer (LGA-50) and N-acetylmuramyl-L-alanyl-D-isoglutamine (muramyl dipeptide: MDP), and immuno-embolic material, were injected into cats unilaterally via the common carotid artery. Histological changes of duplication of the internal elastic lamina could be seen mainly in the terminal portion of the ICA in the animals injected with rod-shaped LGA-50 containing MDP. No angiographic changes were seen in any of the animals. These findings suggest that the immunological reaction induced by MDP caused histological changes in the intima of the ICA similar to those observed in moyamoya disease. This experimental study, however, could not clarify the development of the basal collateral vessels.
Descriptors: acetylmuramyl alanyl isoglutamine, immunologic adjuvants, carotid arteries, cats, animal disease models, moyamoya disease, carotid arteries, cerebral angiograpHy, drug combinations, intra arterial injections, lactic acid, polyglycolic acid, polymers, tunica intima.

Kaneko, K., H. Ando, Y. Watanabe, T. Seo, and T. Harada (2000). Pathologic changes in the common bile duct of an experimental model with pancreaticobiliary maljunction without biliary dilatation. Pediatric Surgery International 16(1-2): 26-8. ISSN: 0179-0358.
Abstract: Pancreaticobiliary maljunction (PBM), a congenital anomaly, causes regurgitation of pancreatic juice into the biliary tract, where it exerts a hazardous influence. However, changes in the common bile duct (CBD) remain obscure due to a lack of suitable experimental models. Using cats, we have developed an experimental model of PBM without bile-duct dilatation that allows the pure effects of PBM to be studied. Histologic and cellular kinetic changes in the CBD were analyzed in 6 controls and 9 experimental animals that survived for more than 6 months. CBD sections were stained with hematoxylin and eosin and a monoclonal antibody to the proliferating cell nuclear antigen (PCNA). Invaginations of the bile-duct epithelium or parietal sacculi increased, and peribiliary glands were well-developed. PCNA-positive cells significantly increased in the CBD, especially in the parietal sacculi and glands. It is concluded that PBM increases the cell cycle in CBD epithelium and subsequently developed peribiliary glands. These developed glands may be associated with the formation of protein plugs, often seen in patients with PBM.
Descriptors: biliary tract diseases, common bile duct, cats, common bile duct, dilatation, pathologic, animal disease models, epithelium, immunohistochemistry, pancreatic diseases, proliferating cell nuclear antigen analysis.

Karanjia, N.D., A.L. Widdison, F.J. Lutrin, and H.A. Reber (1994). Dopamine in models of alcoholic acute pancreatitis. Gut 35(4): 547-51. ISSN: 0017-5749.
NAL Call Number: RC799 G8
Abstract: Acute oedematous pancreatitis and acute haemorrhagic pancreatitis were studied using the low pressure duct perfusion models of alcoholic pancreatitis in cats. After creating either form over 24 hours, each pancreas was histologically graded and assigned an inflammatory score (0-16; absent-severe). Urinary trypsinogen activation peptide concentrations were also used as a measure of severity. Using the model of acute haemorrhagic pancreatitis, it was previously shown that low dose dopamine (5 micrograms/kg.m) reduced the inflammatory score at 24 hours and that this effect was mediated by a reduction in pancreatic microvascular permeability acting via dopaminergic and beta adrenergic receptors. Further studies were conducted and are reported here. In experiment 1 different doses of dopamine in established alcoholic acute haemorrhagic pancreatitis were studied. In group 1 control cats (no dopamine), the inflammatory score was 10.5 (interquartile range (IQR)4). In groups 2, 3, and 4, haemorrhagic pancreatitis was induced. Twelve hours later dopamine was infused for six hours, in the doses of 2 micrograms/kg.min, 5 micrograms/kg.min, and 50 micrograms/kg.min respectively. The inflammatory score in group 2 was 7 (IQR 0.5, p < 0.05 v group 1), in group 3 it was 7 (IQR 2, p < 0.05 v group 1), and in group 4 it was 7 (IQR 4, p < 0.05 v group 1). This was matched by significantly lower levels of urinary tripsinogen activation peptide at 24 hours. In experiment 2 (group 5) we tried to reduce microvascular permeability further by combining dopamine with antihistamines, but there was no improvement in the inflammatory score. As oedematous pancreatitis is the commoner and milder form of acute pancreatitis in clinical practice, in experiment 3 we looked at the effect of dopamine in this model. In group 6 control cats (no treatment), the inflammatory score was 7 (IQR 3, p < 0.05 v group 1). In group 7 cats given dopamine (5 micrograms/kg.min for six hours) from 12 hours after the onset of actue oedematous pancreatitis, the inflammatory score was reduced to 4(IQR 2, p < 0.05 v group 6). This was matched by a significant reduction in the 24 hour urinary tripsin activation peptide concentration.
Descriptors: dopamine, pancreatitis, acute disease, cats, animal disease models, dose response relationship, drug, combination, edema, ethanol, hemorrhage, histamine antagonists, pancreatic diseases, pancreatitis.

Kataoka, N. (1994). Regional differences in seizure threshold following systemic and topical administration of penicillin in cats. The Hokkaido Journal of Medical Science, [Hokkaido Igaku Zasshi] 69(1): 84-94. ISSN: 0367-6102.
Abstract: The regional differences of epileptic seizure susceptibilities in various brain structures were investigated by using the feline model of systemic and local applications of penicillin (PC). After PC application, "repetitive isolated discharges" (RIDs) were observed and thereafter, it developed to "sustained high-frequency discharge" (SHD). The following results were obtained. 1. After the intraperitoneal application of PC, the areas involved by RIDs in order of frequency were cerebral cortex, hippocampus, mesencephalic reticular formation, centro-median nucleus of thalamus, amygdaloid nucleus, dorsal median nucleus of thalamus and globus pallidus. SHD was firstly arising from cerebral cortex (100%), especially from suprasylvian gyrus of 13 out of 16 cats (18.2%). SHD immediately propagated to either the other cortical areas or subcortical structures. Hippocampus, centro-median nucleus and dorsal median nucleus of thalamus were rapidly involved by SHD from cerebral cortex in comparison with the other subcortical structures. 2. PC was applied topically on the surface of several different cortical areas. RIDs tended to appear in posterior suprasylvian gyrus. On the other hand, SHD arose from posterior ectosylvian gyrus in most cases. The mechanisms of initiation and propagation of epileptic discharge were discussed in conjunction with epileptic seizure susceptibility in various neuronal structures.
Descriptors: brain, epilepsy, penicillins, topical administration, cats, electroencephalography, injections, intraperitoneal, maximum allowable concentration, seizures.
Language of Text: Japanese.

Khan, T., R.M. Havey, S.T. Sayers, A. Patwardhan, and W.W. King (1999). Animal models of spinal cord contusion injuries. Laboratory Animal Science 49(2): 161-72. ISSN: 0023-6764.
NAL Call Number: 410.9 P94
Abstract: BACKGROUND AND PURPOSE: Traumatic spinal cord injury causes initial mechanical disruption of tissue, leading to a complex secondary sequence of pathophysiologic changes and neurologic impairment. These sequelae depend on the impact force delivered to the spinal cord at the time of injury. Successful clinical evaluation of the efficacy of any therapeutic regimen depends on the reliability and reproducibility of an experimental animal model. We describe a trauma device and the biomechanical parameters required to induce severe or moderate spinal cord contusion injury in cats and rats. METHODS: Recovery after injury was determined by behavioral, electrophysiologic, and histologic evaluations. RESULTS: Behavioral and electrophysiologic tests after injury clearly identified the experimental groups. A stable severe paraplegic state (defined as 6 months for cats and 8 weeks for rats), without evidence of behavioral or electrophysiologic recovery, was induced by a 65-Newton (N) load for cats and a 35-N load for rats. Moderate spinal cord contusion injury, from which cats and rats partially recovered after approximately 3 months and 4 weeks, respectively, was induced by a 45- and 25-N load, respectively. CONCLUSION: Use of these injury conditions provides reliable animal models for studies designed to evaluate potential therapeutic regimens for spinal cord injury.
Descriptors: contusions, animal disease models, spinal cord injuries, spinal cord injuries, spinal cord injuries, animal behavior, biomechanics, cats, electrophysiology, evoked potentials, motor, evoked potentials, somatosensory, paraplegia, rats, rats, sprague dawley, spinal cord, spinal cord, time factors.

Khanna, C. and K. Hunter (2005). Modeling metastasis in vivo. Carcinogenesis 26(3): 513-523. ISSN: 0143-3334.
NAL Call Number: RC268.5 .C38
Descriptors: animal models, cat, computational biology, tumor biology, metastasis, neoplastic disease, in vivo modelling, mathematical and computer techniques, grave prognosis, xenografts.

Kiroi, V.N. and E.I. Belova (1998). Spektral'nye kharakteristiki EKoG koshki v modeli emotsional'nogo stressa [Spectral EEG characteristics in emotional stress model in cats]. Rossiiskii Fiziologicheskii Zhurnal Imeni I/M/ Sechenova Rossiiskaia Akademiia Nauk 84(12): 1377-85. ISSN: 0869-8139.
NAL Call Number: QP1.F58
Abstract: Emotional stress induced a global activation of the brain electrical activity: a decrease in the power of the theta-, alpha-, and beta-1-frequency bands in animals with active behaviour, and a decrease in the power of the theta- and alpha-frequency bands in animals with behavioural inhibition. The findings suggest that two forms of emotional behaviour correspond to different patterns of the brain activity. Appearance of spindle-like activity in passive animals' parietal and occipital leads suggests a hypothetical suppression in associative parietal and visual neocortical areas involved in processing the sensory information.
Descriptors: electroencephalography, psychological stress, brain mapping, cats, heart rate, motor activity.
Language of Text: Russian.

Kittleson, M.D., K.M. Meurs, M.J. Munro, J.A. Kittleson, S.K. Liu, P.D. Pion, and J.A. Towbin (1999). Familial hypertrophic cardiomyopathy in maine coon cats: An animal model of human disease. Circulation 99(24): 3172-3180. ISSN: 0009-7322.
NAL Call Number: RC681 .A1C8
Abstract: BACKGROUND: A naturally occurring animal model of familial hypertrophic cardiomyopathy (FHCM) is lacking. We identified a family of Maine coon cats with HCM and developed a colony to determine mode of inheritance, phenotypic expression, and natural history of the disease. METHODS AND RESULTS: A proband was identified, and related cats were bred to produce a colony. Affected and unaffected cats were bred to determine the mode of inheritance. Echocardiography was used to identify affected offspring and determine phenotypic expression. Echocardiograms were repeated serially to determine the natural history of the disease. Of 22 offspring from breeding affected to unaffected cats, 12 (55%) were affected. When affected cats were bred to affected cats, 4 (45%) of the 9 were affected, 2 (22%) unaffected, and 3 (33%) stillborn. Findings were consistent with an autosomal dominant mode of inheritance with 100% penetrance, with the stillborns representing lethal homozygotes that died in utero. Affected cats usually did not have phenotypic evidence of HCM before 6 months of age, developed HCM during adolescence, and developed severe HCM during young adulthood. Papillary muscle hypertrophy that produced midcavitary obstruction and systolic anterior motion of the mitral valve was the most consistent manifestation of HCM. Cats died suddenly (n=5) or of heart failure (n=3). Histopathology of the myocardium revealed myocardial fiber disarray, intramural coronary arteriosclerosis, and interstitial fibrosis. CONCLUSIONS: HCM in this family of Maine coon cats closely resembles the human form of FHCM and should prove a valuable tool for studying the gross, cellular, and molecular pathophysiology of the disease.
Descriptors: cats, animal disease models, hypertrophic cardiomyopathy, echocardiograpHy, hypertropHy, muscle fibers, myocardium, papillary muscles, pedigree, phenotype.

Klinke, R., R. Hartmann, S. Heid, J. Tillein, and A. Kral (2001). Plastic changes in the auditory cortex of congenitally deaf cats following cochlear implantation. Audiology and Neuro Otology 6(4): 203-206. ISSN: 1420-3030.
Descriptors: auditory cortex, cochlear implantation, deafness congenital, deafness surgery, neuronal plasticity, brain stem, cats, electric stimulation, neurons, postoperative period, reflex.

Kobelt, F., U. Schreck, and H.A. Henrich (1994). Involvement of liver in the decompensation of hemorrhagic shock. Shock 2(4): 281-8. ISSN: 1073-2322.
Abstract: In a hemorrhagic shock model without adequate volume resuscitation we investigated the question whether a biochemical stabilization of liver function by applying 2-mercaptopropionyl-glycine (2MPG) may influence the shock dynamics especially the transition from compensated to decompensated shock and the development of multiple organ failure (MOF). The application of a bolus of 10 mg/kg 2MPG just after hemorrhage had significantly beneficial effects on shock dynamics. All measured blood parameters demonstrate a less severe liver dysfunction. We found a decisive recovery of systemic pH, prolonged high levels of blood glucose, a better ammonia detoxification, arterial ketone ratios (acetoacetate/beta-OH-butyrat) above about 0.25, and a significantly increased survival time from 200 +/- 10 min to more than 240 min after hemorrhage. Decompensation of the 2MPG group started about 60 min after decompensation of the shock group. The transition to decompensation was combined in the shock group as well as in the 2MPG group with a severe liver dysfunction indicated by an arterial ketone ratio below .25. Decreasing levels of blood thiobarbituric reactive material in compensated shock of both groups demonstrate that production of free radicals did not primarily cause decompensation, but increasing levels of thiobarbituric reactive material during decompensation seems to be one of the factors mediating MOF. Our data support the hypothesis of the liver being a barrier against decompensation of shock and MOF.
Descriptors: blood pressure, liver, mitochondria, liver, shock, hemorrhagic, thiopronine, acetoacetates, ammonia, glucose, cats, diastole, hydroxybutyrates, liver, liver, liver circulation, mitochondria, liver, biological models, oxidation reduction, perfusion, shock, hemorrhagic, splanchnic circulation, systole, thiobarbituric acid reactive substances analysis, uric acid.

Koirala, T.R., K. Nakagaki, T. Ishida, S. Nonaka, S. Morikawa, and T. Tabira (2001). Decreased expression of MAP-2 and GAD in the brain of cats infected with feline immunodeficiency virus. The Tohoku Journal of Experimental Medicine 195(3): 141-51. ISSN: 0040-8727.
Abstract: HIV-1 infection is often complicated by the dysfunction of central nervous system (CNS). Degenerative neuronal changes as well as neuronal loss have been documented in individuals with acquired immunodeficiency syndrome. Feline immunodeficiency virus (FIV) causes similar CNS manifestation and FIV infected cats provide an animal model for human immunodeficiency virus infection in humans. In this study, we examined the brain of FIV-infected cats and controls with immunohistochemical techniques using antibodies to microtubule-associated protein 2 (MAP-2) and glutamic acid decarboxylase (GAD). We found a significant decrease in expression of MAP-2 and GAD in neurons of infected animals compared to controls. In contrast, the expression of neurofilaments and glial fibrillary acidic protein was rather increased. The changes observed in the brain were similar to those seen in humans undergoing the normal aging process as well as those suffering from neurological diseases like Alzheimer's disease and other dementing disorders. These changes in the feline brain give insight into the deleterious effects of FIV on the CNS.
Descriptors: brain, feline acquired immunodeficiency syndrome, glutamate decarboxylase, microtubule associated proteins, cats, glial fibrillary acidic protein, immunohistochemistry, neurofilament proteins, neurons, reference values.

Kotter, R. and F.T. Sommer (2000). Global relationship between anatomical connectivity and activity propagation in the cerebral cortex. Philosophical Transactions of the Royal Society of London/ Series B Biological Sciences 355(1393): 127-34. ISSN: 0962-8436.
NAL Call Number: 501 L84Pb
Abstract: Anatomical connectivity is a prerequisite for cooperative interactions between cortical areas, but it has yet to be demonstrated that association fibre networks determine the macroscopical flow of activity in the cerebral cortex. To test this notion, we constructed a large-scale model of cortical areas whose interconnections were based on published anatomical data from tracing studies. Using this model we simulated the propagation of activity in response to activation of individual cortical areas and compared the resulting topographic activation patterns to electrophysiological observations on the global spread of epileptic activity following intracortical stimulation. Here we show that a neural network with connectivity derived from experimental data reproduces cortical propagation of activity significantly better than networks with different types of neighbourhood-based connectivity or random connections. Our results indicate that association fibres and their relative connection strengths are useful predictors of global topographic activation patterns in the cerebral cortex. This global structure-function relationship may open a door to explicit interpretation of cortical activation data in terms of underlying anatomical connectivity.
Descriptors: cerebral cortex, computer simulation, models, neurological, nerve net, brain mapping, cats, convulsants, epilepsy, neural pathways, strychnine.

Krebs, F.C., H. Ross, J. McAllister, and B. Wigdahl (2000). HIV-1-associated central nervous system dysfunction. Advances in Pharmacology 49: 315-385. ISSN: 0568-0123.
Abstract: Despite more than 15 years of extensive investigative efforts, a complete understanding of the neurological consequences of HIV-1 CNS infection remains elusive. Although the resources of numerous investigators have been focused on studies of HIV-1-associated CNS disease, the complex nature of the disease processes that underlie the clinical, pathological, and cellular manifestations of HIV-1 CNS infection have required a larger volume of studies than was initially envisioned. Several major areas remain as the focus of current research efforts. One of the more pressing issues facing researchers and clinicians alike is the search for correlates to the development of HIV-1-associated CNS neuropathology and the onset of HIVD. Although numerous parameters have been studied, none have been shown to be absolute predictors or markers of HIV-1-related CNS dysfunction. The identification of solid correlates of HIVD is an important goal that would permit clinical identification of individuals at risk for developing potentially crippling, life-threatening CNS abnormalities and would facilitate early treatment of nascent neurological problems. A more complete comprehension of the cellular foundations of CNS dysfunction and HIVD is also a fundamental part of strategies designed to treat or prevent HIV-1-associated CNS disease. Future investigations will strive to expand the body of knowledge concerning the complex interactions between infected and uninfected neuroglial cells and the roles of numerous cytokines, chemokines, and other soluble agents that are deregulated during HIV-1 CNS infection. In particular, a thorough understanding of the mechanisms of neurotoxicity may facilitate the development of new therapies that alleviate or eliminate the clinical consequences of CNS infection. Finally, investigators will continue to study HIVD within the context of single and combination drug therapies used in the treatment of HIV-1 infection and AIDS. As newer and more effective systemic treatments for HIV-1 infection and AIDS are introduced, the effects of these treatments on the onset, incidence, and severity of HIVD will also require intensive study. The impact of drug therapies on the ability of the CNS to act as an HIV-1 reservoir will also need to be addressed. Introduction of each new drug or drug combination will necessitate studies of drug penetration into the CNS and efficacy against the development of CNS abnormalities. Furthermore, as more effective treatments prolong the lifespan of individuals infected with HIV-1, the impact of extended survival on the occurrence and severity of HIVD will also require further investigations. The quest for answers to these and other questions will be complicated by the diversity of experimental systems used to study different aspects of HIV-1 CNS infection and HIVD. Each system has its own unique strengths and weaknesses. Clinical observations provide a continuous spectrum of symptomatic findings but reveal little about the underlying mechanisms of disease. In vivo imaging techniques, such as CT and MRI, also provide a continuum of observations, but the images are limited in their resolution. Neuropathological examinations of postmortem HIV-1-infected brains offer gross, cellular, and molecular views (including phenotypic and genotypic analyses of CNS viral isolates) of the diseased brain, but only provide a snapshot of the end-stage neurologic dysfunction. Studies that rely on animal surrogates for HIV-1, including SIV, simian-HIV (SHIV), feline immunodeficiency virus (FIV), visna virus, and HIV-1 SCID-hu models, permit experimental protocols that cannot be carried out in humans, but are limited by the fidelity with which each virus and animal model emulates the conditions and events observed in the human host. Finally, in vitro techniques, which include the use of primary cells and cell lines, adult or fetal human cell cultures, and BBB barrier model systems, are also convenient means by which aspe
Descriptors: AIDS dementia complex, acquired immunodeficiency syndrome, brain diseases, HIV 1 pathogenicity, AIDS dementia complex, acquired immunodeficiency syndrome, antiretroviral therapy, highly active, astrocytes, brain, brain, brain diseases, ccaat enhancer binding protein beta, gene expression regulation, viral, HIV 1, magnetic resonance imaging, microglia, receptors, chemokine, tomography, x ray computed, transcription factor, sp1.

Kriebel, R.M. and J.P.2. McAllister (2000). Pathology of the hippocampus in experimental feline infantile hydrocephalus. Neurological Research 22(1): 29-36. ISSN: 0161-6412.
Abstract: Hydrocephalus is responsible for many pediatric neurological deficits presumed to be caused by neocortical pathophysiology. Relatively little is known about the role of non-neocortical CNS structures in this condition. In the present work experimental infantile hydrocephalus produced by intracisternal kaolin injection was studied in a neonate kitten model. The hippocampal formation was processed for electron microscopy, and the neuropil of the CA3 region was examined in untreated, severely hydrocephalic and age-matched normal animals. Both macroscopically and microscopically the thickness of the hippocampus was not decreased. Hippocampal pyramidal neurons were found in varying stages of cytoplasmic densification, and dendritic and axonal processes exhibited hydropic cellular deterioration. The number of synaptic contacts was decreased. However, there was no indication of edematous extracellular space and the ependymal covering of the hippocampus was intact. The macroscopic structural integrity of the hippocampus, as well as the dendritic, axonal and synaptic alterations, suggest that the dark pyramidal neurons are the result of deafferentation, which may have profound effects on learning and memory.
Descriptors: hippocampus, hydrocephalus, pyramidal cells, animals, newborn, axons, axons ultrastructure, cats, dendrites, dendrites ultrastructure, hippocampus ultrastructure, neuropil, neuropil ultrastructure, pyramidal cells ultrastructure.

Kuriakose, M., D. Banks, and B. Matthews (1994). Behavioural responses to tooth-pulp stimulation in cats. Society for Neuroscience Abstracts 20(1-2): 762. ISSN: 0190-5295.
NAL Call Number: QP351. S6
Descriptors: behavior, cats, tooth pulp, nervous system, sense organs, behavioral response, nociception model, pain .

Laser, M., C.D. Willey, W. Jiang, G. Cooper, D.R. Menick, M.R. Zile, and D. Kuppuswamy (2000). A potential mechanism for focal complex formation in hypertrophying myocardium. Circulation 102(18 Supplement): II.290. ISSN: 0009-7322.
NAL Call Number: RC681. A1C8
Descriptors: cardiovascular system, circulation, myocardial hypertropHy, Cardiomegaly, heart disease, arginyl glycyl aspartic acid induced, mechanism, right ventricular pressure overload.
Notes: Meeting Information: Abstracts from American Heart Association Scientific Sessions 2000, New Orleans, Louisiana, USA; November 12-15, 2000.

Lee, A. (2000). Animal models of gastroduodenal ulcer disease. Clinical Gastroenterology 14(1): 75-96. ISSN: 0192-0790.
Abstract: Animal models have played a significant role in research that aims to understand peptic ulceration. Firstly, they have helped define basic mechanisms of gastric mucosal defence and repair. The basis for gastric injury following NSAID administration was facilitated by animal models that correlated well with disease in humans. In early studies, ulceration was induced by grossly damaging insults to the gastric mucosa that were unphysiological. With refinement these models provided a clearer appreciation of stress ulceration. The discovery of Helicobacter pylori (H. pylori), as the cause of most ulcers, resulted in a need to re-evaluate the early literature and to look for new models. To date, these have contributed little to our understanding of the pathogenesis of H. pylori-induced ulcer. A major aim of this chapter is to suggest that thorough understanding of the animal models of Helicobacter infection may provide important new insights, in particular the factors controlling gastritis, the essential precursor lesion of ulceration. Available models include primates, cats, guinea pigs, ferrets and pigs. The mouse models provide opportunity for identifying both essential bacterial and host factors. The most severe pathologies are seen in the H. pylori-infected Mongolian gerbil with ulcers being formed in most animals. This is likely to become the standard animal model for investigation of peptic ulcer disease.
Descriptors: animal disease models, duodenal diseases, duodenal diseases microbiology, stomach ulcer, stomach ulcer microbiology, cats, ferrets, gerbillinae, helicobacter infections, helicobacter pylori, mice, swine.

Lee, A. (1998). Animal models for host-pathogen interaction studies. British Medical Bulletin 54(1): 163-73. ISSN: 0007-1420.
Abstract: There is no model of Helicobacter pylori infection that exactly mimics the human diseases. In a particular, there are no good models of ulceration or gastric adenocarcinoma. Patterns of gastritis induced in the animals tend to be lymphocytic and lack the neutrophil infiltration typical of H. pylori infection in the adult. However, the animal models are starting to provide valuable information with respect to factors involved in the colonisation of the gastric mucosa and the importance of host factors in the development of gastric atrophy, as well as making possible the screening of potential therapeutic agents and vaccine candidates. Models include gnotobiotic piglets, primates, cats, dogs, ferrets and a range of rodents. Recent advances in the mouse models mean that they will allow us to dissect bacterial host interactions in a novel manner due to the availability of a wide range of immunological reagents and numerous mutant or transgenic strains.
Descriptors: animal disease models, helicobacter infections microbiology, helicobacter pylori, stomach diseases microbiology, cats, dogs, ferrets, mice, mice, mutant strains, mice, transgenic, swine.

Lee, S.K., D.I. Kim, S.Y. Kim, D.J. Kim, J.E. Lee, and J.H. Kim (2004). Reperfusion cellular injury in an animal model of transient ischemia. American Journal of Neuroradiology 25(8): 1342-7. ISSN: 0195-6108.
Abstract: BACKGROUND AND PURPOSE: Early thrombolytic therapy is encouraged in hyperacute stroke, although this might result in delayed reperfusion injury. Our purpose was to investigate the serial changes in cerebral perfusion following transient ischemia by means of MR imaging and to correlate them with the histologic findings obtained by using the TdT-mediated dUTP-biotin nick-end labeling (TUNEL) assay. METHODS: One-hour transient occlusion of the middle cerebral artery was produced in 10 cats. Serial perfusion-weighted MR imaging was performed for 3 days after reperfusion. The reperfusion characteristics in each region of the brain were classified into four groups according to the serial perfusion MR imaging status: normal perfusion (N), continuous hyperperfusion (I), early hyperperfusion and gradual decrease (II), and persistent hypoperfusion (III). After the last imaging session, a specimen was obtained, and TUNEL staining was performed. TUNEL-positive cells were counted under a high-power-field (HPF) light microscope (x200). The degree of TUNEL positivity was compared among the four reperfusion groups classified on the basis of serial perfusion-weighted imaging findings. RESULTS: Group N had 16.8 +/- 5.1 TUNEL-positive cells per HPF. Groups I and II had a statistically significant increase in TUNEL positivity (39.5 +/- 13.4 and 43.6 +/- 16.7 cells per HPF; P < .01, one-way analysis of variance), whereas group III had a statistically insignificant increase in TUNEL positivity (23.3 +/- 6.9 cells per HPF). CONCLUSION: Reperfusion followed by hyperperfusion induced cellular damage, although the initial MR imaging findings were normal. The inclusion of anti-reperfusion injury therapy should be considered in thrombolytic treatment.
Descriptors: animal disease models, ischemic attack, transient diagnosis, reperfusion injury diagnosis, cats, in situ nick end labeling, ischemic attack, transient, ischemic attack, transient, reperfusion injury, reperfusion injury.

Lefer, A.M., A.S. Weyrich, and M. Buerke (1994). Selectin blockade in myocardial ischemia-reperfusion injury. Journal of Cellular Biochemistry Supplement 0(18D): 262. ISSN: 0733-1959.
NAL Call Number: QH504 .J67
Descriptors: circulation, cardiovascular system, immune system, cardioprotective agents, cardiovascular agents, cell adhesion, coronary angioplasty, feline model, immunologic agents, monoclonal antibodies, therapy potential, thrombolysis .

Leung, J.W., E.D. Libby, D.W. Morck, S.G. McKay, Y. Liu, K. Lam, and M.E. Olson (2000). Is prophylactic ciprofloxacin effective in delaying biliary stent blockage? Gastrointestinal Endoscopy 52(2): 175-82. ISSN: 0016-5107.
Abstract: BACKGROUND: Late stent blockage is a major complication of endoscopic stent insertion for malignant obstructive jaundice. Stents block as a result of bacterial infection and biofilm formation. We report a randomized but unblinded study using an animal model to evaluate the effect of prophylactic ciprofloxacin, which selectively suppresses gram-negative bacteria, in an attempt to prolong stent patency. METHOD: Ten adult cats underwent surgical implantation of 5F polyethylene stents through common bile duct strictures created around the choledochotomy, with the tip of the stent left in the duodenum. Five animals received intravenous ciprofloxacin perioperatively and were then maintained on oral ciprofloxacin 25 mg twice daily. Control cats were not given antibiotics. The animals were sacrificed when signs of biliary obstruction or cholangitis persisted for more than 3 days or at the end of the 16-week study period. Stents were removed and examined for patency. In addition, the stents were cultured to recover the adherent bacteria. RESULTS: All control animals developed stent blockage within 4 weeks. Two ciprofloxacin-treated cats developed stent blockage at 21 and 42 days, respectively, whereas the other 3 cats had patent stents for the entire study period. There was a significant difference between the median stent patency of 112 days for the ciprofloxacin group versus 16 days for the control group (p < 0.02). Bacteriologic cultures showed that the bile and blocked stents from the control group had predominantly gram-negative bacteria, whereas the bile and stents of the ciprofloxacin group had gram-positive and anaerobic bacteria, with an absence of gram-negative bacteria (p < 0.01). CONCLUSION: Ciprofloxacin prophylaxis eliminates gram-negative bacterial infection in bile and minimizes sludge formation and may have a potential benefit in delaying stent blockage.
Descriptors: anti infective agents, antibiotic prophylaxis, ciprofloxacin, common bile duct diseases surgery, postoperative, stents, oral administration, cats, animal disease models, drug administration schedule, equipment safety, follow up studies, infusions, intravenous, random allocation, reference values, nonparametric statistics.

Levine, D.F., D.E. Witherspoon, J.L. Gutmann, and A.M. Iacopino (2001). Interleukin-1beta production in periradicular lesions in a human immunodeficiency virus/acquired immune deficiency syndrome model compared with a noninfected host. Journal of Endodontics 27(8): 499-502. ISSN: 0099-2399.
Abstract: This study elucidates the role of interleukin-1 (IL-1) in developing periradicular lesions in immunocompetent and immunocompromised (human immunodeficiency virus/acquired immune deficiency syndrome) hosts. Eight cats were immunosuppressed with steroids before infection with feline immunodeficiency virus (FIV). Eight uninoculated cats served as controls. Periradicular lesions were induced around the canine teeth. At 1 and 4 wk periradicular exudate was sampled via the root canals. IL-1beta levels were measured with ELISA. Data were analyzed using the Mann-Whitney U test and the Wilcoxon signed rank test. Statistically significant differences existed in cytokine levels between the FIV and non-FIV groups (p < 0.001). Cytokines were below detectable levels in the FIV group. A significant decrease in IL-1beta levels at 4 wk compared with 1 wk occurred in the non-FIV group (p < 0.05). In conclusion decreased IL-1beta production was obtained in the FIV group. In the non-FIV group decreases in IL-1beta levels were encountered at the chronic stage of the periradicular lesion compared with the acute stage.
Descriptors: feline acquired immunodeficiency syndrome, interleukin 1 biosynthesis, periapical periodontitis, acute disease, cats, chronic disease, animal disease models, enzyme linked immunosorbent assay, feline acquired immunodeficiency syndrome, immunocompromised host, nonparametric statistics.

Lewis, G.P., C.S. Sethi, D.G. Charteris, K.A. Linberg, K.C. Talaga, and S.K. Fisher (2002). Repeated retinal detachment and reattachment in an animal model as an experimental paradigm for complex detachments in humans. In: Annual Meeting Abstract Search and Program Planner: Annual Meeting of the Association For Research in Vision and Ophthalmology, May 5, 2002-May 10, 2002, Fort Lauderdale, Florida, USA; Vol. 2002, p. Abstract No. 4540.
Descriptors: feline model, sense organs, sensory reception, retinal detachment, Retinal Detachment, eye disease, immunocytochemical analysis, immunologic techniques, laboratory techniques, retinal reattachment, clinical techniques, cellular response, visual recovery.

Lexa, F.J., R.I. Grossman, and A.C. Rosenquist (1994). Dyke Award paper. MR of wallerian degeneration in the feline visual system: characterization by magnetization transfer rate with histopathologic correlation. American Journal of Neuroradiology 15(2): 201-12. ISSN: 0195-6108.
Abstract: PURPOSE: To examine the utility of measuring magnetization transfer ratio for for delineating the dynamic changes of wallerian degeneration which occur after controlled injury in a feline model in which anatomic pathways are well understood. METHODS: Using standard neurosurgical techniques, discrete lesions were made to ablate the visual cortex. Gradient imaging was performed serially at 1.5 T, with and without a saturation pulse to create a magnetization transfer effect. At varying intervals, the animals were killed for histologic analysis. RESULTS: Within the first 2 weeks there is a statistically significant increase in magnetization transfer ratio relative to the control hemisphere within the white matter connections between the lateral geniculate nucleus and the visual cortex at a time when no effects are visually detectable on spin-echo images. Between 16 and 28 days, this reverses to a decrease in magnetization transfer ratio in both the lateral geniculate nucleus itself and the adjacent superolateral white matter. More remote white matter tracts remained stable, without significant change. CONCLUSIONS: Magnetization transfer ratio seems to be more sensitive for early detection of degeneration than conventional spin-echo imaging. Moreover, temporal changes in magnetization transfer ratio seem to correspond well with known histologic phases of wallerian degeneration.
Descriptors: geniculate bodies, magnetic resonance imaging instrumentation, visual cortex, wallerian degeneration, brain mapping instrumentation, cats, dominance, cerebral, electron microscopy, neuroglia ultrastructure, neurons ultrastructure, stereotaxic techniques instrumentation, visual pathways.

Li, P., K.F. Pitsillides, S.V. Rendig, H.L. Pan, and J.C. Longhurst (1998). Reversal of reflex-induced myocardial ischemia by median nerve stimulation: a feline model of electroacupuncture. Circulation 97(12): 1186-94. ISSN: 0009-7322.
NAL Call Number: RC681. A1C8
Abstract: BACKGROUND: Acupuncture is reported to reduce myocardial ischemia, arrhythmias, and hypertension. To investigate the physiological mechanisms underlying these observations, a model of reflex-induced, reversible myocardial ischemia was developed to test the effects of median nerve stimulation as a surrogate for electroacupuncture. METHODS AND RESULTS: Chloralose-anesthetized cats were instrumented to measure arterial blood pressure, left ventricular pressure, left ventricular dP/dt, heart rate, left anterior descending (LAD) coronary blood velocity, and regional wall motion. The LAD artery either was partially occluded or a small diagonal branch was ligated. Subsequently, transient reflex activation of the cardiovascular system was evoked by application of bradykinin (typically 1 microg/mL) to the gallbladder, which significantly increased myocardial oxygen demand (double product), left ventricular dP/dt, and coronary blood velocity and caused ischemia-induced regional dysfunction, evidenced by significant (P<.05) reduction in normalized wall thickening (10.7+/-4.2% versus -23.6+/-2.9%; control versus ischemia; n=7). However, when median nerves were stimulated with low frequency (5 Hz) to mimic electroacupuncture, bradykinin-induced change in normalized wall thickening was significantly improved (-23.6+/-2.9% versus 9.8+/-4.9%; ischemia versus median nerve stimulation, P<.05) and remained augmented > or = 1 hour. Results were similar in partial and complete occlusion groups. Significant improvement in wall thickening was associated with unchanged increment of coronary blood velocity and significantly diminished increments of double product and diastolic blood pressure. CONCLUSIONS: These results suggest that stimulation of the median nerve to mimic electroacupuncture diminishes regional myocardial ischemia triggered by a sympathetically mediated increase in cardiac oxygen demand. The mechanism of this effect is related to reduction in cardiac oxygen demand, secondary to a diminished pressor response. These data provide the first documentation of the physiological mechanisms underlying the possible beneficial effect of electroacupuncture in the context of restricted coronary blood flow and augmented myocardial oxygen demand.
Descriptors: electroacupuncture, median nerve, myocardial ischemia, reflex, arterial occlusive diseases, arterial occlusive diseases therapy, arterial occlusive diseases ultrasonography, bradykinin, cats, coronary vessels, coronary vessels, electric stimulation, heart innervation, median nerve, myocardial ischemia ultrasonography, neurons, afferent.

Li, R., N. Fujitani, J.T. Jia, and H. Kimura (1998). Immunohistochemical indicators of early brain injury: an experimental study using the fluid-percussion model in cats. The American Journal of Forensic Medicine and Pathology 19(2): 129-36. ISSN: 0195-7910.
Abstract: To detect early changes in neurons and astrocytes by immunohistochemical methods using antibodies against the neuron-specific enolase (NSE), neurofilament, glial fibrillary acid protein (GFAP), and S-100 protein, a fluid-percussion injury model in cats was chosen, in which a severe grade of injury (3.5-5.5 atm) was produced. Neuropathologic changes were produced through brain deformation by pressure gradients at the time of injury. The neuronal NSE immunoreactivity in the parietal cortex and the brain stem began to decrease at 1 to 2 hours after injury and were reduced markedly or even lost 4 hours after injury. Axons in the cerebral white matter and corpus callosum and in the hemorrhage regions at the brain stem were waved and enlarged <4 hours after injury. From 4 hours after injury, retraction balls were found after staining by antibody for the neurofilament. The GFAP-positive astrocytes appeared in the impact site in the parietal cortex and in the brain stem from 4 hours after injury, whereas S-100-positive astrocytes were not markedly changed, indicating that early after the injury, astrocytes manifested reactive hypertrophy without proliferation. These results suggest that immunochemical studies on NSE, neurofilament, GFAP, and S-100 are useful in pathologic and forensic practice in a patient who survives for a short time after a fatal head injury but without obvious focal damage.
Descriptors: brain injuries, glial fibrillary acidic protein, neurofilament proteins, phosphopyruvate hydratase, s100 proteins, astrocytes, astrocytes, biological markers, brain injuries, brain stem, brain stem, cats, cerebral cortex, cerebral cortex, animal disease models, hemorrhage, immunoenzyme techniques, neurons, neurons.

Li, Z., A. Phadke, E.A. Weaver, J.M. Ball, and E.W. Collisson (2005). Feline CD8(+) cells induced with FIV infected, irradiated T cells produce multiple anti-FIV factors. Developmental and Comparative Immunology 29(9): 809-24. ISSN: 0145-305X.
Abstract: Feline immunodeficiency virus (FIV) infection in cats is the only non-primate, small animal model for HIV-AIDS. Replication of FIV has been shown to be optimally suppressed by soluble factors produced by inducer cell-stimulated feline CD8(+) cells from FIV-infected cats. The nature of this dose-dependent suppression of FIV was examined. Antiviral factors, produced in serum-free medium, were shown to be either heat stable or heat labile. Suppressing activity was identified in a heparin-bound fraction and the non-bound fraction and in fractions separated by reverse-phase HPLC. The FIV suppression could not be correlated with IFN type I or II. Neither alpha nor beta chemokines were likely candidates because molecular size exclusion centrifugation indicated that the major factors were larger than 50kD. Identified qualitative differences in the properties of the soluble suppressive activity generated from feline lymphocytes indicated that multiple factors are responsible for the non-cytolytic CD8(+) T cell suppression of FIV replication.

Lin, S., F. Gaschen, and J.M. Burgunder (1998). Utrophin is a regeneration-associated protein transiently present at the sarcolemma of regenerating skeletal muscle fibers in dystrophin-deficient hypertrophic feline muscular dystrophy. Journal of Neuropathology and Experimental Neurology 57(8): 780-90. ISSN: 0022-3069.
Abstract: Utrophin, an autosomal homologue of dystrophin, has been suggested as a possible therapeutic replacement of dystrophin in Duchenne or Becker muscular dystrophies (DMD/BMD). We have undertaken this study to examine the expression of utrophin in the skeletal muscle of dystrophin-deficient cats, a spontaneous animal model for dystrophinopathy. Dystrophin was normal in size, but very low in quantity by immunohistochemistry and Western blot. Utrophin was heterogeneously overexpressed at extrajunctional sarcolemma of regenerating muscle fibers, as defined by overexpression of the myogenic markers: vimentin, desmin, and developmental isoform of myosin heavy chain (MHCd). Muscle regeneration occurred in 6 stages as assessed by fiber size, and immunolabeling of desmin, vimentin, and MHCd. Differential developmental patterns of utrophin, alpha-sarcoglycan, and beta-dystroglycan expression were seen with an increase followed by a decrease and with changes in their respective location. These results suggest that utrophin is a regeneration-associated protein. It can functionally replace dystrophin in anchoring dystrophin-associated proteins (DAPs). However, the expression of utrophin and its anchored DAPs is restricted to the period of muscle regeneration and tends to decrease in late stages. This study therefore suggests a novel role of utrophin during skeletal muscle regeneration.
Descriptors: cytoskeletal proteins analysis, membrane proteins analysis, muscle fibers, muscle, skeletal, muscular dystrophy, animal, nerve tissue proteins analysis, regeneration, Western blot, cats, dystropHin deficiency, hypertropHy, immunohistochemistry, muscle fibers, muscle proteins analysis, muscle, skeletal, muscular dystrophy, animal, muscular dystrophy, animal, sarcolemma, time factors, utropHin.

Lin, Y.L., D. Noel, C. Mettling, B. Reant, J. Clot, C. Jorgensen, and P. Corbeau (2004). Feline immunodeficiency virus vectors for efficient transduction of primary human synoviocytes: application to an original model of rheumatoid arthritis. Human Gene Therapy 15(6): 588-96. ISSN: 1043-0342.
Abstract: The potential of gene therapeutics is hindered by the limitations of the delivery systems presently available. Recently, human immunodeficiency virus (HIV) vectors have been developed that allow the efficient and stable transduction of primary nondividing cells in vivo. Because of the safety concerns raised by HIV vectors, we developed a gene delivery system derived from the ungulate lentivirus feline immunodeficiency virus (FIV). We describe in the present study the optimization of the safety and efficiency of this system that proved to be as potent as HIV vectors to transduce nondividing cells, with titers over 10(8) transducing units per ml. We used this tool to transduce TNF-alpha into human primary synoviocytes, and showed a high efficiency of transduction. TNF-alpha-transduced synoviocytes injected into the knee joints of severe combined immunodeficient (SCID) mice induced cell proliferation, as well as cartilage and bone erosion as soon as day 7, creating a standardized, humanized animal model relevant for rheumatoid arthritis. FIV vectors appear to be promising tools for biologic research and gene therapy.
Descriptors: arthritis, rheumatoid, animal disease models, genetic vectors, feline immunodeficiency virus, synovial membrane, transduction, genetic, tumor necrosis factor alpha, arthritis, rheumatoid therapy, bone and bones, cartilage, cell proliferation, mice, mice, scid, synovial membrane, synovial membrane, tumor necrosis factor alpha.

Linenberger, M.L. and J.L. Abkowitz (1995). Haematological disorders associated with feline retrovirus infections. Bailliere's Clinical Haematology 8(1): 73-112. ISSN: 0950-3536.
Abstract: Feline oncornavirus and lentivirus infections have provided useful models to characterize the virus and host cell factors involved in a variety of marrow suppressive disorders and haematological malignancies. Exciting recent progress has been made in the characterization of the viral genotypic features involved in FeLV-associated diseases. Molecular studies have clearly defined the causal role of variant FeLV env gene determinants in two disorders: the T-lymphocyte cytopathicity and the clinical acute immunosuppression induced by the FeLV-FAIDS variant and the pure red cell aplasia induced by FeLV-C/Sarma. Variant or enFeLV env sequences also appear to play a role in FeLV-associated lymphomas. Additional studies are required to determine the host cell processes that are perturbed by these variant env gene products. In the case of the FeLV-FAIDS variant, the aberrant env gene products appear to impair superinfection interference, resulting in accumulation of unintegrated viral DNA and cell death. In other cases it is likely that the viral env proteins interact with host products that are important in cell viability and/or proliferation. Understanding of these mechanisms will therefore provide insights to factors involved in normal lymphohaematopoiesis. Similarly, studies of FeLV-induced haematological neoplasms should reveal recombination or rearrangement events involving as yet unidentified host gene sequences that encode products involved in normal cell growth regulation. These sequences may include novel protoncogenes or sequences homologous to genes implicated in human haematological malignancies. The haematological consequences of FIV are quite similar to those associated with HIV. As with HIV, FIV does not appear to directly infect myeloid or erythroid precursors, and the mechanisms of marrow suppression likely involve virus, viral antigen, and/or infected accessory cells in the marrow microenvironment. Studies using in vitro experimental models are required to define the effects of each of these microenvironmental elements on haematopoietic progenitors. As little is known about the molecular mechanisms of FIV pathogenesis, additional studies of disease-inducing FIV strains are needed to identify the genotypic features that correlate with virulent phenotypic features. Finally, experimental FIV infection in cats provides the opportunity to correlate in vivo virological and haematological changes with in vitro observations in a large animal model that closely mimics HIV infection in man.
Descriptors: feline acquired immunodeficiency syndrome, feline acquired immunodeficiency syndrome transmission, feline immunodeficiency virus, leukemia virus, feline, leukemia, feline, leukemia, feline transmission, antibodies, viral biosynthesis, antibodies, viral, bone marrow, bone marrow, cats, genes, viral, cellular immunity, feline immunodeficiency virus, feline immunodeficiency virus, leukemia virus, feline classification, leukemia virus, feline, leukemia virus, feline, lymphoma epidemiology, lymphoma, lymphoma, myelodysplastic syndromes, myelodysplastic syndromes, red cell aplasia, pure, red cell aplasia, pure, retroviridae classification, retroviridae proteins, retroviridae proteins, spumavirus pathogenicity.

Liu, B. (2003). Effects of nitric oxide synthase inhibitor to esophagus in a feline esophagitis model. Diseases of the Esophagus 16(4): 312-4. ISSN: 1120-8694.
Abstract: The present study explores the effects of nitric oxide synthase inhibitor on esophageal motility in a feline model with esophagitis. Perfusion of the esophagus with acid produced inflammatory changes of esophageal mucosa. The esophageal motility was measured before and after the perfusion. One group of cats was given nitric oxide inhibitor orally at the same time as the perfusion of acid. The control group was given water instead. Esophagitis impairs the motility of the esophagus. However, the esophageal motility of the cats that were given nitric oxide synthase inhibitor decreased less than that of the control group. The results suggested that during esophagitis there is an alteration of the nitric oxide synthase/nitric oxide pathway in the esophagus, which may be one of the important mechanisms of esophageal motility dysfunction.
Descriptors: enzyme inhibitors, esophagitis, esopHagogastric junction, nitric oxide synthase, nitroarginine, cats, esophagitis, esophagitis, esopHagogastric junction, esopHagogastric junction, gastrointestinal motility, gastrointestinal motility, hydrochloric acid, models, animal.

Liu, B., X. Liu, C. Tang, J. Liu, H. Wang, and P. Xie (2002). Esophageal dysmotility and the change of synthesis of nitric oxide in a feline esophagitis model. Diseases of the Esophagus 15(3): 193-8. ISSN: 1120-8694.
Abstract: The present study explores the changes of nitric oxide synthesis and esophageal dysmotility in a feline model of esophagitis. Perfusion of the esophagus with acid produced inflammatory changes of esophageal mucosa. The esophageal motility was measured before and after the perfusion. The nitric oxide synthase activity, the l-arginine uptake, and the content of cyclic guanine monophosphate of the muscle and the mucous membrane were determined and the NADPH-diaphorase was stained. Esophagitis impairs the motility of the esophagus. The nitric oxide synthase activity, the content of cyclic guanine monophosphate, the NADPH-diaphorase stain and the maximum velocity of l-arginine uptake of lower esophageal sphincter of the cats in the acid perfusion group were higher than those of the control group. The maximum velocity of l-arginine transport and the content of cyclic guanine monophosphate of the mucosa in the acid perfusion group were lower than those of the control group. The results suggested that during esophagitis there is an alteration of the l-arginine/nitric oxide synthase/nitric oxide pathway in the esophagus, which may be one of the important mechanisms of esophageal motility dysfunction.
Descriptors: esophageal motility disorders, esophagitis, esophagitis, nitric oxide biosynthesis, nitric oxide synthase, arginine analysis, cyclic gmp analysis, animal disease models, esophageal motility disorders, nitric oxide analysis, nitric oxide synthase analysis, probability, random allocation, reference values, sensitivity and specificity.

Liu, S.K. (2002). Animal hypertrophic cardiomyopathy: ideal model of human disease. Chinese Journal of Veterinary Science 22(6): 626-635. ISSN: 1005-4545.
NAL Call Number: SF604 .C58
Descriptors: animal models, arteries, cardiomyopathy, clinical aspects, fibrosis, heart, human diseases, lesions, myocardium, cats, dogs, man.
Language of Text: Chinese; Summary in English.

Lloyd, J., L. Askie, J. Smith, and W. Tarnow-Mordi (2003). Supplemental oxygen for the treatment of prethreshold retinopathy of prematurity. Cochrane Database of Systematic Reviews(2): 3482.
Online: http://www.cochrane.org
Abstract: Oxygen has long been implicated in the pathogenesis of retinopathy of prematurity (ROP) and is rigorously monitored in today's neonatal intensive care units. Recent research using a feline model has shown an improvement in ROP outcome of kittens treated with supplemental oxygen. Current treatment for ROP by retinal ablation is not without complications so a non-invasive method of treatment is preferred. The possible effects of long term oxygen supplementation on chronic lung disease, length of hospital stay and growth and development are, however, unknown. OBJECTIVES: To determine whether, in preterm or low birth weight infants with prethreshold ROP, targeting higher as compared to normal transcutaneous oxygen levels or pulse oximetry levels when using supplemental oxygen reduces the progression of ROP to threshold disease and improves visual outcome without any adverse effects. SEARCH STRATEGY: The standard search strategy of the Cochrane Neonatal Review Group was used. This included searches of the Oxford Database of Perinatal Trials, MEDLINE, previous reviews including cross references, abstracts, conferences and symposia proceedings, expert informants and journal handsearching. An additional literature search of the MEDLINE (1966-June 2002), EMBASE (1980-April 2002), and CINAHL (1982-April 2002) databases was conducted in order to locate any trials in addition to those provided by the Cochrane Controlled Trials Register (CENTRAL/CCTR, The Cochrane Library Issue 2, 2002). SELECTION CRITERIA: All randomised or quasi randomised studies comparing higher versus normal target oxygen levels in preterm or low birthweight infants with prethreshold ROP were eligible for inclusion. DATA COLLECTION AND ANALYSIS: The methodological quality of the one eligible trial was assessed independently by two authors for the degree of selection, performance, attrition and detection bias. Data regarding clinical outcomes including progression to threshold ROP, blindness or severe visual impairment, mortality, respiratory morbidities and long term growth were extracted and reviewed independently by two authors. Results were compared and differences resolved as required. Data analysis was conducted according to the standards of the Cochrane Neonatal Review Group. MAIN RESULTS: The one trial included in this review enrolled 649 infants. There was a trend for supplemental oxygen to reduce the progression to threshold ROP, however this did not reach statistical significance (RR 0.84, 95% CI 0.70, 1.02). A subgroup analysis of those infants without plus disease showed significantly fewer infants progressing to threshold ROP in infants treated with supplemental oxygen. However this analysis was not pre-specified so these results should be interpreted with caution. No significant effects were detected on blindness or severe visual function at three months corrected age, mortality, pneumonia, chronic lung disease or weight gain. Adverse pulmonary events were more common in the higher oxygen saturation group and these infants were in hospital and on supplemental oxygen for longer. Longer term visual outcomes were not reported. REVIEWER'S CONCLUSIONS: The results of this systematic review do not show a statistically significant reduction in the rate of progression to threshold ROP with supplemental oxygen treatment, but reveal increased adverse pulmonary sequelae with higher oxygen targeting in this group of preterm infants. Future research needs to be directed towards the question of whether infants without plus disease are more likely to respond to supplemental oxygen therapy than those with plus disease.
Descriptors: infant, low birth weight, infant, premature, oxygen, retinopathy of prematurity, infant, newborn, randomized controlled trials.

Lu, D., M. Solomonow, B. Zhou, R.V. Baratta, and L. Li (2004). Frequency-dependent changes in neuromuscular responses to cyclic lumbar flexion. Journal of Biomechanics 37(6): 845-55. ISSN: 0021-9290.
NAL Call Number: TA166. J6
Abstract: Repetitive lifting in the workplace has been identified to be a cause of low back disorders. Epidemiologic data further supports an hypothesis that higher repetition rate (i.e. frequency) is an added risk factor. The objective of this study was to provide experimental data testing the above hypothesis. An in vivo feline model was subjected to 20-min of cyclic lumbar loading at frequencies of 0.1 Hz and 0.5 Hz while monitoring the EMG from the L-3/4-L-5/6 multifidus muscles and the creep at the L-4/5 level. Seven hours of rest were allowed after the cyclic flexion/extension was terminated. During this rest period, a single test cycle was performed every hour to assess recovery of EMG and lumbar creep. The results demonstrate that cyclic lumbar flexion elicits a transient neuromuscular disorder consisting of EMG spasms during the cyclic loading and initial and delayed muscular hyperexcitabilities during the rest period. Cyclic loading at 0.5 Hz resulted in significant (p<0.05) increase in the hyperexcitability magnitude and duration during the recovery period. It was concluded that repetitive lumbar loading at fast rates is indeed a risk factor as it induces larger creep in the lumbar viscoelastic tissues which in turn intensify the resulting neuromuscular disorder.
Descriptors: cumulative trauma disorders, low back pain, lumbar vertebrae, cats, electromyogrphy, models, animal, neuromuscular junction, united states, workplace.

Maitland, M.E., T. Leonard, C.B. Frank, N.G. Shrive, and W. Herzog (1998). Method to assess in vivo knee stability longitudinally in an animal model of ligament injury. Journal of Orthopaedic Research 16(4): 441-7. ISSN: 0736-0266.
Abstract: The purpose of this study was to develop a method to prospectively quantify passive knee stability in an animal model of joint injury over time. Knee stability is defined here as the amount of translation or rotation of the tibia relative to the femur for a given application of force or moment, respectively. Five animals that had undergone transection of the anterior cruciate ligament and three control animals that had undergone a sham operation were anaesthetized and positioned in a stereotaxic frame. Motion of the tibia relative to the femur was quantified with use of reflective markers secured to modified bone pins and a three-dimensional motion analysis system. External forces and moments in the transverse plane of the tibia were measured with use of force transducers based on a strain-gauge design. Longitudinal measurements of knee stability were made before either sham surgery (control animals) or transection of the ligament (experimental animals), immediately after surgery, and at 2 and 4 months after transection. The results showed that the animals tolerated the procedures well and that systematic measurements could be obtained. The method described here has the practical advantage over cross-sectional experimental designs in that the number of subjects can be decreased while maintaining statistical power and has the further conceptual advantage that individual changes can be accounted for over time.
Descriptors: anterior cruciate ligament injuries, joint instability, knee injuries, knee joint, anterior cruciate ligament, anterior cruciate ligament surgery, cats, animal disease models, equipment design, knee joint surgery, longitudinal studies, range of motion, articular, videotape recording, weight bearing.

Makarova, L.P. and V.E. Pogorelyi (2004). Neuroprotector action of an asparagic acid derivative during the model reperfusive cerebral damage in cats. Eksperimental'Naia I Klinicheskaia Farmakologiia 67(5): 13-16. ISSN: 0869-2092.
Abstract: Neuroprotector properties of a new phosphorylated derivative of asparagic acid (PIR 87-65-0) were studied on a model of acute brain ischemia in cats. PIR 87-5-0 has proved to be more effective than the reference drug vinpocetin in preventing the reperfusive damage, which was manifested by decreased postischemic hypergycemia, activated utilization of oxygen and glucose in the brain, and suppressed postischemic metabolic lactate acidosis.
Descriptors: asparagic acid, brain ischemia model, reperfusive damage, PIR 87 65 0, vinpocetin .
Language of Text: Russian.

Manganiello, P.D., B.L. Sueoka, D.R. Valentine, and T.P. Hoopes (1998). A bipolar radiofrequency catheter fails to occlude a feline uterine horn: A model for fallopian tube occlusion. The Journal of the American Association of Gynecologic Laparoscopists 5(3): 269-73. ISSN: 1074-3804.
Abstract: We developed a retrograde transvaginal-transcervical-transuterine sterilization technique capable of causing occlusive fibrosis and stricture in the human fallopian tube. The procedure is required to induce a lesion at the intramural-isthmic portion of the tube at sufficient depth to damage epithelium underlying the submucosa and inner muscular layer, without acute damage to the outer muscular layer and serosal surface. Nineteen nulliparous purpose-bred cats were induced and maintained in an anestrus state with testosterone cypionate 5 mg/kg intramuscularly and a 6-18-hour light-dark cycle. After laparotomy, all animals had focal radiofrequency lesioning of uterine horns. Ten of 30 treated uterine horns appeared grossly occluded at the time of sacrifice; however, histologic assessment demonstrated only 6 complete occlusions, and 4 horns showed lack of complete lumen occlusion with or without evidence of recanalization. Although no complications were encountered, bipolar radiofrequency failed to provide a consistent obstructive lesion in a tubular structure similar in size and morphology to the human fallopian tube.
Descriptors: catheter ablation, sterilization, tubal, cats, biological models, pilot projects.

Maniglia, A.J., H. Abbass, T. Azar, M. Kane, P. Amantia, S. Garverick, W.H. Ko, W. Frenz, and T. Falk (1999). The middle ear bioelectronic microphone for a totally implantable cochlear hearing device for profound and total hearing loss. American Journal of Otology 20(5): 602-611. ISSN: 0192-9763.
Descriptors: equipment, instrumentation, sensory reception, profound hearing loss, ear disease, bioelectronic middle ear micropHone, efficacy, totally implantable cochlear hearing device, prosthetic .

March, P.A., M.A. Thrall, D.E. Brown, T.W. Mitchell, A.C. Lowenthal, and S.U. Walkley (1997). GABAergic neuroaxonal dystrophy and other cytopathological alterations in feline Niemann-Pick disease type C. Acta Neuropathologica 94(2): 164-72. ISSN: 0001-6322.
Abstract: Feline Niemann-Pick disease type C (NPC) is an autosomal recessive lysosomal storage disease which shares many of the clinical, biochemical and pathological features of the corresponding human disorder. Cytopathological alterations in distinct neuronal cell populations were investigated in this animal model to gain a better understanding of the pathogenesis of brain dysfunction. Golgi and immunocytochemical methods were employed to characterize the cell architectural changes occurring in neuronal somata, dendrites and axons at different stages of disease progression. Cortical pyramidal neurons in laminae II, III, and V exhibited various degrees of meganeurite and/or swollen axon hillock formation with or without ectopic dendritogenesis. Enlarged axon hillock regions with neuritic processes and spines were recognized early in the progression of feline NPC but were less prevalent in mid to late stages of the disease. Glutamic acid decarboxylase (GAD) immunocytochemistry demonstrated immunoreactive spheroids in numerous GABAergic axons in neocortex, subcortical areas, and cerebellum. Parvalbumin-immunoreactive axonal spheroid distribution in brain closely mirrored results from the GAD studies, whereas calbindin D-28k-immunoreactive spheroids were conspicuously absent in most cortical and subcortical areas examined. Purkinje cell axonal spheroid formation progressed in a distal to proximal direction, with eventual involvement of recurrent axon collaterals. Purkinje cell death and a concomitant decrease in the numbers of spheroids in the cerebellum were observed late in the disease course. Clinical neurological signs in feline NPC occur in parallel with neuronal structural alterations and suggest that GABAergic neuroaxonal dystrophy is a contributor to brain dysfunction in this disease.
Descriptors: neuroaxonal dystropHies, niemann pick diseases, age factors, brain diseases, brain diseases, cats, child, preschool, animal disease models, golgi apparatus, golgi apparatus ultrastructure, immunohistochemistry, neuroaxonal dystropHies, neuroaxonal dystropHies, neurons, neurons ultrastructure, niemann pick diseases, gamma aminobutyric acid.

Marinelli, E.R., R. Neubeck, B. Song, T. Wagler, R.S. Ranganathan, K. Sukumaran, P. Wedeking, A. Nunn, V.M. Runge, and M.F. Tweedle (2000). Synthesis, characterization, and imaging performance of a new class of macrocyclic hepatobiliary MR contrast agents. Investigative Radiology 35(1): 8-24. ISSN: 0020-9996.
Abstract: RATIONALE AND OBJECTIVES: To investigate the effect of substituent lipophilicity, substituent position, and overall charge on the hepatobiliary clearance and tolerance of a series of aromatic ring-containing macrocyclic Gd chelates to select a candidate compound for evaluation as a hepatobiliary imaging agent. METHODS: Hepatobiliary clearance was studied in rats. Tissue distribution and tolerance were studied in mice. Imaging was performed in cats, rabbits, and Rhesus monkeys using T1-weighted pulse sequences or T1-weighted breath-hold pulse sequences. RESULTS: All the compounds were excreted bimodally. Gd-2,5-BPA-DO3A (15d) was found to have the optimal combination of hepatobiliary clearance (47% in rats, 29% in mice) and tolerance (minimum lethal dose 5.0 mmol/kg). Initial imaging studies in cats demonstrated the feasibility of Gd-2,5-BPA-DO3A for hepatic imaging. In rabbits with implanted VX-2 adenocarcinoma as a model for metastatic liver disease, Gd-2,5-BPA-DO3A provided sustained hepatic signal intensity (SI) enhancement and lesion conspicuity over a 120-minute imaging time course. In Rhesus monkeys with normal liver function, Gd-2,5-BPA-DO3A afforded sustained hepatic SI enhancement and a time-dependent increase in gallbladder SI over the entire 90-minute imaging time course. CONCLUSIONS: Gd-2,5-BPA-DO3A provides dramatic and sustained SI enhancement of hepatic tissue in cats, rabbits, and Rhesus monkeys that was superior in all respects to the extracellular space MRI agent, Gd-HP-DO3A, that was employed as a control.
Descriptors: contrast media chemical synthesis, contrast media, magnetic resonance imaging, biliary tract, cats, gadolinium, heterocyclic compounds diagnostic use, liver, liver neoplasms, Macaca mulatta, mice, organometallic compounds chemical synthesis, organometallic compounds, organometallic compounds diagnostic use, rabbits, rats, tissue distribution.

Marks, S.L., A.K. Cook, R. Reader, P.H. Kass, A.P. Theon, C. Greve, and Q.R. Rogers (1999). Effects of glutamine supplementation of an amino acid-based purified diet on intestinal mucosal integrity in cats with methotrexate-induced enteritis. American Journal of Veterinary Research 60(6): 755-63. ISSN: 0002-9645.
NAL Call Number: 41.8 Am3A
Abstract: OBJECTIVE: To determine effects of glutamine-supplemented and glutamine-free amino acid-based purified diets, compared with a dry expanded diet, on intestinal structure and function in a model that used cats with methotrexate-induced enteritis. ANIMALS: 18 adult specific-pathogen-free cats. PROCEDURE: 12 cats were given intragastric feedings of an amino acid-based purified diet supplemented with glutamine (7% [wt:wt]) or an isonitrogenous amount of glycine and alanine; 6 cats consumed a dry expanded diet. After 21 days, cats received methotrexate (MTX; 11 mg/kg of body weight, IV). Intestinal permeability testing was performed immediately before and 66 hours after MTX administration. Celiotomy was performed 72 hours after MTX administration for aseptic removal of mesenteric lymph nodes, collection of full-thickness intestinal biopsy specimens, determination of intestinal cellular proliferation, and collection of aortic and portal venous blood samples for determination of arteriovenous amino acid concentrations across the intestine. RESULTS: Administration of MTX was associated with severe enterotoxicosis manifested as diarrhea (8/12 cats), vomiting (12/12), and positive results for bacterial culture of mesenteric lymph nodes (12/12) in cats receiving the purified diets, independent of glutamine supplementation. Diet did not affect villus tip length and villus surface area in the small intestine or cellular proliferation. Administration of MTX was associated with significantly increased intestinal permeability, which was not attenuated by glutamine supplementation. CONCLUSIONS: Feeding of a glutamine-supplemented amino acid-based purified diet was unable to preserve intestinal function in cats with MTX-induced enteritis. CLINICAL RELEVANCE: Intestinal morphologic alterations correlate poorly with intestinal function as measured by means of bacterial translocation and intestinal permeability.
Descriptors: enteritis, glutamine, intestinal mucosa, methotrexate toxicity, amino acids, analysis of variance, animal feed, cats, cell division, dietary supplements, duodenum, duodenum, glutamine, intestinal mucosa, lymph nodes.

Martin Jimenez, T. and J.E. Riviere (2001). Mixed effects modeling of the disposition of gentamicin across domestic animal species. Journal Veterinary Pharmacology and Therapy 24(5): 321-332. ISSN: 0140-7783.
NAL Call Number: SF915. J63
Abstract: An interspecies pharmacokinetic model for gentamicin was developed using the mixed effects modeling approach and serum disposition data obtained from the Food Animal Residue Avoidance Databank (FARAD). Data that met a priori quality criteria was obtained from the database and analysed using the traditional double logarithmic analysis and the mixed effects modeling approach. Body weight, brain weight and fever were the covariates of interest in our study. Population pharmacokinetic models across species were developed and validated with swine data. The parameter volume of distribution was modeled as a function of body weight. The total clearance was initially modeled as a function of body weight. The predictability performance of the model improved dramatically when the parameter brain weight was included in the covariate model for clearance. This was a surprising finding worthy of further study. The covariate fever seemed to influence the magnitude of the volume of distribution, although the scarcity of data pertaining to diseased animals makes this finding uncertain. We conclude that the pharmacokinetic characteristics of drugs such as gentamicin, can be predicted across species using a population pharmacokinetics modeling approach, and that clinical features that affect species in a similar manner can be also explored in this fashion.
Descriptors: gentamicin, models, prediction, species differences, rabbits, cats, dogs, goats, sheep, horses, body weight, brain, fever.

Martin, W.J. and R.T. Glass (1995). Acute encephalopathy induced in cats with a stealth virus isolated from a patient with chronic fatigue syndrome. Pathobiology Journal of Immunopathology, Molecular and Cellular Biology 63(3): 115-8. ISSN: 1015-2008.
NAL Call Number: RB125.P37
Abstract: A simian cytomegalovirus-related stealth virus, isolated from a patient with the chronic fatigue syndrome, induced an acute neurological illness when inoculated into cats. Histological examination of brain tissue showed foci of cells with cytoplasmic vacuolization and an absence of any inflammatory reaction. Electron microscopy confirmed the presence of herpes-like viral particles and viral-like products in the brain of an inoculated animal. These findings support the role of stealth viruses in the pathogenesis of human neurological diseases and provide an animal model to evaluate potential antiviral therapy.
Descriptors: brain diseases, cytomegalovirus, fatigue syndrome, chronic, acute disease, cats, cytomegalovirus infections.

Matteucci, D., M. Pistello, P. Mazzetti, S. Giannecchini, D.L.I. Mauro, L. Zaccaro, C. Pollera, S. Specter, and M. Bendinelli (1997). Studies of AIDS vaccination using and ex vivo feline immunodeficiency virus model: protection conferred by a fixed-cell vaccine against cell-free and cell-associated challenge differs in duration and is not easily boosted. Journal of Virology 71(11): 8368-8376. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Descriptors: vaccination, immune response, cell mediated immunity, immunity , immunization , immunostimulation , immunotherapy , therapy , lymphocyte transformation.

Matteucci, D., M. Pistello, P. Mazzetti, S. Giannecchini, P. Isola, A. Merico, L. Zaccaro, A. Rizzuti, and M. Bendinelli (1999). Aids vaccination studies using feline immunodeficiency virus as a model: immunisation with inactivated whole virus suppresses viraemia levels following intravaginal challenge with infected cells but not following intravenous challenge with cell-free virus. Vaccine 18(1-2): 119-130. ISSN: 0264-410X.
NAL Call Number: QR189.V32
Descriptors: infection , AIDS , acquired immunodeficiency syndrome, immune system disease, feline acquired immunodeficiency syndrome, intravaginal virus challenge, WIV immunisation.

Maulik, S.K., R. Kumari, M. Maulik, S.C. Manchanda, and S.K. Gupta (2001). Captopril and its time of administration in myocardial ischaemic-reperfusion injury. Pharmacological Research 44(2): 123-8. ISSN: 1043-6618.
NAL Call Number: RS122
Abstract: The present study was designed to investigate the role of captopril in an in vivo model of myocardial ischaemic-reperfusion injury with respect to its time of administration. In open-chest pentobarbitone anaesthetized cats, the left anterior descending coronary artery was occluded for 15 min followed by 60 min of reperfusion. Vehicle (saline) or captopril (4 mg kg(-1)) was administered 10 min before instituting ischaemia (pre-treatment) or 5 min before reperfusion (post-treatment). In the vehicle-treated group, ischaemic-reperfusion injury (IRI) was evidenced by enhanced plasma renin activity, depression of global haemodynamic function (mean arterial pressure, left ventricular-end-diastolic-pressure, peak positive and negative dP/dt) along with depletion of myocardial high energy phosphate (HEP) compounds. Oxidant stress in IRI was evidenced by raised levels of myocardial thiobarbituric acid reactive substances (TBARS) and depletion of endogenous myocardial antioxidants (glutathione, superoxide dismutase and catalase). Pre-treatment with captopril prevented (i) loss of myocardial haemodynamic function, (ii) rise in TBARS and (iii) depletion of myocardial HEP compounds. However, in the post-treatment group, only partial recovery of myocardial haemodynamic function, with no significant reduction in TBARS, was observed. Glutathione, superoxide dismutase and catalase were unaffected by either treatment schedules. The results of the present study suggest that captopril is more effective in attenuating ischaemic-reperfusion injury when administered before ischaemia rather than before reperfusion.
Descriptors: angiotensin converting enzyme inhibitors, captopril, myocardial reperfusion injury, adenosine triphosphate, angiotensin converting enzyme inhibitors, pressure, captopril, catalase, cats, creatine kinase, glutathione, heart rate, lactates, myocardial reperfusion injury, myocardial reperfusion injury, phosphocreatine, superoxide dismutase, thiobarbituric acid reactive substances, time factors, left ventricular function.

Mazzetti, P., S. Giannecchini, D. Del Mauro, D. Matteucci, P. Portincasa, A. Merico, C. Chezzi, and M. Bendinelli (1999). Aids vaccination studies using an ex vivo feline immunodeficiency virus model: detailed analysis of the humoral immune response to a protective vaccine. Journal of Virology 73(1): 1-10. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Descriptors: cats, immune response, antibodies, antigens, immunity , immunological factors, epitopes , viral antigens.

McCall, C.A., K.E. Stedman, D.E. Bevier, G.A. Kunkle, C.S. Foil, and L.D. Foil (1997). Correlation of feline IgE, determined by FceRI alpha-based ELISA technology, and IDST to Ctenocephalides felis salivary antigens in a feline model of flea bite allergic dermatitis. Compendium on Continuing Education for the Practicing Veterinarian 19(11): 29-32. ISSN: 0193-1903.
NAL Call Number: SF601 .C66
Descriptors: cats, hypersensitivity, arthropoda, ctenocepHalides felis, saliva, allergens, dermatitis, immunoglobulins, elisa, skin tests, diagnosis, heat, temperature resistance, antigens , body fluids, body parts, ctenocepHalides , glycoproteins , immunoenzyme techniques, immunological diseases, immunological factors, immunological techniques, insecta , organic diseases, proteins , pulicidae , resistance to injurious factors, siphonaptera , skin diseases, temperature , arthropod allergies, heat stability.

McIntyre, J.A. and J. Castaner (2003). Efaproxiral sodium. Allosteric hemoglobin modifier radiosensitizer. Drugs of the Future 28(12): 1159-1167. ISSN: 0377-8282.
Descriptors: feline models, oncology, human medicine, brain metastasis, neoplastic disease, cardiac ischemia, heart disease, cerebral ischemia, vascular disease, glioblastoma multiforme, nervous system disease, non small cell lung cancer, respiratory system disease, radiotherapy, tissue oxygen .

Megyesi, J.F., B. Vollrath, D.A. Cook, and J.M. Findlay (2000). In vivo animal models of cerebral vasospasm: a review. Neurosurgery 46(2): 448-61. ISSN: 0148-396X.
Abstract: BACKGROUND: Cerebral vasospasm is delayed-onset cerebral arterial narrowing in response to blood clots left in the subarachnoid space after spontaneous aneurysmal subarachnoid hemorrhage (SAH). Ideally, studies on the pathogenesis and treatment of cerebral vasospasm in humans should be conducted using human cerebral arteries. Because in vivo experiments using human vessels are not possible, and postmortem pathological examination of human arteries in vasospasm provides only a limited amount of information, a number of animal models of vasospasm have been developed. METHODS: The literature was searched to find all references to in vivo animal models of SAH and vasospasm. An online search of the medical database MEDLINE was initially performed using the key words "cerebral," "vasospasm," "subarachnoid," "hemorrhage," "animal," and "model." References were checked to determine the first description of each in vivo animal model. RESULTS: Fifty-seven models of SAH and vasospasm were identified. These models used one of three techniques to simulate SAH: 1) an artery was punctured allowing blood to escape and collect around the artery and its neighbors; 2) an artery was surgically exposed, and autologous blood obtained from another site was placed around the artery; or 3) blood from another site was injected into the subarachnoid space and was allowed to collect around arteries. Each technique has advantages and disadvantages. The majority of animal models of SAH and vasospasm use intracranial arteries; however, extracranial arteries have also been used recently in vasospasm experiments. These studies seem easier and less costly to perform, but concerns exist regarding the physiological dissimilarity between systemic and cerebral arteries. CONCLUSION: The model of SAH and vasospasm used most frequently is the canine "two-hemorrhage" model, in which two injections of blood into the dog's basal cistern performed 48 hours apart result in greater arterial vasoconstriction than that effected by a single injection of blood. On the basis of its ability to accurately predict what occurs in human SAH, the best model of vasospasm seems to be the primate model in which a blood clot is surgically placed around the large cerebral vessels at the base of the monkey's brain.
Descriptors: animal disease models, vasospasm, intracranial, cats, cerebral arteries, dogs, haplorhini, rabbits, rats, subarachnoid hemorrhage, swine, vasoconstriction.

Mijnes, J.D.F. and R.J. De Groot (1999). Structure-function analysis of the feline herpesvirus virulence factors gE and gI. Veterinary Microbiology 69(1-2): 89-91. ISSN: 0378-1135.
NAL Call Number: SF601. V44
Descriptors: feline herpesvirus, infection, heterologous expression, cloned genes, disulfide bonded gI, cell to cell transmission.

Miller, C.A., P.J. Abbas, and B.K. Robinson (2001). Response properties of the refractory auditory nerve fiber. Journal of the Association for Research in Otolaryngology 2(3): 216-32. ISSN: 1525-3961.
Abstract: The refractory characteristics of auditory nerve fibers limit their ability to accurately encode temporal information. Therefore, they are relevant to the design of cochlear prostheses. It is also possible that the refractory property could be exploited by prosthetic devices to improve information transfer, as refractoriness may enhance the nerve's stochastic properties. Furthermore, refractory data are needed for the development of accurate computational models of auditory nerve fibers. We applied a two-pulse forward-masking paradigm to a feline model of the human auditory nerve to assess refractory properties of single fibers. Each fiber was driven to refractoriness by a single (masker) current pulse delivered intracochlearly. Properties of firing efficiency, latency, jitter, spike amplitude, and relative spread (a measure of dynamic range and stochasticity) were examined by exciting fibers with a second (probe) pulse and systematically varying the masker-probe interval (MPI). Responses to monophasic cathodic current pulses were analyzed. We estimated the mean absolute refractory period to be about 330 micros and the mean recovery time constant to be about 410 micros. A significant proportion of fibers (13 of 34) responded to the probe pulse with MPIs as short as 500 micros. Spike amplitude decreased with decreasing MPI, a finding relevant to the development of computational nerve-fiber models, interpretation of gross evoked potentials, and models of more central neural processing. A small mean decrement in spike jitter was noted at small MPI values. Some trends (such as spike latency-vs-MPI) varied across fibers, suggesting that sites of excitation varied across fibers. Relative spread was found to increase with decreasing MPI values, providing direct evidence that stochastic properties of fibers are altered under conditions of refractoriness.
Descriptors: cochlear nerve, nerve fibers, cats, cochlear implantation, electric stimulation instrumentation, evoked potentials, auditory, perceptual masking, sensory thresholds, time factors.

Mitchell, D.E., G. Gingras, and P.C. Kind (2001). Initial recovery of vision after early monocular deprivation in kittens is faster when both eyes are open. Proceedings of the National Academy of Sciences of the United States of America 98(20): 11662-7. ISSN: 0027-8424.
NAL Call Number: 500 N21P
Abstract: A comparison was made of the speed of visual recovery in the deprived eye of kittens after a 6-day period of monocular deprivation imposed at 5-9 weeks of age in two postdeprivation conditions. In one condition, binocular recovery (BR), both eyes were open, whereas in the other condition, reverse lid-suture (RLS), the formerly nondeprived eye was closed to force the animal to use the originally deprived eye. In littermate pairs, BR kittens began to recover form vision 12 to 30 h before those subjected to RLS. The vision of the deprived eye of the BR animals remained superior to that of their RLS littermates for 4-8 days. Although this finding is difficult to reconcile with competitive mechanisms of synaptic plasticity, it supports a prediction of an alternative model of synaptic plasticity [Bienenstock, E. L., Cooper, L. N. & Munro, P. W. (1982) J. Neurosci. 2, 32-48] for slower initial recovery with RLS because of the time required to reset the modification threshold.
Descriptors: sensory deprivation, visual acuity, visual perception, aging, cats, time factors, vision, binocular, vision, monocular.

Mitchell, R.W., P. Cozzi, I.M. Ndukwu, S. Spaethe, A.R. Leff, and P.A. Padrid (1998). Differential effects of cyclosporine A after acute antigen challenge in sensitized cats in vivo and ex vivo. British Journal of Pharmacology 123(6): 1198-204. ISSN: 0007-1188.
Abstract: 1. We determined the effect of cyclosporine A (CsA) treatment on mast cell degranulation and lung resistance (R(L)) in vivo, and tracheal smooth muscle (TSM) contraction ex vivo after antigen challenge in sensitized cats. We also determined the direct effects of addition of CsA to the tissue bath on antigen-induced responses of TSM in vitro. 2. Cats (n=10) were sensitized by i.m. injection of Ascaris suum antigen (AA); 5 cats (CsA+) received CsA twice daily for 2 weeks before acute antigen challenge in doses sufficient to suppress interleukin-2 secretion from feline peripheral blood mononuclear cells ex vivo. 3. Lung resistance increased comparably within 10 min of exposure to AA (P<0.03). Histamine content in bronchoalveolar lavage fluid from both groups increased comparably within 30 min of antigen challenge, from undetectable levels to 542+/-74 pg ml(-1) post AA for CsA+ and from 74+/-19 pg ml(-1) at baseline, to 970+/-180 pg ml(-1) post AA CsA- (P<0.05; P=NS vs CsA+). 4. In excised TSM, active tension elicited by exposure to AA in vitro was 107+/-38% KCl in the CsA+ group vs 144+/-56% KCl in the CsA- group (P=NS). However, contraction of TSM (n=4) harvested from both groups was abolished or greatly diminished after AA challenge when tissues were pre-incubated with 1 microM CsA in vitro (8+/-8% KCl, P<0.05 vs CsA+ and CsA-). This was associated with inhibited release of 5-hydroxytryptamine into the organ bath fluid of tissues treated with CsA in vitro only. 5. We demonstrated that CsA treatment in vivo does not inhibit the early phase asthmatic response or mast cell degranulation following antigen challenge in sensitized cats. Additionally, the effects of CsA on mast cell function ex vivo do not reflect lack of effects of CsA on mast cell function in vivo in this animal model of atopic asthma.
Descriptors: antigens, helminth, cyclosporine, ascaris suum, asthma, cats, cell degranulation, mast cells, muscle, smooth, muscle, smooth, muscle, smooth, serotonin, trachea, trachea, trachea.

Mitsikostas, D.D. and M. Sanchez del Rio (2001). Receptor systems mediating c-fos expression within trigeminal nucleus caudalis in animal models of migraine. Brain Research 35(1): 20-35. ISSN: 0926-6410.
Abstract: In intracranial structures unmyelinated C- and Adelta-fibers of the trigeminal nerve transmit pain stimuli from meninges to the trigeminal nucleus caudalis (Sp5C). Peripheral nerve endings surround meningeal vessels (the so-called trigeminovascular system) and contain vasoactive neuropeptides (calcitonin gene-related peptide, substance P and neurokinin A). Activation of the trigeminovascular system promotes a meningeal sterile inflammatory response through the release of neuropeptides by peripheral endings. Orthodromic conduction along trigeminovascular fibers transmits information centrally with induction of immediate early c-fos gene within post-synaptic Sp5C neurons, as a marker of neuronal activity within central nociceptive pathways. In laboratory animals the system is activated by either electrical stimulation of the TG, chemical stimulation of the meninges, electrical or mechanical stimulation of the superior sagittal sinus or by induction of cortical spreading depression. All these techniques induce c-fos within Sp5C and are used as a rodent/feline model of vascular headache in humans. Up-to-date there is evidence that at least ten receptors (5-HT(1B), 5-HT(1D), 5-HT(lF), 5-HT(2B), NK-1, GABA(A), NMDA, AMPA, class III metabotropic glutamate receptors, and opioids mu receptors) modulate c-fos expression within Sp5C. These receptors represent potential targets for anti-migraine drugs as shown by triptans (5-HT(1B/1D/1F)) and ergot alkaloids (5-HT(1A1B/1D/1F)). This review discusses the importance of c-fos expression within Sp5C as a marker of cephalic nociception, the different cephalic pain models that induce c-fos within Sp5C, the receptors involved and their potential role as targets for anti-migraine drugs.
Descriptors: migraine, proto oncogene proteins c fos, receptors, cell surface, trigeminal caudal nucleus, animal disease models.

Miyabe, M., J.R. Kirsch, S. Mori, P.C.M. Van Zijl, R.C. Koehler, and R.J. Traystman (1994). Magnetic resonance imaging of water diffusion constants in a reversible middle cerebral artery occlusion model in cats. Anesthesiology 81(3A): A896. ISSN: 0003-3022.
Descriptors: effect of heat processing, Maillard reaction, antibiotics, diets, taurine, adult cats, cardiovascular system, ischemia, meeting abstract.
Notes: Meeting Information: Annual Meeting of the American Society of Anesthesiologists, San Francisco, California, USA; October 15-19, 1994.

Miyazawa, T. (2002). Infections of feline leukemia virus and feline immunodeficiency virus. Frontiers in Bioscience 7: 504-518. ISSN: 1093-4715.
Online: http://www.bioscience.org/
Descriptors: feline retrovirus infection, infectious disease, viral disease, immunodeficiency, immune system disease, retroviral persistance.

Moon, D.G., H.S. Byun, and J.J. Kim (1999). Akatp-channel opener as a potential treatment modality for erectile dysfunction. British Journal of Urology International 83(7): 837-841. ISSN: 1464-4096.
Descriptors: pharmacology, urology, human medicine, feline model, erectile dysfunction, reproductive system disease, male, diagnosis, treatment, intracavernosal pressure, pinacidil, acetylcholine, PGE1, L arginine.

Moon, D.G., H.S. Byun, and J.J. Kim (1999). A KATP-channel opener as a potential treatment modality for erectile dysfunction. British Journal of Urology International 83(7): 837-41. ISSN: 1464-4096.
Abstract: OBJECTIVES: To assess the effects of pinacidil (a KATP-channel opener) for the treatment of penile erectile dysfunction and to examine the role of the K+-channel in cavernosal smooth muscle contractility. MATERIALS AND METHODS: Using a feline model, the magnitude of penile erection caused by pinacidil was compared with that caused by erectogenic drugs, e.g. acetylcholine, prostaglandin E1 (PGE1) and L-arginine. The effects of K+-channel blockers (4-aminopyridine, glibenclamide and tetraethylammonium) and pinacidil on penile erections induced by the drugs were investigated. RESULTS: The intra-arterial injection of pinacidil caused a dose-dependent increase in intracavernosal pressure (ICP) and the increase in ICP induced by pinacidil with acetylcholine, PGE1 or L-arginine was more pronounced than with the compounds alone. Furthermore, pinacidil (1 mmol/L) effectively reversed the inhibitory effects of the K+-channel blockers on the cavernosal relaxation induced by acetylcholine, PGE1 or L-arginine (P<0.01). Notably, pinacidil induced cavernosal relaxation after injecting the drugs even in cases refractory to higher concentrations (0.1 mol/L) of the drugs (n=11, P<0.01). CONCLUSIONS: These results suggest that pinacidil is effective in relaxing feline erectile tissue in vivo, probably via increased K+ permeability and subsequent hyperpolarization. Further comparative studies with erectogenic compounds on human erectile tissue and clinical testing are required to determine whether K+-channel openers can be used in the diagnosis and treatment of erectile dysfunction. However, pinacidil seems promising as an intracavernosal agent combined with PGE1 to produce synergistic effects.
Descriptors: impotence, vasculogenic, pinacidil, vasodilator agents, cats, dose response relationship, drug, muscle contraction, muscle, smooth, penile erection, potassium channels.

Moriello, K.A., D.J. Deboer, R. Schenker, J.L. Blum, and L.M. Volk (2004). Efficacy of pre-treatment with lufenuron for the prevention of Microsporum canis infection in a feline direct topical challenge model. Veterinary Dermatology 15(6): 357-362. ISSN: 0959-4493.
NAL Call Number: SF901 .V47
Descriptors: feline, Microsporum canis, lufenuron, pre-treatment, topical, dermatology.

Muller, T., M. Stetter, M. Hubener, F. Sengpiel, T. Bonhoeffer, I. Godecke, B. Chapman, S. Lowel, and K. Obermayer (2000). An analysis of orientation and ocular dominance patterns in the visual cortex of cats and ferrets. Neural Computation 12(11): 2573-95. ISSN: 0899-7667.
Abstract: We report an analysis of orientation and ocular dominance maps that were recorded optically from area 17 of cats and ferrets. Similar to a recent study performed in primates (Obermayer & Blasdel, 1997), we find that 80% (for cats and ferrets) of orientation singularities that are nearest neighbors have opposite sign and that the spatial distribution of singularities deviates from a random distribution of points, because the average distances between nearest neighbors are significantly larger than expected for a random distribution. Orientation maps of normally raised cats and ferrets show approximately the same typical wavelength; however, the density of singularities is higher in ferrets than in cats. Also, we find the well-known overrepresentation of cardinal versus oblique orientations in young ferrets (Chapman & Bonhoeffer, 1998; Coppola, White, Fitzpatrick, & Purves, 1998) but only a weak, not quite significant overrepresentation of cardinal orientations in cats, as has been reported previously (Bonhoeffer & Grinvald, 1993). Orientation and ocular dominance slabs in cats exhibit a tendency of being orthogonal to each other (Hubener, Shoham, Grinvald, & Bonhoeffer, 1997), albeit less pronounced, as has been reported for primates (Obermayer & Blasdel, 1993). In chronic recordings from single animals, a decrease of the singularity density and an increase of the ocular dominance wavelength with age but no change of the orientation wavelengths were found. Orientation maps are compared with two pattern models for orientation preference maps: bandpass-filtered white noise and the field analogy model. Bandpass-filtered white noise predicts sign correlations between orientation singularities, but the correlations are significantly stronger (87% opposite sign pairs) than what we have found in the data. Also, bandpass-filtered noise predicts a deviation of the spatial distribution of singularities from a random dot pattern. The field analogy model can account for the structure of certain local patches but not for the whole orientation map. Differences between the predictions of the field analogy model and experimental data are smaller than what has been reported for primates (Obermayer & Blasdel, 1997), which can be explained by the smaller size of the imaged areas in cats and ferrets.
Descriptors: brain mapping, cats, ferrets, vision, binocular, visual cortex, visual pathways, algorithms, cats, ferrets, nephelometry and turbidimetry, oxygen consumption, species specificity, visual cortex, visual cortex.

Murao, K., K. Shingu, E. Miyamoto, S. Ikeda, S. Nakao, M. Masuzawa, and M. Yamada (2002). Anticonvulsant effects of sevoflurane on amygdaloid kindling and bicuculline-induced seizures in cats: comparison with isoflurane and halothane. Journal of Anesthesia 16(1): 34-43. ISSN: 0913-8668.
Abstract: PURPOSE: We compared the anticonvulsant effects of sevoflurane with those of isoflurane and halothane in amygdaloid kindling and bicuculline-induced seizures in cats. METHODS: In a crossover design, the effects of 70% nitrous oxide, and 0.3, 0.6, and 1.5 minimum alveolar concentration (MAC) of volatile anesthetics were studied in five cats in which the amygdala was electrically stimulated at the current used for establishing the kindled state. The effects of 0.6 and 1.5 MAC of volatile anesthetics were studied in another five cats, in which 0.2 mg.kg(-1) of bicuculline was administered i.v.. RESULTS: In the amygdaloid kindling model, all four anesthetics decreased the duration of after-discharge (AD), the rise of multiunit activity in midbrain reticular formation (R-MUA), and the behavior scores compared with findings without anesthetics. Halothane, at 1.5 MAC, significantly decreased the number of cats showing AD ( P < 0.05). In the bicuculline-induced seizure model, all five cats showed repetitive spikes during 1.5 MAC of sevoflurane, whereas only two and three cats, respectively, showed the repetitive spikes during 1.5 MAC of isoflurane and halothane. All three volatile anesthetics decreased the rise of R-MUA, the duration of the repetitive spikes, and the behavior scores. The suppression of the rise in R-MUA and the behavior scores with 1.5 MAC of sevoflurane was significantly less than that with 1.5 MAC of isoflurane. CONCLUSION: The anticonvulsant effects of sevoflurane were less potent than those of halothane in the amygdaloid kindling model and less potent than those of isoflurane in the bicuculline-induced seizure model.
Descriptors: cat, amygdaloid kindling model, seizure model, halothane, sevoflurane, anticonvulsant, isoflurane, anesthetics.

Murao, K., K. Shingu, K. Tsushima, K. Takahira, and S. Ikeda (1995). Anticonvulsant effects of volatile anesthetics on a penicillin-induced epilepsy model in cats. Anesthesiology 83(3A): A321. ISSN: 0003-3022.
Descriptors: animal care, nervous system, toxicology, cats, anesthetic drug, isoflurane, sevoflurane, penicillin induced, epilepsy model .

Murohara, T., M. Buerke, and A.M. Lefer (1996). Cardioprotective actions of oligotide, a single stranded polydeoxyribonucleotide complex, in myocardial ischaemia and reperfusion injury. British Journal of Pharmacology 117(6): 1000-8. ISSN: 0007-1188.
Abstract: 1. The efficacy of oligotide, a single stranded polydeoxyribonucleotide complex, was examined in a feline model of myocardial ischaemia (MI: 90 min) and reperfusion (R: 270 min). Oligotide (15 mg kg-1 bolus) was administered intravenously 80 min after occlusion of the left anterior descending (LAD) coronary artery (i.e., 10 min prior to R) and continued for an additional 280 min (10 mg kg-1 h-1 infusion). 2. Oligotide-treated cats showed significantly smaller myocardial necroses and lower cardiac myeloperoxidase activities (significantly lower neutrophil infiltration) in the necrotic zone as compared to MI+R cats receiving only vehicle. 3. LAD coronary arteries isolated from MI+R cats exhibited a significant endothelial dysfunction (i.e., reduced endothelium-dependent relaxation), and significantly increased adherence of polymorphonuclear neutrophils (PMNs) ex vivo. However, oligotide significantly preserved endothelial function and attenuated PMN adherence in ischaemic LAD coronary arteries. 4. Oligotide attenuated P-selectin expression on thrombin-stimulated platelets as well as PMN adherence to thrombin-stimulated coronary endothelium. Immunohistochemical examination in vivo revealed that oligotide treatment also significantly inhibited coronary endothelial P-selectin expression after 90 min MI and 20 min R. 5. Oligotide exerted a significant cardioprotection in MI+R injury. The mechanism appears to be related to attenuation of PMN-endothelial interaction and eventual infiltration into the ischaemic myocardium.
Descriptors: coronary vessels, heart, myocardial reperfusion injury, oligodeoxyribonucleotides, acetylcholine, cats, endothelium, vascular, flow cytometry, neutrophils, oligodeoxyribonucleotides, p selectin analysis, peroxidase analysis, thrombin, vasodilation.

Murphy, K.M., K.R. Duffy, and D.G. Jones (2004). Experience-dependent changes in NMDAR1 expression in the visual cortex of an animal model for amblyopia. Visual Neuroscience 21(4): 653-670. ISSN: 0952-5238.
Abstract: When normal binocular visual experience is disrupted during postnatal development, it affects the maturation of cortical circuits and often results in the development of poor visual acuity known as amblyopia. Two main factors contribute to the development of amblyopia: visual deprivation and reduced binocular competition. We investigated the affect of these two amblyogenic factors on the expression of the NMDAR1 subunit in the visual cortex because activation of the NMDA receptor is a key mechanism of developmental neural plasticity. We found that disruption of binocular correlations by monocular deprivation promoted a topographic loss of NMDAR1 expression within the cortical representations of the central visual field and the vertical and horizontal meridians. In contrast, binocular deprivation, which primarily affects visual deprivation, promoted an increase in NMDAR1 expression throughout the visual cortex. These different changes in NMDAR1 expression can be described as topographic and homeostatic plasticity of NMDA expression, respectively. In addition, the changes in NMDA expression in the visual cortex provide a greater understanding of the neural mechanisms that underlie the development of amblyopia and the potential for visual recovery.
Descriptors: amblyopia, n methyl d aspartate receptors, vision, visual cortex, amblyopia, cats, animal disease models, homeostasis, immunohistochemistry, neuronal plasticity, sensory deprivation, staining and labeling, tissue distribution, monocular vision.

Mushahwar, V.K., D.M. Gillard, M.J. Gauthier, and A. Prochazka (2002). Intraspinal micro stimulation generates locomotor-like and feedback-controlled movements. Institute of Electrical and Electronics Engineers Transactions on Neural Systems and Rehabilitation Engineering 10(1): 68-81. ISSN: 1534-4320.
Abstract: Intraspinal microstimulation (ISMS) may provide a means for improving motor function in people suffering from spinal cord injuries, head trauma, or stroke. The goal of this study was to determine whether microstimulation of the mammalian spinal cord could generate locomotor-like stepping and feedback-controlled movements of the hindlimbs. Under pentobarbital anesthesia, 24 insulated microwires were implanted in the lumbosacral cord of three adult cats. The cats were placed in a sling leaving all limbs pendent. Bilateral alternating stepping of the hindlimbs was achieved by stimulating through as few as two electrodes in each side of the spinal cord. Typical stride lengths were 23.5 cm, and ample foot clearance was achieved during swing. Mean ground reaction force during stance was 36.4 N, sufficient for load-bearing. Feedback-controlled movements of the cat's foot were achieved by reciprocally modulating the amplitude of stimuli delivered through two intraspinal electrodes generating ankle flexion and extension such that the distance between a sensor on the cat's foot and a free sensor moved back and forth by the investigators was minimized. The foot tracked the displacements of the target sensor through its normal range of motion. Stimulation through electrodes with tips in or near lamina IX elicited movements most suitable for locomotion. In chronically implanted awake cats, stimulation through dorsally located electrodes generated paw shakes and flexion-withdrawals consistent with sensory perception but no weight-bearing extensor movements. These locations would not be suitable for ISMS in incomplete spinal cord injuries. Despite the complexity of the spinal neuronal networks, our results demonstrate that by stimulating through a few intraspinal microwires, near-normal bipedal locomotor-like stepping and feedback-controlled movements could be achieved.
Descriptors: electric stimulation, hindlimb, implants, locomotion, spinal cord, cats, electromyogrphy, feedback, lumbar vertebrae surgery, microelectrodes, movement, sacrum surgery, stress, mechanical.

Nagashima, G. (1994). Cumulative effect of repetitive ischemia: pathophysiological findings. The Bulletin of Tokyo Medical and Dental University 41(2): 23-36. ISSN: 0040-8921.
Abstract: The cumulative effect of ischemia on the brain was investigated in cats using a repetitive transient global ischemia model. The cats were submitted to three series of repetitive ischemia of 5.0, 7.5 and 10.0-minute durations at 1-hour intervals by intrathoracic clamping of the innominate and subclavian arteries. Pathophysiological changes during and after the ischemic episodes were evaluated by monitoring the electroencephalograms (EEG), cerebral blood flow (CBF), specific gravity and 31P-MR spectroscopy (MRS). Transient 5.0, 7.5, and 10.0-minute ischemias appeared to produce a slightly more severe energy failure on the 31P MRS measurement in the animals that had previously experienced an ischemic injury than those that had not. Additionally, repetition of ischemic episodes at 1-hour intervals led to a progressive lengthening of the duration of the spontaneous electrocortical suppression that followed each ischemic episode. However, preischemic hypoxia (5% O2 for 5 minutes) resulted in minor changes in the levels of phosphocreatine and intracellular inorganic phosphate on the MRS measurement, otherwise the EEG activity declined progressively. This shut-down response of the EEG can be concluded to serve in preserving the energy state of the brain although it is not capable of preventing the development of postischemic brain edema and neuronal death.
Descriptors: ischemic attack, transient, adenosine triphosphate, anoxia, brain edema, cats, cerebrovascular circulation, electroencephalography, energy, hydrogen ion concentration, ischemic attack, transient, magnetic resonance spectroscopy, recurrence.

Nakagaki, K., K. Nakagaki, K. Takahashi, D. Schols, E. De Clercq, and T. Tabira (2001). CXCR4 is the primary receptor for feline immunodeficiency virus in astrocytes. Journal of Neurovirology 7(5): 487-92. ISSN: 1355-0284.
Abstract: Feline astrocytes were productively infected with the Crandell feline kidney (CrFK) cell-adapted feline immunodeficiency virus (FIV) Petaluma strain in a primary culture. They expressed mRNA of CXCR4, and the FIV infection was blocked by stromal cell-derived factor 1alpha (SDF-1alpha), SDF-1beta, or the bicyclam AMD3100 in a dose-dependent manner. These observations suggest that, like FIV infection in CrFK cells and lymphocytes, the virus uses CXCR4 as a primary receptor for infecting astrocytes and this can be a possible natural model for AIDS dementia complex.
Descriptors: astrocytes, feline immunodeficiency virus, nerve tissue proteins, receptors, virus, AIDS dementia complex, astrocytes, cats, cells, cultured, chemokines, cxc, cytokines, animal disease models, dose response relationship, drug, gene products, gag biosynthesis, gene products, gag, heterocyclic compounds, microglia, microglia, RNA, messenger biosynthesis, biosynthesis, receptors, CXCR4, receptors, virus biosynthesis, receptors, virus, specific pathogen free organisms.

Nakagama, H., T. Saito, and S. Tanaka (2000). Effect of imbalance in activities between on- and off-center lgn cells on orientation map formation. Biological Cybernetics 83(2): 85-92. ISSN: 0340-1200.
Descriptors: models and simulations, computational biology, cats, nervous system, neural coordination, computer simulation, orientation map formation, activity imbalance, spatial periodicity, self organization model, visual cortex.

Nakao, M., T. Takizawa, K. Nakamura, N. Katayama, and M. Yamamoto (2001). An optimal control model of 1/f fluctuations in heart rate variability. Institute of Electrical and Electronics Engineers :Engineering in Medicine and Biology Magazine 20(2): 77-87. ISSN: 0739-5175.
Descriptors: heart rate, models, cardiovascular, analysis of variance, biomedical engineering, pressure, cats, computer simulation, nonlinear dynamics, pressoreceptors, sympathetic nervous system.

Nedrud, J.G. (1999). Animal models for gastric Helicobacter immunology and vaccine studies. Federation of European Microbiological Societies : Immunology and Medical Microbiology 24(2): 243-50. ISSN: 0928-8244.
NAL Call Number: QR180.F46
Abstract: Over the last decade animal models have been used extensively to investigate disease processes and therapy for Helicobacter pylori infections. The H. pylori animal models which have been used in pathogenesis and vaccine studies include the gnotobiotic pig, non-human primates, cats, dogs, and several species of rodents including mice, rats, gerbils and guinea pigs. H. felis infection of mice and H. mustelae infection of ferrets have also been used. Recently, investigators have begun using transgenic mice and gene-targeted 'knock-out' mice to investigate Helicobacter infections. Each of these animal models has distinct advantages and disadvantages which are discussed in this minireview. The choice of an animal model is dictated by factors such as cost and an understanding of how each model will or will not allow fulfillment of experimental objectives.
Descriptors: bacterial vaccines, animal disease models, helicobacter, helicobacter infections, stomach diseases, cats, dogs, guinea pigs, helicobacter infections, mice, rats, stomach diseases.

Neilsen, M.E., M. Buse, D.R. Menick, and G.I. Cooper (2001). Role of microtubules in the trafficking of the insulin-responsive glucose transporter, glut4, in cardiocytes. Federation of American Societies for Experimental Biology Journal 15(5): A1118. ISSN: 0892-6638.
NAL Call Number: QH301 .F3
Descriptors: cardiovascular system, transport and circulation, cardiac hypertropHy, feline cardiocytes, nocodazole, heart disease, model, microtubule based protein trafficking, glucose transporter, GLUT1, GLUT4, cardiac isoforms, insulin.

Nemzek, J.A., S.P. Arnoczky, and C.L. Swenson (1994). Retroviral transmission by the transplantation of connective-tissue allografts. An experimental study. The Journal of Bone and Joint Surgery/ American Volume 76(7): 1036-41. ISSN: 0021-9355.
Abstract: The transmission of a retrovirus by the transplantation of allografts of connective tissues was studied in a feline model with use of the feline leukemia virus, a retrovirus with a replication cycle and pathological characteristics similar to those of the human immunodeficiency virus. The retrovirus was used to infect four specific-pathogen-free cats that were subsequently used as tissue donors. Fresh allografts of menisci, patellar ligaments, and patellar ligament and bone composites were harvested from infected donors and were transplanted into the knee joints of twelve specific-pathogen-free cats. A fresh cancellous-bone allograft was transplanted into the proximal part of the tibia of four additional specific-pathogen-free cats, which served as positive control animals. Additional grafts from infected donors were harvested and were stored at -80 degrees Celsius for ten weeks. A fresh-frozen graft was then transplanted into the knee of twelve other specific-pathogen-free cats. Samples of plasma were obtained weekly from all twenty-eight cats and were tested with both an enzyme-linked immunosorbent assay to detect the presence of viral antigen and an immunofluorescent antibody assay to determine exposure to the virus. All types of fresh and fresh-frozen connective-tissue allografts from the infected donors resulted in transmission of the retrovirus to the recipient cats. The recipients had evidence of viral antigen or rising antibody titers as early as two weeks after the transplantation. Histological examination of specimens of the allografts revealed normal incorporation of the transplanted tissues, with no sign of rejection of the graft.
Descriptors: connective tissue microbiology, connective tissue transplantation, leukemia virus, feline, leukemia, feline transmission, viral antigens, bone transplantation, cats, enzyme linked immunosorbent assay, fluorescent antibody technique, freezing, leukemia, feline microbiology, menisci, tibial microbiology, menisci, tibial transplantation, patellar ligament microbiology, patellar ligament transplantation, specific pathogen free organisms, tissue preservation, transplantation, homologous.

Nicoll, R.G., M.W. Jackson, B.S. Knipp, J.A. Zagzebski, H. Steinberg, and R.T. O' Brien (1998). Quantitative ultrasonography of the liver in cats during obesity induction and dietary restriction. Research in Veterinary Science 64(1): 1-6. ISSN: 0034-5288.
NAL Call Number: 41.8 R312
Descriptors: ultrasonography, liver, obesity, disease models, diagnostic techniques, ultrasonic diagnosis, nutritional disorders, cats.

Nilsson, B., E. Theodorsson, L. Jivegard, A. Thune, S. Friman, and J. Svanvik (1994). Vasoactive intestinal peptide-antiserum inhibits fluid secretion by the inflamed gallbladder mucosa. Regulatory Peptides 49(3): 179-84. ISSN: 0167-0115.
NAL Call Number: QP552 .P4
Abstract: The inflammatory fluid secretion by the gallbladder mucosa in experimental cholecystitis is induced by an increased prostaglandin formation and is mediated by intramural nerves. In the present study the effect of VIP-antiserum on the inflammatory fluid secretion in the gallbladder was tested in a validated experimental model in cats. The animals were studied in acute experiments 6 weeks after a procedure when the cystic duct was tied and gallstones were implanted in the gallbladder. During basal conditions there was a continuous secretion of fluid into the lumen of the inflamed gallbladder averaging 0.43 +/- 0.18 ml/h. Injection of VIP antiserum, obtained from immunized rabbits and diluted with saline 1:10 in a bolus of 4 ml into the coeliac artery reversed this secretion into an absorption of 1.72 +/- 0.44 ml h-1 (P < 0.001). VIP-antiserum did not affect the fluid adsorption in control animals with an intact gallbladder and injection of control serum from rabbits not immunized to VIP did not affect fluid secretion in the inflamed gallbladders. The results support the idea that the inflammatory fluid secretion in the gallbladder mucosa is mediated by VIP-ergic nerve fibres.
Descriptors: cholecystitis, exudates and transudates secretion, gallbladder secretion, vasoactive intestinal peptide, bile secretion, cats, animal disease models, immune sera, mucous membrane secretion, rabbits, vasoactive intestinal peptide.

Nishimura, T. (1997). Comparative study of neurons in the rabbit and feline parasympathetic ganglia. Journal of the Autonomic Nervous System 65(2-3): 126. ISSN: 0165-1838.
Descriptors: cell biology, nervous system, urinary system, chemical coordination, animal model, electrophysiology, excretory system, morphology, nervous system, feline parasympathetic ganglion, urinary bladder.

Nonaka, I. (1998). Animal models of muscular dystrophies. Laboratory Animal Science 48(1): 8-17. ISSN: 0023-6764.
NAL Call Number: 410.9 P94
Abstract: Recent advances in molecular biology have indicated that many mutant animal models of muscular dystrophy share common genetic and protein abnormalities similar to those of the human disease. The best example is a model of Duchenne muscular dystrophy (DMD), the mdx mouse. Similar to dystrophic muscle in DMD patients, dystrophin protein is not expressed along the surface membrane, even though the mdx mouse has no apparent signs of muscular dysfunction. Because clinical and pathologic findings in the dystrophic (mxd) dog are similar to those in DMD patients, it also has been regarded as a good model for therapeutic trials. The best known and most extensively studied dy+dy+ mouse lacks merosin (laminin alpha2), which is one subunit of a basement membrane protein, laminin. Because approximately half of all patients with the classical form of congenital muscular dystrophy also lack merosin, availability of this animal has revived interest in the study of the pathologic mechanism of fiber necrosis resulting from this membrane defect. The dystrophic hamster is a model of limb-girdle muscular dystrophy with sarcoglycan deficiency in which one of the dystrophin-associated glycoproteins, delta-sarcoglycan, is defective. Because these animal models have common protein and genetic defects similar to those seen in people with muscular dystrophies, they have been widely used to examine the effectiveness of gene therapy and the administration of pharmacologic and trophic factors.
Descriptors: animal disease models, muscular dystrophy, animal, cats, chickens, dogs, dystrophin, hamsters, laminin deficiency, laminin, mice, mice, knockout, mice, mutant strains.

Norris, C.R., J.R. Byerly, K.C. Decile, R.D. Berghaus, W.F. Walby, E.S. Schelegle, D.M. Hyde, and L.J. Gershwin (2003). Allergen-specific IgG and IgA in serum and bronchoalveolar lavage fluid in a model of experimental feline asthma. Veterinary Immunology and Immunopathology 96(3/4): 119-127. ISSN: 0165-2427.
NAL Call Number: SF757.2. V38
Descriptors: allergens, allergic reactions, asthma, bronchoalveolar lavage, IgA, IgG, mucosa, cats.

North, T.W. and R.A. LaCasse (1995). Testing anti-HIV drugs in the FIV model. Nature Medicine 1(5): 410-411. ISSN: 1078-8956.
Descriptors: HIV infections, animal models, acquired immune deficiency syndrome, therapy, treatment, analogues, enzyme inhibitors, zidovudine, drug resistance, nucleosides, nucleoside analogues, reverse transcriptase inhibitors, Retroviridae, Lentivirus, human immunodeficiency virus, cats, man.

Nuttall, J.D., L.K. Brumfield, N.L. Fazzalari, J.J. Hopwood, and S. Byers (1999). Histomorphometric analysis of the tibial growth plate in a feline model of mucopolysaccharidosis type VI. Calcified Tissue International 65(1): 47-52. ISSN: 0171-967X.
Abstract: Mucopolysaccharidosis type VI (MPS VI) is a genetically inherited lysosomal storage disorder. Severely affected children exhibit a range of skeletal abnormalities including short stature, facial dysmorphia, and dysostosis multiplex. Naturally occurring and transgenic animal models of MPS VI are also found which exhibit pathology similar to the human disorder. In this paper we have characterized the formation of trabecular bone from growth plate cartilage in a feline model of MPS VI. Tibial trabecular bone was shown to be osteopenic in MPS VI animals with a bone mineral volume (BV/TV) of 4.51% compared with a BV/TV of 15.64% in normal animals. In addition to osteopenia, a rearrangement of trabecular bone architecture was also observed in MPS VI tibiae, with fewer, thinner trabeculae noted; bone formation rate was also decreased. These observations support those previously made in the L5 vertebrae of MPS VI animals. When the sequential formation of growth plate cartilage structural elements, their transition into primary bone spongiosa, and remodeling into secondary bone spongiosa was characterized, no difference between normal and MPS VI could be detected in the number of cartilage septae and their arrangement in the proliferative and hypertrophic regions of the growth plate or trabecular elements in the primary spongiosa. However, a deviation from normal was observed in the resting zone of the growth plate and in the secondary spongiosa of bone. Thus, the osteopenia observed in MPS VI bone appears to arise primarily from a defect in bone production within the metaphysis and diaphysis rather than the creation of an abnormal template in the preceding growth plate cartilage.
Descriptors: animal disease models, growth plate, mucopolysaccharidosis vi, tibia, bone density, metabolic bone diseases, metabolic bone diseases, cats, growth plate, mucopolysaccharidosis vi, osteogenesis, tibia.

Ohkura, T., Y.S. Shin, N. Wakamiya, N. Iwa, and T. Kurimura (1997). Detection of proviruses and viral RNA in the early stages of feline immunodeficiency virus infection in cats: a possible model of the early stage of HIV infection. Experimental Animals: Japanese Association for Laboratory Animal Science 46(1): 31-9. ISSN: 1341-1357.
NAL Call Number: QL55.J55
Abstract: Feline immunodeficiency virus (FIV) infection in cats has been reported to be a useful animal model for human AIDS studies, especially in the early stages of infection. We examined the temporal changes in provirus detection in peripheral blood mononuclear cells (PBMC) and the distribution of FIV-DNA and RNA in feline tissues by the polymerase chain reaction at 10, 35, 70 days after intravenous inoculation of FIV. Viral DNA in the PBMC was detected three to four weeks after infection and its fluctuation was demonstrated for the first time. Ten days after infection, before seroconversion, proviruses were detected only in the mesenteric lymph nodes and intestines. At 35 and 70 days after infection, after seroconversion, proviruses were detected in most lymphoid organs and the salivary glands, but the expression of FIV-RNA was limited to the thymus at 70 days after infection. These results show that FIV-RNA is transcribed from proviral DNA exclusively in the thymus at this stage. We suggest that the quantitative changes in detectable proviruses in the PBMC depend on the relation between the decrease in infected cells caused by cytolytic T lymphocytes and/or apoptosis and their increase caused by the release of a new supply of lymphocytes from the thymus.
Descriptors: cats, animal disease models, feline acquired immunodeficiency syndrome, feline immunodeficiency virus, feline immunodeficiency virus, proviruses, RNA, viral analysis, antibodies, viral, DNA, viral analysis, kinetics, leukocytes, mononuclear, polymerase chain reaction, tissue distribution.

Oreskovic, D., M. Klarica, M. Vukic, and J. Marakovic (2003). Evaluation of ventriculo-cisternal perfusion model as a method to study cerebrospinal fluid formation. Croatian Medical Journal 44(2): 161-4. ISSN: 0353-9504.
Abstract: AIM: To evaluate ventriculo-cisternal perfusion as a method for measuring cerebrospinal fluid formation rate, calculated by means of the Heisey et al equation. Method. All experiments were carried out on anesthetized domestic cats fixed in the sphinx position in a stereotaxic frame. Ventriculo-cisternal perfusion was used at an intracranial pressure of -10 cm H2O at different perfusion rates (32.0, 65.5, 125.0, and 252.0 microL/min). Dextran blue was applied as an indicator substance and the concentration of the indicator was measured with a spectrophotometer at a wavelength of 635 nm. Cerebrospinal fluid formation rate was calculated with the equation of Heisey et al. Results. The indicator substance was less diluted at a higher perfusion rate, and the calculated cerebrospinal fluid formation rate was lower. The increase in perfusion rate from 65.5 to 125.0 to 252.0 microL/min increased the concentration of indicator substance from 0.75 to 0.89 to 0.97 mg/mL and decreased calculated cerebrospinal fluid formation rate from 21.8 to 15.4 to 7.8 microL/min. This reduction was linear and an increase in the perfusion rate by 1.0 microL/min decreased the cerebrospinal formation rate by 0.05 microL/min. Conclusion. The calculated cerebrospinal fluid formation rate depends on different perfusion rates. The increase in the perfusion rate diminishes the calculated formation rate. Ventriculo-cisternal perfusion may not be a suitable method to calculate the cerebrospinal fluid formation rate according to the equation of Heisey et al.
Descriptors: cerebral ventricles, cerebrospinal fluid, intracranial pressure, biological models, cats, croatia, perfusion, spectropHotometry, stereotaxic techniques.

Orton, E.C. (1995). Small Animal Thoracic Surgery, Williams and Wilkins: Baltimore, Maryland, USA, 256 p. ISBN: 0683066706.
NAL Call Number: SF991.O88 1995
Descriptors: dogs, cats, cardiopulmonary pathophysiology, anesthesia and analgesia, disorders of the thoracic wall, pnuemothroax, digestive system, esophgus, hiatal hernia, respiratory system, cardiovascular system.

Pan, J., C. Zhong, Z. Chang, and P. Roy Burman (2003). A potential therapeutic strategy to combat leukemia virus infection. Cancer Biology and Therapy 2(1): 92-9. ISSN: 1538-4047.
Abstract: To test the concept that a replication-competent retrovirus carrying a suicide gene could have potential utility in the control of the natural virus infection in mammalian species, we constructed derivatives of a feline leukemia virus (FeLV) that is commonly associated with leukemia-lymphomas in this species. The FeLV, Rickard strain, subgroup A (FRA) genome contained at the 3' end of the envgene, an insert of an internal ribosomal entry site (IRES) linked to cDNA sequence of either herpes simplex virus thymidine kinase (HSV-TK) or a truncated HSV-TK (HSV-ATK) or yeast cytosine deaminase (CD). These constructs were transfected into feline fibroblast cells (H927). The viruses produced were determined to be replication-competent. The stable propagation of the full-length transgene was, however, dependent on the size of the insert, IRES-CD being the smallest in size (1031 bp) exhibiting maximal stability for at least up to six months. The protein products of the transgenes could be detected, despite the appearance of deleted proviruses at late passages. The transduced cells were susceptible to cytotoxic killing when the appropriate prodrug, ganciclovir (GCV), acyclovir (ACV) or 5-fluorocytosine (5-FC) was added to the culture medium. H927 cells, infected with another subgroup of FeLV, namely, FeLV-B or FeLV-C, could be superinfected by the FRA-suicide gene viruses and thus, subjected to killing. Interestingly, at an early stage of infection by the parental FRA, H927 cells could also be reinfected by the same subgroup FRA constructs to induce the suicide effect. Among the three constructs, the vector with the CD gene was determined to be superior to others in terms of stability, therapeutic index and bystander effect in the cell culture test system. While the in vivo correlates of the therapeutic effect in the feline model remain to be determined, our results do encourage investigation of the same concept in the control of HTLV and, perhaps even, HIV infection in humans.
Descriptors: leukemia virus, feline, retroviridae infections therapy, retroviridae proteins, oncogenic, tumor virus infections therapy, viral envelope proteins, virus replication, acyclovir, Western blot, cats, cells, cultured, cytosine deaminase, DNA primers, fibroblasts, flucytosine, ganciclovir, gene expression regulation, viral, genetic vectors, luminescent proteins, nucleoside deaminases, nucleoside deaminases, polymerase chain reaction, prodrugs, retroviridae infections, retroviridae proteins, oncogenic, ribosomes, saccharomyces cerevisiae, simplexvirus, thymidine kinase, thymidine kinase, thymidine kinase, transfection, transgenes, tumor virus infections, viral envelope proteins.

Parodi, A.L., F. Femenia, A. Moraillon, F. Crespeau, and J.J. Fontaine (1994). Histopathological changes in lymph nodes of cats experimentally infected with the feline immunodeficiency virus (fiv). Journal of Comparative Pathology 111(2): 165-174. ISSN: 0021-9975.
NAL Call Number: 41.8 J82
Descriptors: blood and lymphatics, cell biology, feline immunodeficiency virus, immune system, animal model, kittens, HIV, cd4 lymphocyte, cd8 lymphocyte, follicular hyperplasia, generalized lymphadenopathy, hyperactive follicular center, immunocytochemistry, interfollicular proliferation, lymphocytic mantle cell, medullary plasmacytosis.

Pascal, J., A. Bourgeade, M. Lagier, and C. Legros (1998). Linear and nonlinear model of the human middle ear. Journal of the Acoustical Society of America 104(3 PART 1): 1509-1516. ISSN: 0001-4966.
Descriptors: mathematical biology, computational biology, cats, acoustic field, eardrum impedance, linear model: mathematical model, middle ear transfer function data, nonlinear model, sound pressure levels.

Patel, A.G., M.T. Toyama, C. Alvarez, T.N. Nguyen, P.U. Reber, S.W. Ashley, and H.A. Reber (1995). Pancreatic interstitial pH in human and feline chronic pancreatitis. Gastroenterology 109(5): 1639-45. ISSN: 0016-5085.
NAL Call Number: RC799. G37
Abstract: BACKGROUND & AIMS: Advanced chronic pancreatitis is associated with a reduction in pancreatic blood flow. To determine the physiological significance of this decrease, pancreatic interstitial pH was measured in a model of obstructive chronic pancreatitis in cats and in patients with chronic pancreatitis. METHODS: In cats, pancreatic interstitial pH and blood flow were measured serially under basal conditions and after secretory stimulation as chronic pancreatitis evolved. Basal pancreatic interstitial pH was also measured in patients undergoing an operation for chronic pancreatitis or periampullary cancer (controls). RESULTS: In normal cats, pancreatic interstitial pH was 7.41 +/- 0.01 and blood flow was 124 mL.min-1.(100 g pancreas-1). With the evolution of chronic pancreatitis, interstitial pH and blood flow progressively decreased to 7.21 +/- 0.04 (P < 0.007) and 75 +/- 11 (P < 0.007), respectively. From 1 to 2 weeks, secretory stimulation reduced pancreatic interstitial pH and blood flow further, but as secretory function was lost, this effect disappeared. In patients with chronic pancreatitis, the interstitial pH was lower (7.02 +/- 0.06) than in controls (7.25 +/- 0.04; P < 0.05). CONCLUSIONS: These observations are consistent with the hypothesis that, in chronic pancreatitis, acidic metabolites associated with pancreatic secretion accumulate within the pancreas, probably because of impaired blood flow.
Descriptors: pancreas, pancreatitis, adult, aged, cats, chronic disease, hydrogen ion concentration, middle aged, pancreas supply, pancreatitis.

Persidsky, Y., H.S. Nottet, V.G. Sasseville, L.G. Epstein, and H.E. Gendelman (1995). The development of animal model systems for HIV-1 encephalitis and its associated dementia. Journal of Neurovirology 1(3-4): 229-43. ISSN: 1355-0284.
Abstract: The human immunodeficiency virus (HIV) is neuroinvasive and can be neurovirulent. Indeed, 20-30% of individuals with the acquired immune deficiency syndrome (AIDS) develop cognitive and motor dysfunction (termed the AIDS dementia complex or HIV dementia) coincident with advanced immunosuppression. Despite massive research efforts to discern viral neuropathogenic mechanisms, much remains incompletely understood. Recently, we and others developed animal model systems to elucidate how HIV infection within the brain can lead to impairment of central nervous system function. In this report, we evaluate each of the published animal models for their ability to mirror HIV dementia. Ease of handling and expense were also under consideration. Ultimately, studies in animal systems should permit a better understanding of the nature of HIV-1-induced neurological injury and aid in the development of effective treatments for this dreaded complication of HIV infection.
Descriptors: AIDS dementia complex, encephalitis, viral, HIV 1, cats, animal disease models, haplorhini, mice.

Pistello, M., D. Matteucci, F. Bonci, P. Isola, P. Mazzetti, L. Zaccaro, A. Merico, D. Mauro del, N. Flynn, and M. Bendinelli (2003). AIDS vaccination studies using an ex vivo feline immunodeficiency virus model: protection from an intraclade challenge administered systemically or mucosally by an attenuated vaccine. Journal of Virology 77(20): 10740-10750. ISSN: 0022-538X.
NAL Call Number: QR360. J6
Descriptors: acquired immune deficiency syndrome, animal models, disease models, immune response, immunity, immunization, live vaccines, vaccination, vaccine development, cats, feline immunodeficiency virus.

Plechner, A.J. (2003). An effective veterinary model may offer therapeutic promise for human conditions: roles of cortisol and thyroid hormones. Medical Hypotheses 60(3): 309-14. ISSN: 0306-9877.
Abstract: For nearly three decades, the author has treated multiple serious diseases of cats and dogs by correcting an unrecognized endocrine-immune imbalance originating with a deficiency or defect of cortisol. The cortisol abnormality creates a domino effect on feedback loops involving the hypothalamus-pituitary-adrenal axis. In this scenario estrogen becomes elevated, thyroid hormone becomes bound, and B and T cells become deregulated. Diseases with this aberration as a primary etiological component range from allergies and strange behavior to severe cases of autoimmunity and cancer. Successful treatment and control, even in critical cases, have been consistently achieved with a long-term physiologic (not pharmacologic) replacement with cortisone along with thyroid hormone (in dogs). The treatment represents a major healing modality for many seemingly unrelated chronic diseases of animals. In humans, this endocrine-immune dysfunction appears to exist and, as in veterinary medicine, has been overlooked by researchers and clinicians. Testing and treatment patterned after the animal model may offer significant clinical benefits for challenging human afflictions.
Descriptors: animal disease models, hydrocortisone, hydrocortisone, thyroid hormones, cats, dogs, biological models, models, theoretical, thyroid hormones.

Plotnikov, M.B., V.I. Smol'iakova, G.A. Chernysheva, and A.D. Avdoshin (1999). Effect of Polyosm preparation on the viscoelastic properties of the craniospinal system in the model of acute hypertensive encephalopathy [Vliianie preparata Poliosm na viazkoelasticheskie svoistva kraniospinal'noi sistemy na modeli ostroi gipertonicheskoi entsefalopatii]. Biulleten' Eksperimental'Noi Biologii i Meditsiny 127(5): 499-502. ISSN: 0007-4888.
NAL Call Number: 442.8 B87AE
Descriptors: brain edema, cerebrospinal fluid, hypertension, polyethylene glycols, acute disease, pressure, brain edema, brain edema, brain edema, cats, cerebrospinal fluid, elasticity, hypertension, hypertension, hypertension, intracranial pressure, norepinephrine, venous pressure, viscosity.
Language of Text: Russian.

Podell, M., M. Hadjiconstantinou, M.A. Smith, and N.H. Neff (2003). Proton magnetic resonance imaging and spectroscopy identify metabolic changes in the striatum in the MPTP feline model of parkinsonism. Experimental Neurology 179(2): 159-66. ISSN: 0014-4886.
NAL Call Number: RC321. E96
Abstract: We administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to adult, male cats to model Parkinson's disease (PD), and utilized proton magnetic resonance imaging (MRI) and spectroscopy (MRS) at a field strength of 1.5 T to identify metabolic degenerative changes in the striatum in vivo. Neurologic status and somatosensory-evoked potentials in vivo, as well as postmortem striatal histopathological and immunohistochemical parameters, were examined. Nine cats were equally divided into three groups and treated daily for 10 days as follows: saline, MPTP, and pargyline (a monoamine oxidase inhibitor) plus MPTP. The MPTP-treated cats displayed bradykinesia, head tremor, and reduced oculovestibular reflex activity. MRI showed a diffuse increase of the T2-weighted signal in the striatum of two MPTP-treated cats. Analysis of the MRS spectra indicated significantly lower N-acetylaspartate/creatine (CR) and glutamine-glutamate complex/CR ratios than the control baseline. Two MPTP-treated cats had low choline-containing compounds/CR ratio, whereas a lactate peak was present in all MPTP-treated cats. In the striatum of the MPTP-treated cats, there was a significant decline of tyrosine hydroxylase immunoreactivity and histological evidence for a diffuse cytotoxic reaction. Pretreatment with pargyline attenuated the MPTP-induced clinical signs, MRI and MRS changes, and the histopathological and immunoreactivity alterations. We conclude that proton MRI/MRS is a sensitive, noninvasive measure of neural toxicity and biochemical alteration of the striatum in a feline model of PD.
Descriptors: aspartic acid, corpus striatum, magnetic resonance imaging, magnetic resonance spectroscopy diagnostic use, parkinsonian disorders diagnosis, parkinsonian disorders, 1 methyl 4 pHenyl 1,2,3,6 tetrahydropyridine, aspartic acid, aspartic acid, brain, brain, brain, cats, choline analysis, choline, corpus striatum, corpus striatum, creatine analysis, creatine, animal disease models, disease progression, inositol analysis, inositol, neurologic examination, pargyline, parkinsonian disorders, predictive value of tests, protons, tyrosine 3 monooxygenase biosynthesis.

Poirier, P., F.K. Samson, and T.J. Imig (2003). Spectral shape sensitivity contributes to the azimuth tuning of neurons in the cat's inferior colliculus. Journal of Neurophysiology 89(5): 2760-77. ISSN: 0022-3077.
Abstract: We recorded high-best-frequency single-unit responses to free-field noise bursts that varied in intensity and azimuth to determine whether inferior colliculus (IC) neurons derive directionality from monaural spectral-shape. Sixty-nine percent of the sample was directional (much more responsive at some azimuths than others). One hundred twenty-nine directional units were recorded under monaural conditions (unilateral ear plugging). Binaural directional (BD) cells showed weak monaural directionality. Monaural directional (MD) cells showed strong monaural directionality, i.e., were much more responsive at some directions than others. Some MD cells were sensitive to both monaural and binaural directional cues. MD cells were monaurally nondirectional in response to tone bursts that lack direction-dependent variation in spectral shape. MD cells were unresponsive to noise bursts at certain azimuths even at high intensities showing that particular spectral shapes inhibit their responses. Two-tone inhibition was stronger where MD cells were unresponsive to noise stimulation than at directions where they were responsive. According to the side-band inhibition model, MD cells derive monaural directionality by comparing energy in excitatory and inhibitory frequency domains and thus should have stronger inhibitory side-bands than BD cells. MD and BD cells showed differences in breadth of excitatory frequency domains, strength of nonmonotonic level tuning, and responsiveness to tones and noise that were consistent with this prediction. Comparison of these data with previous findings shows that strength of spectral inhibition increases greatly between the level of the cochlear nucleus and the IC, and there is relatively little change in strength of spectral inhibition among the IC, auditory thalamus, and cortex.
Descriptors: form perception, inferior colliculus, inferior colliculus, neurons, acoustic stimulation, cats, electrophysiology, laterality, sound localization.

Ponti, W., T. Rubino, M. Bardotti, G. Poli, and D. Parolaro (2001). Cannabinoids inhibit nitric oxide production in bone marrow derived feline macrophages. Veterinary Immunology and Immunopathology 82(3-4): 203-14. ISSN: 0165-2427.
NAL Call Number: SF757.2. V38
Abstract: Feline immunodeficiency virus (FIV) infection causes a widespread natural immunodeficiency syndrome in cats that is considered a suitable animal model for studying human immunodeficiency virus (HIV) infection and pathogenesis. Short term cultures of bone marrow derived feline macrophages stimulated with recombinant feline interferon-gamma (r-IFN-gamma) and lipopolysaccharide (LPS) were shown to produce nitric oxide. Feline macrophages were shown to express cannabinoid receptors, and nitric oxide production decreased after in vitro exposure to synthetic cannabinoid CP-55940. Both cannabinoid receptors, CB1 and CB2, were involved in this process, since the inhibition was reversed by selective cannabinoid antagonists for both of these receptors.
Descriptors: bone marrow cells, cannabinoids, feline acquired immunodeficiency syndrome, macrophages, nitric oxide biosynthesis, bornanes, cats, cyclohexanols, animal disease models, histocytochemistry, immunosuppressive agents, macrophages, nitric oxide, phagocytosis, piperidines, pyrazoles, receptors, cannabinoid, receptors, drug.

Post, R.M. (2004). Neurobiology of seizures and behavioral abnormalities. Epilepsia 45(Suppl 2): 5-14. ISSN: 0013-9580.
Abstract: Seizures are both caused by and induce a complex set of neurobiological alterations and adaptations. The animal model of amygdala kindling provides insight into the spatiotemporal evolution of these changes as a function of seizure development and progression. Intracellular, synaptic, and microstructural changes are revealed as related to both the primary pathophysiology of kindled seizure evolution and compensatory secondary, or endogenous anticonvulsant adaptations. At the level of gene expression, the balance of these pathological and adaptive processes (as augmented by exogenous medications) probably determines whether seizures will be manifest or suppressed and could account for aspects of their intermittency. As anxiety and emotion modulation are subserved by many of the same neuroanatomic substrates involved in the evolution of complex partial seizures, particularly those of the medial temporal lobe, it is readily conceptualized how vulnerability to a range of psychiatric disorders could be related to the primary or secondary neurochemical alterations associated with seizure disorders. The discrete and methodologically controlled elucidation of the cascades and spatiotemporal distributions of neurobiological alterations that accompany seizure evolution in the kindling model may help resolve some of the difficulty and complexity of elucidating these biobehavioral relationships in the clinic.
Descriptors: animal behavior, kindling neurology, seizures, amygdala, anticonvulsants, anticonvulsants, animal behavior, bipolar disorder, brain, brain, cats, cocaine, cocaine, animal disease models, drug tolerance, mental disorders, rats, seizures, seizures.

Potts, J.T., I.E. Fuchs, J. Li, B. Leshnower, and J.H. Mitchell (1999). Skeletal muscle afferent fibres release substance p in the nucleus tractus solitarii of anaesthetized cats. Journal of Physiology 514(3): 829-841. ISSN: 0022-3751.
NAL Call Number: 447.8 J82
Descriptors: nervous system, anesthesia, chloralose, substance P, mean arterial pressure, vagal nerves, carotid sinus nerves, neurones, neural coordination, barorecepters, nucleus tractus solitarii, tachykininergic modulation .

Power, C., K. Zhang, and G. van Marle (2004). Comparative neurovirulence in lentiviral infections: The roles of viral molecular diversity and select proteases. Journal of Neurovirology 10(Suppl 1): 113-7. ISSN: 1355-0285.
Abstract: All lentiviruses infect the brain, causing chronic neurological disease in their respective hosts. To examine the relationship(s) between lentivirus molecular diversity and the development of neurological disease, we examined in vitro and in vivo models of lentivirus neurovirulence using different recombinant viruses derived from human (HIV-1) and feline (FIV) immunodeficiency viruses. Both in vitro and in vivo studies of FIV neurovirulence showed that the FIV envelope derived from a neurovirulent strain was a principal determinant of neuropathogenesis, although systemic immunosuppression was also an integral feature of FIV neurovirulence. Studies of HIV-1 envelope sequences derived from brain or blood indicate that molecular diversity is greater in viruses from patients with HIV-associated dementia (HAD), compared to nondemented individuals. Moreover, the hypervariable V3 domain of HIVgp120, regardless of the HIV-1 clade from which it was derived, was an important region for mediating neurotoxicity in vitro but the level of viral replication did not influence neurotoxicity. For both the HIV-1 and FIV envelopes and HIV-1 Tat, induction of matrix metalloproteinase (MMP)-2 in macrophages was a consistent finding. Neurotoxicity caused by supernatants from HIV-infected or transfected macrophages, containing MMP-2, was greater than direct neurotoxicity levels caused by direct exposure of neurons to virus in assays of total neuronal death, but not in assays of neuronal apoptosis. Proteinase-activated receptor (PAR)-1 and its ligand thrombin were also induced during HIV infection, chiefly on astrocytes. PAR-1 activation resulted in gliosis and neurobehavioral changes in an animal model and resulted in N-methyl-D-aspartate (NMDA) receptor-mediated neuronal death. These findings suggest that the lentivirus envelope, which is a domain of extensive molecular diversity in brain-derived lentivirus isolates, directly influences neuropathogenesis through the activation of select proteases, underscoring the importance of concentrating on individual viral genes and proteases in the development of neuroprotective agents for HIV-related neurological disease.
Descriptors: feline acquired immunodeficiency syndrome, HIV infections, HIV 1 pathogenicity, feline immunodeficiency virus pathogenicity, matrix metalloproteinases, cats, feline acquired immunodeficiency syndrome, HIV infections, HIV 1, feline immunodeficiency virus, receptors, proteinase activated, variation, virulence.

Preuss, T.M. (2000). Taking the measure of diversity: comparative alternatives to the model-animal paradigm in cortical neuroscience. Brain, Behavior and Evolution 55(6): 287-299. ISSN: 0006-8977.
Descriptors: cerebral cortex, biological models, cats, cerebral cortex, haplorhini, rats, species specificity.

Prochazka, A. and V.K. Mushahwar (2001). Activation of paralyzed muscles with intraspinal microstimulation after chronic spinal transection. Society for Neuroscience Abstracts 27(2): 2482. ISSN: 0190-5295.
NAL Call Number: QP351. S6
Descriptors: spinal cord injury, animal model, cats, nervous system, muscle paralysis, muscle disease, chronic spinal transection, surgical method, intraspinal microstimulation, stimulation method, amplitude modulated pulse train, neural firing rate.
Notes: Meeting Information: 31st Annual Meeting of the Society for Neuroscience, San Diego, California, USA; November 10-15, 2001.

Prospero Garcia, O., N. Herold, T.R. Phillips, J.H. Elder, F.E. Bloom, and S.J. Henriksen (1994). Sleep patterns are disturbed in cats infected with feline immunodeficiency virus. Proceedings of the National Academy of Science of the United States of America 91(26): 12947-12951. ISSN: 0027-8424.
NAL Call Number: 500 N21P
Abstract: Human immunodeficiency virus (HIV)-related sleep disturbances have been reported early in AIDS. Likewise, the feline immunodeficiency virus (FIV), a natural lentivirus pathogen of cats, produces a similar immunodeficiency syndrome with neurological sequelae. To identify the neurophysiological substrate of FIV infection in brain, pathogen-free cats were infected with the Maryland strain of FIV. Eight weeks after inoculation, all FIV-infected cats seroconverted and virus was detected in the cerebrospinal fluid and in the mononuclear cells of peripheral blood. Ten to 12 months after the FIV inoculation, inoculated and control cats were surgically implanted with electrodes to record the sleep/wake cycle. These sleep recordings were obtained under conditions controlling for environmental variables and instrumental adaptation. FIV-infected cats spent 50% more time awake than the sham-inoculated controls and exhibited many more sleep/waking stage shifts--i.e., 40% more than controls. In addition, FIV-infected cats showed approximately 30% of rapid eye movement (REM) sleep reduction compared to controls. The latency to sleep and REM sleep onset was also significantly delayed in FIV-infected cats. In addition, a remarkable increase in cortically recorded spindle activity (8-13 Hz) was observed during slow-wave sleep in some infected subjects, similar to changes described in HIV-infected humans. Moreover, infected cats exhibited no overt signs of systemic morbidity, such as hyperpyrexia or body weight loss. These results indicate that FIV-infected cats exhibit sleep abnormalities similar to the sleep disturbances previously described in AIDS patients and further support the feline preparation as a.
Descriptors: cats, feline immunodeficiency virus, infections, sleep, neurophysiology, electrophysiology, electroencephalography, rapid eye movement, latency to sleep.

Prost, C. (1998). Allergy diagnosis in companion animals: clinical experience with the basophil activation model. Veterinary Dermatology 9(3): 213-215. ISSN: 0959-4493.
NAL Call Number: SF901 .V47
Descriptors: diagnosis, pet animals, hypersensitivity, granulocytes, cats, dogs, immunoglobulins, Dermatophagoides farinae, Dermatophagoides pteronyssinus, pollen, allergens, acarina, antigens, arachnida, astigmata , cells, dermatophagoides, gametes, glycoproteins, immunological diseases, immunological factors, leukocytes , pyroglyphidae, basophils, assays, IGE .

Quattrochi, J.J., J. Shapiro, R.L. Verrier, and J.A. Hobson (2000). Transient cardiorespiratory events during NREM sleep: a feline model for human microarousals. Journal of Sleep Research 9(2): 185-91. ISSN: 0962-1105.
Abstract: Microarousals (MAs) are brief transient events that occur during normal sleep in humans and with increased frequency in disordered sleep, especially in association with sleep apnoea. In a feline model, we discovered transient cardiorespiratory events during nonrapid eye movement (NREM) sleep that exhibited consistent features with similarities to human MAs. It was observed that MAs have two distinct phases. Phase I (MAI) is characterized by an abrupt increase in electromyogram (EMG) amplitude (> 50%), increased electrooculogram (EOG) activity and accelerated frequency of hippocampal electroencephalographic (EEG) activity. MAI lasts 4.1 +/- 0.3 s. Phase II (MAII), lasting 9.8 +/- 0.8 s, is characterized by high frequency EEG activity, but EMG, EOG and hippocampal activity remain at baseline levels. Mean inspiratory rate begins to increase 15 s before the onset of the MA, followed 10 s later by the increase in mean heart rate. Mean respiratory rate decreases sharply through MAII, and returns to baseline levels 15 s after the MA. During MAII mean heart rate decreases quickly; there is increased respiratory irregularity, followed by a prolonged ventilatory overshoot. The abrupt shift in heart rate is coincident with the change in breath timing seen during MAII. Heart rate returns to baseline levels 10 s following the MA. Integrating our findings with those described previously in humans, we propose that MAs may serve as a homeostatic mechanism which is designed to restore cardiorespiratory function allowing the continuity of sleep.
Descriptors: arousal, brain, heart rate, biological models, respiration, sleep, rem, cats, electroencephalography, electromyogrphy, electrooculography, homeostasis, polysomnography, time factors.

Reading, S.A. and J.K. Barclay (2002). The inotropic effect of nitric oxide on mammalian papillary muscle is dependent on the level of beta1-adrenergic stimulation. Canadian Journal of Physiology and Pharmacology 80(6): 569-577. ISSN: 0008-4212.
NAL Call Number: 444.8 C16
Descriptors: nitric oxide, cAMP, cGMP, Krebs Henseleit bicarbonate buffer, inotropic effects, cardiovascular system, feline ventricular papillary muscle.

Reber, P.U., A.G. Patel, M.T. Toyama, S.W. Ashley, and H.A. Reber (1999). Feline model of chronic obstructive pancreatitis: effects of acute pancreatic duct decompression on blood flow and interstitial pH. Scandinavian Journal of Gastroenterology 34(4): 439-44. ISSN: 0036-5521.
Abstract: BACKGROUND: The mechanism by which duct decompression (DD) relieves pain in patients with chronic pancreatitis (CP) is unknown. CP is associated with increased tissue pressure (IP), low pancreatic microvascular blood flow (PMBF), and interstitial pH (pH(I)). The aims of this study were to examine the effects of acute DD on PMBF, increased IP, and pH(I) in cats with CP. METHODS: The main pancreatic duct was partially obstructed. At 6 weeks PMBF (ml/min/100g H2 gas clearance), IP (mmHg needle electrode), and pH(I) (microelectrode) were measured before and after secretin stimulation. The duct was then opened, and the studies were repeated. RESULTS: PMBF normally increased with secretin stimulation (118 +/- 20 versus 271 +/- 52, P < 0.05). IP was unaltered, and pH(I) decreased as hydrogen ions produced during bicarbonate secretion were dissipated (7.41 +/- 0.01 versus 7.38 +/- 0.01, P < 0.05). In CP, basal PMBF was lower than normal (51 +/- 6 versus 118 +/- 20, P < 0.05) and decreased with stimulation (51 +/- 3.5 versus 31 +/- 3.5, P < 0.05). Basal pancreatic IP was increased (3.47 +/- 0.7 versus 0.05 +/- 0.3, P < 0.05) and increased further with secretory stimulation (3.47 +/- 0.7 versus 4.41 +/- 0.7, P < 0.05) (a compartment syndrome). The low basal pancreatic pH(I) (7.23 +/- 0.02) did not change with secretin stimulation, since bicarbonate secretion was minimal. DD decreased IP (3.66 +/- 0.5 versus 2.81 +/- 0.5, P < 0.05) and increased PMBF (50 +/- 6 versus 79 +/- 6, P < 0.05) and pH(I) (7.24 +/- 0.02 versus 7.34 +/- 0.02, P < 0.05). The normal increase in PMBF after stimulation was restored (79 +/- 6 versus 218 +/- 54, P < 0.05). pH(I) now increased with stimulation (7.34 +/- 0.002 versus 7.37 +/- 0.002, P < 0.05), perhaps due to the marked hyperaemic response. CONCLUSIONS: DD acutely restored basal and stimulated PMBF and IP towards normal. Basal pancreatic pH(I) also improved and reflects the underlying ischaemia.
Descriptors: pancreas supply, pancreatitis, cats, chronic disease, decompression, surgical, hydrogen ion concentration, pancreatic ducts surgery, pancreatitis, pancreatitis.

Rials, S.J., Y. Wu, N. Ford, F.J. Pauletto, S.V. Abramson, A.M. Rubin, R.A. Marinchak, and P.R. Kowey (1995). Effect of left ventricular hypertrophy and its regression on ventricular electrophysiology and vulnerability to inducible arrhythmia in the feline heart. Circulation 91(2): 426-30. ISSN: 0009-7322.
NAL Call Number: RC681.A1C8
Abstract: BACKGROUND: Left ventricular hypertrophy (LVH) is associated with an increased risk of death, susceptibility to ventricular arrhythmia, and multiple electrophysiological abnormalities. The purpose of the present study was to determine whether the susceptibility to arrhythmia and electrical abnormalities persists after regression of hypertrophy in an animal model of LVH. METHODS AND RESULTS: We placed constricting bands on the ascending aorta of cats (n = 9) or performed sham operations (n = 9). Serial cardiac echocardiography was performed to measure left ventricular wall thickness. After LVH had developed in the banded animals, the constricting bands were removed and serial echocardiograms were used to monitor for regression of hypertrophy. Electrophysiological studies were performed in cats that showed regression of LVH (Regress, n = 5), those that showed no change in LV wall thickness (No Regress, n = 4), and in the sham-operated animals (Sham). Cats with persistent LVH had a higher incidence of inducible polymorphic ventricular tachycardia (4 of 4) compared with Regress (1 of 5) or Sham (1 of 9) cats (P < .05) and had lower ventricular fibrillation thresholds (9 +/- 2 mA) than Regress (17 +/- 4 mA) or Sham (16 +/- 3 mA) cats (P < .05). Persistent LVH in the No Regress group was associated with prolongation of epicardial monophasic action potential duration (MAPD) in the left but not the right ventricle. Dispersion of refractoriness was greater in the No Regress group (P < .05 versus Regress or Sham). Regress cats were identical to Sham cats in having a low incidence of inducible polymorphic ventricular arrhythmia, high fibrillation threshold, and MAPD measurements (P = NS versus Sham). CONCLUSIONS: LVH produces multiple electrophysiological abnormalities and increased vulnerability to inducible polymorphic ventricular arrhythmia in this model of LVH. Cats that show regression of hyperthrophy have normal ventricular electrophysiology and have the same low vulnerability to inducible ventricular arrhythmia as Sham animals.
Descriptors: arrhythmia, heart, hypertropHy, left ventricular, action potentials, cats, echocardiograpHy, electrophysiology, heart ventricles, hypertropHy, left ventricular ultrasonography, tachycardia, ventricular, ventricular fibrillation diagnosis, ventricular fibrillation.

Rivo, J., E. Zeira, E. Galun, and I. Matot (2004). Activation of A3 adenosine receptors attenuates lung injury after in vivo reperfusion. Anesthesiology 101(5): 1153-9. ISSN: 0003-3022.
Abstract: BACKGROUND: A3 adenosine receptor (AR) activation worsens or protects against renal and cardiac ischemia-reperfusion (IR) injury, respectively. The aims of the current study were to examine in an in vivo model the effect of A3AR activation on IR lung injury and investigate the mechanism by which it exerts its effect. METHODS: The arterial branch of the left lower lung lobe in intact-chest, spontaneously breathing cats was occluded for 2 h and reperfused for 3 h (IR group). Animals were treated with the selective A3 receptor agonist IB-MECA (300 microg/kg intravenously) given 15 min before ischemia or with IB-MECA as described, with pretreatment 15 min earlier with the selective A3AR antagonist MRS-1191, the nonsulfonylurea adenosine triphosphate-sensitive potassium channel-blocking agent U-37883A, or the nitric oxide synthase inhibitor N-nitro-l-arginine benzyl ester. RESULTS: IB-MECA markedly (P < 0.01) reduced the percentage of injured alveoli (IR, 48 +/- 4%; IB-MECA, 18 +/- 2%), wet:dry weight ratio (IR, 8.2 +/- 0.4; IB-MECA, 4 +/- 2), and myeloperoxidase activity (IR, 0.52 +/- 0.06 U/g; IB-MECA, 0.17 +/- 0.04 U/g). This protective effect was completely blocked by pretreatment with the selective A3AR antagonist MRS-1191 and the adenosine triphosphate-sensitive potassium channel blocking agent U-37883A but not the nitric oxide synthase inhibitor N-nitro-l-arginine benzyl ester. CONCLUSIONS: In the feline lung, the A3AR agonist IB-MECA confers a powerful protection against IR lung injury. This effect is mediated by a nitric oxide synthase-independent pathway and involves opening of adenosine triphosphate-sensitive potassium channels. Therefore, selective activation of A3AR may be an effective means of protecting the reperfused lung.
Descriptors: adamantane, adenosine, lung, receptor, adenosine a3 agonists, reperfusion injury, reperfusion injury, adamantane, adenosine, cats, dihydropyridines, enzyme inhibitors, hemodynamic processes, histamine, morpholines, nitric oxide synthase, nitroarginine, potassium channel blockers, potassium channels, pulmonary artery, pulmonary artery, receptor, adenosine a3.

Robinson, W. (1996). The use of FIV infection as an animal model for HIV infection. Australian and New Zealand Council for the Care of Animals in Research and Teaching News 9(2): 4-5. ISSN: 1322-1779.
Online: www.adelaide.edu.au/ANZCCART/
NAL Call Number: SF405.5.A3
Descriptors: HIV infections, human diseases, disease models, animal models, animal diseases, human immunodeficiency virus, feline immunodeficiency virus.

Rubinstein, J.T., C.A. Miller, H. Mino, and P.J. Abbas (2001). Analysis of monophasic and biphasic electrical stimulation of nerve. Institute of Electrical and Electronics Engineers Transactions on Bio Medical Engineering 48(10): 1065-70. ISSN: 0018-9294.
Abstract: In an earlier study, biphasic and monphasic electrical stimulation of the auditory nerve was performed in cats with a cochlear implant. Single-unit recordings demonstrated that spikes resulting from monophasic and biphasic stimuli have different thresholds and latencies. Monophasic thresholds are lower and latencies are shorter under cathodic stimulation. Results from stochastic simulations of a biophysical model of electrical stimulation are similar. A simple analysis of a linear, "integrate to threshold" membrane model accounts for the threshold and latency differences observed experimentally and computationally. Since biphasic stimuli are used extensively in functional electrical stimulation, this analysis greatly simplifies the biophysical interpretation of responses to clinically relevant stimuli by relating them to the responses obtained with monophasic stimuli.
Descriptors: nerve fibers, vestibulocochlear nerve, action potentials, auditory threshold, cats, electric stimulation, models, neurological, reaction time, stochastic processes.

Rudolph, K.K., V.P. Ferrera, and T. Pasternak (1994). A reduction in the number of directionally selective neurons extends the spatial limit for global motion perception. Vision Research 34(24): 3241-3251. ISSN: 0042-6989.
Abstract: Dynamic random-dot targets were used to study neural mechanisms underlying motion perception. Performance of cats with severely reduced numbers of cortical directionally selective neurons (reduced DS) was compared to that of normal animals. We assessed the spatial properties of the residual motion mechanism by measuring direction discriminations at various dot displacements. At small displacements, reduced DS cats' motion integration thresholds for opposite direction discrimination were nearly normal. At larger displacements, their thresholds surpassed those of normal cats and their upper displacement limit (dmax) was increased by 0.35 deg. The accuracy of direction discrimination was reduced at small displacements, but at larger displacements direction difference thresholds of reduced DS cats approached or surpassed those of normals. These data were compared to the performance of humans who showed an extension of dmax for peripherally viewed targets. The data support the hypothesis that expansion in spatial scale of the motion mechanism may contribute to extension of dmax. Additional support for this hypothesis is provided by a modified direction discriminating line-element model. The model also suggests that changes in sampling of motion mechanisms in the reduced DS system may play a role.
Descriptors: motion perception, visual pattern recognition, visual cortex, cats, discrimination psychology, biological models, psychophysics, sensory deprivation, sensory thresholds, time factors, visual fields.

Sahani, M., U.D. Parashar, R. Ali, P. Das, M.S. Lye, M.M. Isa, M.T. Arif, T.G. Ksiazek, and M. Sivamoorthy (2001). Nipah virus infection among abattoir workers in malaysia, 1998-1999. International Journal of Epidemiology 30(5): 1017-1020. ISSN: 0300-5771.
Descriptors: Nipah virus encephalitis, nervous system disease, viral disease, 1998-1999 study period, abattoir worker occurrence.

Sakamoto, N., T. Yamashita, T. Takebayashi, M. Sekine, and S. Ishii (2001). An electrophysiologic study of mechanoreceptors in the sacroiliac joint and adjacent tissues. Spine 26(20): E468-71. ISSN: 0362-2436.
Abstract: STUDY DESIGN: The somatosensory afferent units in the sacroiliac joint of an animal model were investigated using an electrophysiologic technique. OBJECTIVES: To identify the mechanosensitive receptive fields in the sacroiliac joint, and to determine their distribution and characteristics. SUMMARY OF BACKGROUND DATA: The sacroiliac joint is considered to be a source of lower back pain. Although there have been clinical studies on the diagnosis of sacroiliac joint pain, no satisfactory diagnostic method other than joint blocks has been reported. It still is not clear whether the sacroiliac joints actually transmit pain to the central nervous system. The sensory innervation of the sacroiliac joint has not been fully characterized neurophysiologically. METHODS: Experiments were performed on 10 adult cats weighing 2.6 to 4 kg. The animals were anesthetized with intravenous sodium pentobarbital. An L4-L7 laminectomy was performed. The L4-L6 dorsal roots were cut at their proximal ends, split, and draped over a bipolar recording electrode. Glass probes were used to search the sacroiliac joint and adjacent tissues for mechanosensitive units. When units were identified, they were stimulated electrically to obtain conduction velocities and by Semmes-Weinstein monofilaments to determine mechanical thresholds. RESULTS: In the sacroiliac joint and adjacent muscles, 29 discrete mechanosensitive units were identified. Of these 29 units, 26 were found in the posterior sacroiliac ligament and the remaining 3 in the adjacent muscles. Also, 16 units (55%) were identified in the proximal third of the sacroiliac joint. Conduction velocities of the units ranged from 3.1 to 22 m/second (average, 9.2 m/second), and 26 units were group III. Mechanical thresholds of the units ranged from 4.6 to 164.3 g (average, 69.7 g). Whereas 28 units (96.6%) had thresholds higher than 7 g, one unit (3.4%) had a threshold lower than 7 g. CONCLUSIONS: Group III units with mechanical thresholds higher than 7 g may serve as nociceptors, and units with thresholds of lower than 7 g may serve as proprioceptors. The current study showed that most of the units in the sacroiliac joint were high-threshold group III units that perhaps had a nociceptive function. This result suggests that the sacroiliac joint may be a source of lower back pain in humans. This study also showed that the sacroiliac joint has little proprioceptive function.
Descriptors: mechanoreceptors, sacroiliac joint, cats, electrophysiology, ganglia, spinal, ganglia, spinal surgery, laminectomy, lumbar vertebrae surgery, models, animal, neural conduction, nociceptors, pain threshold, sacroiliac joint innervation.

Sandmeyer, L.S., C.L. Keller, and D. Bienzle (2005). Culture of feline corneal epithelial cells and infection with feline herpesvirus-1 as an investigative tool. American Journal of Veterinary Research 66(2): 205-9. ISSN: 0002-9645.
NAL Call Number: 41.8 Am3A
Abstract: OBJECTIVE: To isolate and characterize pure cultures of feline corneal epithelial cells and to assess the extent and nature of feline herpesvirus (FHV)-1 infection in these cells. SAMPLE POPULATION: Healthy eyes from 23 recently euthanatized cats. PROCEDURE: Stroma and epithelium of the rostral portion of the cornea were surgically isolated, and epithelial cells were detached from the stroma by enzymatic incubation. Epithelial cells were cultured in hormone-supplemented media. Cells were passaged, and cytokeratin expression was assessed. Cells were then infected with FHV-1, and cytopathic effects were determined. RESULTS: Cell cultures were readily established from samples obtained from each eye and could be maintained through 6 passages. Cultured cells expressed cytokeratins 3 and 12 but not other cytokeratins. Infection with FHV-1 was rapid and caused widespread cytopathic effects. CONCLUSIONS AND CLINICAL RELEVANCE: Feline corneal cells cultured in vitro during multiple passages maintain consistent morphologic characteristics and intermediate filament expression. They are susceptible to infection with FHV-1 and may provide a useful in vitro model for investigation of ocular drugs.
Descriptors: epithelium, corneal, epithelium, corneal, herpesviridae, cats, cell culture techniques, cytopathogenic effect, viral, epithelium, corneal, immunohistochemistry, keratin.

Sargan, D.R., P.J. Clements, A. Sohal, C.Y. Gregory, S.S. Bhattacharya, and S.M. Petersen Jones (1994). Progressive retinal atrophy: a model for retinitis pigmentosa in companion animals. Gene Therapy 1(Suppl 1): S89. ISSN: 0969-7128.
Abstract: The generalised progressive atrophies (PRA's) are a heterogeneous group of inherited retinopathies in dogs and cats. They show marked similarities to the retinitis pigmentosas (RP) in man, as well as to a number of inherited retinal degenerations of laboratory rodents. Of the various recessively inherited forms of PRA in the dog, that in the Irish setter is due to a nonsense mutation in the gene encoding cGMP-PDE-beta subunit. Mutations at this locus are also known to cause a proportion of human RP cases. We are interested in applying gene therapy to these diseases.
Descriptors: retinitis pigmentosa, 3',5' cyclic GMP phosphodiesterase, animals, domestic, cats, animal disease models, dogs, gene therapy, retinitis pigmentosa, retinitis pigmentosa.

Sbriccoli, P., K. Yousuf, I. Kupershtein, M. Solomonow, B.H. Zhou, M.P. Zhu, and Y. Lu (2004). Static load repetition is a risk factor in the development of lumbar cumulative musculoskeletal disorder. Spine 29(23): 2643-53. ISSN: 0362-2436.
Abstract: STUDY DESIGN: In vivo feline model subjected to variable number of repetitions of a short static lumbar flexion followed by an equally long rest period. OBJECTIVES: The purpose of this study was to determine the influence of the number of repetitions as a risk factor in promoting a cumulative low back disorder in the feline model. SUMMARY OF BACKGROUND DATA: Epidemiologic data point out that the increased number of repetitions of static lumbar loading is a major risk factor in the development of cumulative low back disorder. Biomechanical and physiologic confirmation of the epidemiology is lacking. Recent work demonstrated that repetitive static loading results in accumulation of creep in the lumbar viscoelastic tissues, resulting in a neuromuscular disorder consisting of spasms during loading and hyperexcitability of lumbar muscles during following rest. It was also shown that the load magnitude is a major risk factor. It is hypothesized that increased number of repetitions of static load periods result in increased severity of the resulting neuromuscular disorder. METHODS: Static lumbar flexion of 10 minutes duration followed by 10 minutes rest was repeated three times in one experimental group, six times in the second, and nine times in the third group. In all groups, the creep developing in the lumbar viscoelastic tissues as well as the reflexive EMG from the multifidus were monitored during the flexion/rest periods and throughout a 7-hour recovery period after the repetitions. RESULTS: Creep developed and accumulated during each of the flexion/rest periods in the three experimental protocols, with larger residual creep at the end of the nine repetitions. A residual creep was still present at the end of the 7 hours of recovery allowed in each of the three groups. During the flexion/rest sessions, EMG spasms were present, and the presence of an initial hyperexcitability was detected during the 7 hours of recovery in all the preparations. The presence of a delayed hyperexcitability was revealed only in the group subjected to nine flexion/rest periods, while it was not observed in the groups subjected to three and six flexion/rest repetitions. The statistical analysis (post hoc Fisher test) performed on the normalized integrated EMG and displacement data during the recovery phase showed a significant difference between the nine repetitions group and the other two groups (P < 0.0001). The two-way ANOVA analysis revealed a significant effect of time (P < 0.005) and number of repetitions (P < 0.0001) on all considered parameters. CONCLUSIONS: It was concluded that a cumulative neuromuscular disorder develops because of repetition of static lumbar flexion, and the severity of the disorder provoked is magnified by the number of repetitions. Despite the highly favorable 1:1 work-to-rest ratio and the 7-hour post loading rest period, a full recovery of creep was not obtained in this study.
Descriptors: feline lumbar, static load, EMG, neuromuscular disorder.

Schlichtenbrede, F.C., G.M. Sarra, R.R. Ali, P. Wiedemann, and M.B. Reichel (2002). Fortschritte in der somatischen Gentherapie von Netzhautdegenerationen am Tiermodell. [Progress in somatic gene therapy of retinal degeneration in the animal model]. Der Ophthalmologe Zeitschrift Der Deutschen Ophthalmologischen Gesellschaft 99(4): 259-65. ISSN: 0941-293X.
Abstract: More than 60 genes responsible for human retinal dystrophies have already been identified. Most of them are either expressed in the photoreceptor or in the retinal pigment epithelium (RPE). Therefore these cells have become the target of new therapeutical strategies on a molecular level. The most promising approach at present is somatic gene therapy, which has been developed over the last years and the principle has now been established in animal models. For gene therapy of inherited retinal degeneration, as for gene therapy in general, gene transfer has to be proven to be not only efficient but also safe. This has recently been achieved using the adeno-associated virus (AAV) as a vector to express a therapeutic gene within the photoreceptor cell. It could be demonstrated in mouse and dog models of retinal degeneration that expression of the therapeutic transgene leads to anatomical and functional restitution of degenerating photoreceptors. A significant immune response to AAV has not been detected so far. In this paper the recent success of gene therapy of retinal degeneration in animal models is reviewed.
Descriptors: gene therapy, retinal degeneration therapy, adenoviridae, cats, animal disease models, dogs, gene transfer techniques, mice, photoreceptors, pigment epithelium of eye, retinal degeneration, retinal degeneration, swine.
Language of Text: German.

Schmanke, T.D. and J.R. Villablanca (2001). A critical maturational period of reduced brain vulnerability to injury. A study of cerebral glucose metabolism in cats. Brain Research/ Developmental Brain Research 131(1-2): 127-41. ISSN: 0006-8993.
Abstract: We have developed a feline cerebral hemispherectomy model as an analog to the surgical procedure used in pediatric intractable epilepsy. Previous work with this model has shown a remarkable plasticity associated with an early period of brain development, which we have defined using morphological, cerebral metabolic and behavioral methods. However, the important functional-metabolic bracketing of this period has not yet been performed. We have conducted the present study to answer questions raised by our previous findings using [14C] 2-deoxy-D-glucose autoradiography but only including animals lesioned at day 10 postnatally (P10) or in adulthood. The questions were; (a) is there any age better than P10 for an optimal metabolic outcome?, and (b) can we determine a cutoff point for the beneficial effects of the young age-at-lesion? Twenty-one adult cats were studied. Seven cats served as intact controls, five received a left hemineodecortication at P30, three at P60, three at P90 and three at P120, respectively. Histological analysis indicated that the extent of the lesion was similar between the age groups. Local glucose metabolic rates (LCMR(glc)) were measured in 50 structures bilaterally and used to calculate overall LCMR(glc) for seven grouped sites within the cerebral cortex, thalamus, basal ganglia, mesencephalic tegmentum (and tectum), limbic system and cerebellum. Results indicated a widespread bilateral depression of LCMR(glc) in all age-at-lesion groups. The depression in overall LCMR(glc) across all structures measured in each hemisphere was significant (P<0.05) for the P120 group relative to intacts for both ipsilateral (left) and contralateral (right) sides of the brain. The ipsilateral thalamus was the region most effected by the injury, with significant losses for all age-at-lesion groups. In addition, while there were widespread depressions for all lesion groups, these losses were significant for the P120 group in five groups of structures ipsilaterally (thalamus, basal ganglia, tectum, limbic system, cerebellum) and in three contralaterally (thalamus, tectum, cerebellum). In contrast, significant depressions for the earlier age-at-lesion groups (P30, P60, P90) were found only in the ipsilateral thalamus and bilaterally in the tectum. These results, together with our previous results for the P10 group, indicate a relative sparing of LCMR(glc) after hemineodecortication during the first 60 days of life, with gradually decreasing plasticity thereafter, such that there is some residual sparing at 90 days of age, and afterwards an almost complete loss of metabolic plasticity, with lesions at P120 producing a dismal outcome. These results complement earlier morphological and behavioral studies and support the concept of a 'Critical Maturational Period' of reduced vulnerability to developmental injury.
Descriptors: brain growth and development, brain, brain injuries, critical period psychology, glucose, antimetabolites, basal ganglia growth and development, basal ganglia, brain stem growth and development, brain stem, cats, cerebellum growth and development, cerebellum, cerebral decortication, deoxyglucose, epilepsy, limbic system growth and development, limbic system, neocortex growth and development, neocortex, neuronal plasticity, thalamus growth and development, thalamus.

Schneider, J.H., J.H. Peters, E. Kirkman, C.G. Bremner, and T.R. DeMeester (1999). Are the motility abnormalities of achalasia reversible? An experimental outflow obstruction in the feline model. Surgery 125(5): 498-503. ISSN: 0039-6060.
Abstract: BACKGROUND: Experimental and clinical evidence suggests that the loss of esophageal body function in achalasia may be a result of the outflow obstruction of a nonrelaxing, hypertensive lower esophageal sphincter. The reversibility of such abnormalities has implications to the timing of therapeutic interventions. This study was designed to evaluate the evolution and reversibility of motility abnormalities resulting from esophageal outflow obstruction in cats. METHODS: Twenty adult cats were divided into 2 groups. Group 1 consisted of 4 cats that underwent laparotomy as a sham procedure. Group 2 consisted of 16 cats that underwent surgical placement of a loose Gore-tex expanded polytetrafluoroethylene (W. L. Gore, Elkton, Md) band calibrated to 110% of the circumference of the gastroesophageal junction. The band was removed from 4 randomly selected cats each at 1, 2, 4, and 6 weeks after placement. Esophageal manometry was performed before placement of the band, at weekly intervals after placement of the band, and after removal of the band. The resting pressure and percent relaxation of the lower esophageal sphincter (LES), in addition to amplitude, duration, and propagation of esophageal body contractions, were measured at each interval. Data are expressed as median and interquartile range and compared with use of the Mann-Whitney U test for independent samples. RESULTS: The LES resting pressure remained unchanged after placement of the band, but sphincter compliance was reduced, as manifested by a significant reduction in the percent of sphincter relaxation (98% prebanding, 65% postbanding, P < .05). The median amplitude of esophageal contraction decreased significantly after banding. By 6 weeks after banding the esophagus was markedly dilated and exhibited aperistaltic, low-amplitude esophageal motility typical of that seen in clinical achalasia. Importantly, removal of the bands resulted in a prompt return of both peristalsis and amplitude of contraction. CONCLUSIONS: Loss of compliance of the lower esophageal sphincter produces outflow obstruction with the resultant loss of esophageal contraction amplitude and peristaltic waveform typical of achalasia in humans. These abnormalities were reversible after relief of obstruction in the feline model and may indicate that early relief of outflow obstruction in clinical achalasia may preserve esophageal function in patients.
Descriptors: esophageal achalasia, esophgus, cats, compliance, muscle contraction, pressure.

Sekine, M., T. Yamashita, T. Takebayashi, N. Sakamoto, Y. Minaki, and S. Ishii (2001). Mechanosensitive afferent units in the lumbar posterior longitudinal ligament. Spine 26(14): 1516-21. ISSN: 0362-2436.
Abstract: STUDY DESIGN: The mechanosensitive afferent units in the lumbar posterior longitudinal ligament were investigated in an animal model using an electrophysiologic technique. OBJECTIVES: The objectives of this study were to identify the mechanosensitive receptive fields in the lumbar posterior longitudinal ligament and to investigate their distribution and characteristics. SUMMARY OF BACKGROUND DATA: The lumbar posterior longitudinal ligament has a nerve network originating from the sinuvertebral nerve. These fibers are thin, and most of their terminals are free nerve endings. Some immunohistochemical studies have indicated that they are immunoreactive to calcitonin gene-related peptide and/or substance P, suggesting a nociceptive function. Most of these studies investigated morphologic aspects, and there have been few studies employing electrophysiologic techniques to examine mechanosensitive units. METHODS: We used 13 adult cats. They were anesthetized and then laminectomy was performed. The L5 and L6 dorsal rootlets were draped over a recording electrode. To investigate the receptive fields in the posterior longitudinal ligament, afferent impulses were evoked by mechanical stimulation with a glass probe. When the receptive fields were located, they were stimulated electrically to obtain conduction velocity and were stimulated with a set of 17 nylon filaments to determine their mechanical thresholds. RESULTS: Thirteen units were identified in the lumbar posterior longitudinal ligament. The majority of the units were located around the intervertebral disc level of the posterior longitudinal ligament. The mean mechanical threshold was 47.04 +/- 15.25 g. According to the conduction velocities of the units, 12 units were classified into Group III (0.5-2.5 m/sec) and one unit into Group IV (2.5-20 m/sec). CONCLUSION: Mechanosensitive units classified into Group III or Group IV and with a high mechanical threshold (>7.0 g) were thought to act as nociceptive units. All units identified in this study satisfied these criteria. Our result suggests that afferent fibers from the lumbar posterior longitudinal ligament have a principally nociceptive function.
Descriptors: afferent pathways, longitudinal ligaments innervation, lumbar vertebrae, mechanoreceptors, afferent pathways, cats, electric conductivity, longitudinal ligaments, mechanoreceptors, models, animal.

Shaker, R., B.K. Medda, J. Ren, S. Jaradeh, P. Xie, and I.M. Lang (1998). Pharyngoglottal closure reflex: identification and characterization in a feline model. American Journal of Physiology 275(3 Pt 1): G521-525. ISSN: 0002-9513.
NAL Call Number: 447.8 AM3
Abstract: Earlier studies in humans have shown that pharyngeal stimulation by water at a threshold volume induces a brief vocal cord adduction, i. e., pharyngoglottal closure reflex. The present study was undertaken to 1) develop a suitable animal model for physiological studies of this reflex and 2) delineate its neural pathway and effector organs. Studies were done in cats by concurrent videoendoscopy and manometry followed by electromyographic studies. At a threshold volume (0.3 +/- 0.06 ml), injection of water into the pharynx resulted in a brief closure of the vocal folds, closing the introitus to the trachea. Duration of this closure averaged 1.1 +/- 0.1 s. Bilateral transection of the glossopharyngeal nerve completely abolished this reflex but not swallows induced by pharyngeal water stimulation. The pharyngoglottal closure reflex is present in the cats. The glossopharyngeal nerve is the afferent pathway of this reflex, and the interarytenoid and lateral cricoarytenoid muscles are among its target organs.
Descriptors: glossopHaryngeal nerve, glottis, pharynx, reflex, cats, electromyogrphy, kinetics, microscopy, video, trachea.

Shaker, R., J. Ren, B. Medda, I. Lang, V. Cowles, and S. Jaradeh (1994). Identification and characterization of the esophagoglottal closure reflex in a feline model. American Journal of Physiology 266(1 Pt 1): G147-53. ISSN: 0002-9513.
NAL Call Number: 447.8 AM3
Abstract: To identify a suitable animal model and to delineate the neural pathway and target organs of the esophagoglottal closure reflex we studied three species. Study showed the existence of an esophagoglottal closure reflex in cats. The presence of this reflex could not be documented in the opossum. In monkeys, because of the inadequacy of the available recording devices, its presence could not be ascertained. In the feline model, the closure response of the vocal folds to the abrupt generalized and segmental distension of the esophagus was similar to that of the humans. Study findings indicate that among glottal adductor muscles at least interarytenoid and lateral cricoarytenoid muscles are involved as target organs of the esophagoglottal closure reflex. Decerebration did not change the frequency of glottal closure response to esophageal distension, supporting the notion that this reflex is completely under brain stem control. Bilateral cervical vagotomy abolished the glottal closure induced by esophageal distension indicating that this reflex is mediated by the vagus nerve. Upper esophageal sphincter (UES) pressure response to esophageal distension by air was variable, suggesting that glottal and UES response to esophageal distension, although closely coordinated, are not dependent on one another. In summary, an esophagoglottal closure reflex exists in feline species, and many similarities in the elicitation and mediation of this reflex have been found with that of humans. This model could be used for further physiological studies.
Descriptors: esophgus, glottis, reflex, air, balloon dilatation, cats, electromyogrphy, endoscopy, esopHagogastric junction, esophgus, glottis, injections, macaca, opossums, television.

Shardonofsky, F.R., J. Sato, and D.H. Eidelman (1994). Frequency dependence of pulmonary and chest wall mechanics in young and adult cats. Journal of Applied Physiology 76(5): 2037-46. ISSN: 8750-7587.
NAL Call Number: 447.8 J825
Abstract: The frequency (f) dependence of pulmonary and chest wall mechanics was assessed in nine kittens and four cats. Kittens and cats were anesthetized, paralyzed, and mechanically ventilated at various f between 0.13 and 1.6 Hz and 0.09 and 0.79 Hz, respectively. Resistance and dynamic compliance pertaining to the respiratory system (Rrs and Cdyn,rs), lungs (RL and Cdyn,L), and chest wall (RW and Cdyn,W) were estimated by fitting a single-compartment model to data obtained from regular ventilation. Static lung and chest wall compliances (Cst,L and Cst,W) were computed from quasi-static pressure-volume data. Lung tissue resistance (Rti) was estimated with alveolar capsules in open-chest animals. The f dependence of the two-compartment viscoelastic model of the respiratory system was assessed by computing the effective resistance [Rmod,rs(omega)] and compliance [Cmod,rs(omega)] from data obtained at the lowest experimental f. Both Cdyn,L and Cdyn,W decreased with increasing f in all animals. Cdyn,L/Cst,L and Cdyn,W/Cst,W were lower in kittens than in cats. RL and RW decreased markedly with f in all animals. Rti/RL showed a marked f dependence, its values being similar in both young and adult cats at their respective resting f. CstW/Cst,L ratio was higher in kittens than in cats. A better agreement was found between Cmod,rs(omega) and Cdyn,rs than between Rmod,rs(omega) and Rrs.
Descriptors: aging, lung, respiratory mechanics, thorax, air pressure, airway resistance, cats, lung compliance, lung volume measurements, biological models, plethysmograpHy, pulmonary alveoli, respiration, artificial.

Shevelev, O.A., G.V. Bugorskii, I.L. Privalova, and N.A. Khodorovich (1994). Vliianie ostrogo povrezhdeniia na afferentnye reaktsii zheludka i dvenadtsatiperstnoi kishki [Effect of an acute lesion on afferent reactions of the stomach and duodenum]. Patologicheskaia Fiziologiia i Eksperimental'Naia Terapiia(4): 46-7. ISSN: 0031-2991.
Abstract: By recording the evoked potentials in the cortex and thalamic nuclei, afferent reactions of gastroduodenal components were studied early after acute gastroduodenal lesion in acute feline experiments. A model of acute ulcer in various gastric portions and the duodenal bulb gave rise to inhibition of their afferentation. This phenomenon was most pronounced in pyloric ulcer. It is concluded that the inhibition of the afferent reactions of gastroduodenal components in early periods after their acute lesion is a specific protective reaction of the viscera and appears mainly at the intraorgan level.
Descriptors: duodenal ulcer, duodenum innervation, stomach innervation, stomach ulcer, acute disease, afferent pathways, cats.
Language of Text: Russian.

Shimada, Y. (1995). Experimental study on effects of omental transposition in cats with spinal cord injury. No to Shinkei [Brain and Nerve] 47(9): 863-873. ISSN: 0006-8969.
Abstract: The effects of autogenous omental transposition on spinal cord injury in cats were examined using a cord crush injury model produced by a modification of Allen's weight-dropping technique. Twenty-three cats were divided into two groups: an omental transposition group, and a control group. The animals were sacrificed at 1, 2, 3, and 4 weeks after injury. The injured cords were examined histologically using India ink perfusion, morphometry of the spinal cord cavities and also by somatosensory evoked potential (SEP) studies. After 1 week, hemorrhagic necrosis, cavitation and demyelination of almost the same extent and severity were noted in both groups. These changes diminished with time in the omental transposition group, but tended to persist in the control group. In the omental transposition group, fibrous coats of Goldsmith were newly formed on the injured cord between the incised dura edges. After 3 weeks, the fibrous coat was thickened with active proliferation of fibroblasts and collagen fibers. India ink particles were noticed within the fine vessels of the omentum, fibrous coat and injured cord at 4 weeks. No India ink particles were found in the control group even after 4 weeks. In the somatosensory evoked potentials, biphasic or triphasic waves noted before injury were absent immediately after trauma. At 3 and 4 weeks, 3 of 5 cats with the omentum showed reappearance of the waves, whereas no wave-reappearance was noted in the controls. These results suggest that autogenous omental transposition helps to accelerate the healing process after crush injury to the spinal cord.
Descriptors: omentum transplantation, spinal cord injuries surgery, cats, evoked potentials, somatosensory, spinal cord, spinal cord, spinal cord injuries, spinal cord injuries, wound healing.
Language of Text: Japanese.

Shouse, M.N., P.R. Farber, and R.J. Staba (2000). Physiological basis: how NREM sleep components can promote and REM sleep components can suppress seizure discharge propagation. Clinical Neurophysiology 111(Suppl 2): S9-S18. ISSN: 1388-2457.
Abstract: OBJECTIVES: To describe how the neural generators of different sleep components can provoke seizure discharge propagation during NREM sleep and can suppress it during REM sleep. METHODS: Experimental manipulations of discrete physiological components were conducted in feline epilepsy models (n=64), mostly in the systemic penicillin epilepsy model of primary generalized epilepsy and the amygdala kindling model of the localization-related seizure disorder, temporal lobe epilepsy. Procedures included seizure induction as well as quantifying norepinephrine concentrations (microdialysis) and the sleep-waking state distribution of seizures before and after lesions, systemic and localized drug administration and/or photic stimulation. RESULTS: (1) Neural generators of synchronous EEG oscillations, including tonic background slow waves and phasic 'arousal' events (sleep EEG transients such as sleep spindles, k-complexes), can combine to promote electrographic seizure propagation during NREM and drowsiness; anti-gravity muscle tone permits seizure-related movement. (2) Neural generators of asynchronous neuronal discharge patterns can reduce electrographic seizures during alert waking and REM sleep; skeletal motor paralysis blocks seizure-related movement during REM. (3) Etiology of the seizure disorder can interact with sleep and arousal mechanisms to determine sleep-waking state distribution of interictal and ictal events. CONCLUSIONS: Differential effects of NREM versus REM sleep components on seizure discharge propagation are to some extent non-specific and in other ways specific to seizure etiology.
Descriptors: brain, epilepsy, sleep, rem, cats, animal disease models, electroencephalography.

Shouse, M.N., J.C. Scordato, and P.R. Farber (2004). Sleep and arousal mechanisms in experimental epilepsy: epileptic components of NREM and antiepileptic components of REM sleep. Mental Retardation and Developmental Disabilities Research Reviews 10(2): 117-21. ISSN: 1080-4013.
Abstract: Neural generators related to different sleep components have different effects on seizure discharge. These sleep-related systems can provoke seizure discharge propagation during nonrapid eye movement (NREM) sleep and can suppress propagation during REM sleep. Experimental manipulations of discrete physiological components were conducted in feline epilepsy models, mostly in the systemic penicillin epilepsy model of primary generalized epilepsy and the amygdala kindling model of the localization-related seizure disorder, temporal lobe epilepsy. The sleep-wake state distribution of seizures was quantified before and after discrete lesions, systemic and localized drug administration, and/or photic stimulation, as well as in relation to microdialysis of norepinephrine. We found that (1) neural generators of synchronous EEG oscillations--including tonic background slow waves and phasic "arousal" events (sleep EEG transients such as sleep spindles and k-complexes)--combine to promote electrographic seizure propagation during NREM and drowsiness, and antigravity muscle tone permits seizure-related movement; (2) neural generators of asynchronous neuronal discharge patterns reduce electrographic seizures during alert waking and REM sleep, and skeletal motor paralysis blocks seizure-related movement during REM; (3) there are a number of similarities between amygdala-kindled kittens and children with Landau-Kleffner Syndrome (LKS) that suggest a link among seizures, sleep disorders, and behavioral abnormalities/regression.
Descriptors: arousal, epilepsy, sleep, rem, amygdala, cats, electroencephalography, kindling neurology, landau kleffner syndrome, muscle, skeletal, rats, sleep stages.

Silvotti, L., A. Corradi, G. Brandi, A. Cabassi, M. Bendinelli, M. Magnan, and G. Piedimonte (1997). FIV induced encephalopathy: early brain lesions in the absence of viral replication in monocyte/macrophages. A pathogenetic model. Veterinary Immunology and Immunopathology 55(4): 263-271. ISSN: 0165-2427.
NAL Call Number: SF757.2. V38
Abstract: FIV induced encephalopathy represents a model for the study of the neuropathogenesis of AIDS. It has yet to be determined whether massive viral replication is a prerequisite for the development of early brain lesions. Using a drug delivery system developed by us, we have shown that early encephalic lesions appear in FIV infected subjects even when viral transport within the brain has been markedly reduced or blocked.
Descriptors: feline immunodeficiency virus, cats.

Simon, J.C., K. Saker, and E. Thomas (2000). Sensitivity of specific immune function tests to acute nutrient deprivation as indicators of nutritional status in a feline model. Nutrition Research 20(1): 79-89. ISSN: 0271-5317.
NAL Call Number: QP141.A1N88
Descriptors: cats, starvation, immune function, feline model, nutrition.

Sokov, E.L. and O.A. Shevelev (1994). Osteogennyi mekhanizm vertebrogennykh radikulopatii. [The osteogenic mechanism of vertebrogenic radiculopathies]. Zhurnal Nevropatologii i Psikhiatrii Imeni 94(2): 62-64. ISSN: 0044-4588.
Abstract: Intraosteal block was conducted in 86 patients with pronounced neurological symptoms of lumbar osteochondrosis. To clarify the role of the intraosteal receptors in pathogenesis of the above symptoms and to evaluate the efficacy of the blocks, series of experiments were made on 8 cats. The authors studied evoked potentials in the cerebral cortex and thalamus in response to irritation of the sciatic nerve under the exposure of the sciatic receptors to electrostimulation, intraosteal introduction of physiologic salt solution and trimecaine, electrostimulation following the introduction of the above substances. The pilot experience has been gained on facilitation of afferent current passage from the sciatic nerve under conditions of intraosteal receptor irritation as well as on inhibition of the above effect under anesthetic block of intraosteal receptors. Basing on the above findings, the authors explain osteogenic mechanism of radiculopathy and pathogenicity of the intraosteal blocks.
Descriptors: lumbar vertebrae, nerve compression syndromes, osteochondritis, spinal nerve roots, spondylitis, cats, dexamethasone, electric stimulation, evoked potentials, nerve block, nerve compression syndromes, nociceptors, trimecaine.
Language of Text: Russian.

Solomonow, M., S. Hatipkarasulu, B.H. Zhou, R.V. Baratta, and F. Aghazadeh (2003). Biomechanics and electromyography of a common idiopathic low back disorder. Spine 28(12): 1235-48. ISSN: 0362-2436.
Abstract: STUDY DESIGN: In vivo feline preparation groups loaded into lumbar flexion at different magnitudes and an unloaded control group. OBJECTIVE: To demonstrate that a static, constant load flexion of the lumbar spine results in a complex neuromuscular disorder. SUMMARY OF BACKGROUND DATA: Epidemiology suggests that static lumbar flexion is a cause of low back disorders. There is little direct experimental evidence describing the physiologic and biomechanical processes that elicit the disorder. Recent evidence shows that static flexion of the spine under constant displacement results in muscular spasms and a prolonged recovery period. The response of the spine to flexion under constant load of various magnitudes (as opposed to constant displacement) is not known. It was hypothesized that static lumbar flexion under constant load may elicit creep in spinal ligaments, discs, etc., causing microdamage and development of a neuromuscular disorder. METHODS: The lumbar spine of the feline was subjected to 20 minutes of constant load static flexion at physiologic load intensities from light to heavy while creep of lumbar viscoelastic tissues and EMG from the multifidus muscles of L3-L4 to L5-L6 were recorded. Recordings were continued over a 7-hour rest period after the static flexion was terminated. RESULTS: Spasms and decreasing reflexive EMG were evident during the loading period, and a transient surge of EMG activity occurred at the beginning of the rest period. A second surge of EMG activity was seen 3-4 hours later. The four components of the neuromuscular disorder were present regardless of the load magnitude. A model was developed to quantify the disorder. CONCLUSION: A four-component neuromuscular disorder was elicited by a 20-minute constant load static flexion even when very light loads were applied. The disorder was elicited by creep of the viscoelastic tissues, which resulted in spasms and muscular hyperexcitability lasting for >24 hours. Although the disorder was transient, the physiologic and biomechanical principles associated with its development could also explain cumulative trauma disorders.
Descriptors: low back pain, lumbar vertebrae, neuromuscular diseases, biomechanics, cats, animal disease models, electromyogrphy, muscle contraction, muscle relaxation, stress, mechanical.

Solomonow, M., B. He Zhou, R.V. Baratta, Y. Lu, M. Zhu, and M. Harris (2000). Biexponential recovery model of lumbar viscoelastic laxity and reflexive muscular activity after prolonged cyclic loading. Clinical Biomechanics 15(3): 167-75. ISSN: 0268-0033.
Abstract: OBJECTIVES: To determine the rest duration required for full recovery of reflexive muscular activity and laxity/creep induced in the lumbar viscoelastic structures (e.g., ligaments, discs, etc.) after 50 min of cyclic loading, and to develop a model describing such recovery. BACKGROUND: It is well established that steady, cyclic or vibratory loading of the lumbar spine induces laxity/creep in its viscoelastic structures. It was also shown that such viscoelastic creep does not fully recover when subjected to rest equal in duration to the loading period. Rest periods of 24 h, however, were more than sufficient to allow full recovery. The exact period of time allowing full recovery of viscoelastic laxity/creep, and its pattern is not known. It is also not known what is the duration required for full recovery of reflexive muscular activity lost due to the laxity/creep induced in the spine during cyclic loading. METHODS: The lumbar spine of 'in vivo' feline preparations was subjected to 50 min of 0.25 Hz cyclic loading applied v ia the L4/5 supraspinal ligament. At the end of the loading period the spine was subjected to prolonged rest, interrupted by a single cycle loading applied hourly for measurement purposes until the laxity was fully recovered (>90%). Reflexive EMG activity was recorded with wire electrodes from the L-1-L-7 multifidus muscles. A biexponential model was fitted to the load and EMG recorded in the recovery period in order to represent viscous and elastic components of structures with different architecture (e.g., disc vs. ligament). RESULTS: Full recovery of the laxity induced by 50 min of cyclic loading at 0.25 Hz required 7 h and was successfully fitted with a biexponential model. Similarly, EMG activity was fully recovered in 4 hours, and often exceeded its initial value during the following 3 h. CONCLUSIONS: Full recovery of laxity induced in the lumbar viscoelastic structures by a given period of cyclic loading requires rest periods, which are several folds longer than the loading duration. Similarly, reflexive muscular activity requires 4 h of rest in order to be restored. Meanwhile, significant laxity can be present in the joints, exposing the spine to potential injury and low back pain. Increased EMG activity at the end of the recovery period may indicate that pain was possibly induced in the spinal structures, inducing hyperexcitability of the muscles during passive loading. RELEVANCE: Although the data was derived from a feline model, and its extrapolation to the human model is not straightforward, the general pattern of decreasing reflexive muscular activity with cyclic loading is expected in both species. Therefore, workers who subject their spine to periods of cyclic loading may be exposed to prolonged periods of laxity beyond the neutral zone limits, without protection from the muscles and therefore the risk of possible injury and low back pain. Pain and muscle hyperexcitability could also be a factor associated with cyclic loading, being expressed several hours after work was completed.
Descriptors: intervertebral disk, longitudinal ligaments, lumbar vertebrae, muscle, skeletal, reflex, weight bearing, cats, animal disease models, elasticity, electromyogrphy, follow up studies, joint instability, low back pain, lumbar vertebrae injuries, biological models, recovery of function, sprains and strains, stress, mechanical, time factors, vibration, viscosity.

Solomonow, M., B. Zhou, R.V. Baratta, M. Zhu, and Y. Lu (2002). Neuromuscular disorders associated with static lumbar flexion: a feline model. Journal of Electromyography and Kinesiology 12(2): 81-90. ISSN: 1050-6411.
Abstract: Static flexion of the lumbar spine with constant load applied to the viscoelastic structures for 20 minutes and for 50 minutes resulted in development of spasms and inhibition in the multifidus muscles (e.g., deep erector spinae) and in creep of the supraspinous ligament in the feline model. The development of spasms and inhibition was not dependent on load magnitude. It is suggested that occupational and sports activities which require prolonged static lumbar flexion within the physiological range can cause a "sprain"-like injury to the ligaments, which in turn reflexively induce spasms and inhibition in some erector spinae muscles. Such disorder may take a long time to recover, in the order of days to weeks, depending on the level of creep developed in the tissues.
Descriptors: muscle, skeletal, spasm, stress, cats, animal disease models, electromyogrphy, lumbosacral region, spasm.

Solomonow, M., B.H. Zhou, R.V. Baratta, and E. Burger (2003). Biomechanics and electromyography of a cumulative lumbar disorder: response to static flexion. Clinical Biomechanics 18(10): 890-8. ISSN: 0268-0033.
Abstract: OBJECTIVE: To assess the mechanical and neurological processes active in the development of a cumulative trauma disorder (CTD) associated with repetitive exposure to periods of static lumbar flexion. METHODS: The spine of the feline model was subjected to a series of three 10 min sessions of static lumbar flexion with each session followed by a 10 min rest. A 7 h rest period was implemented after the series of three flexion-rest sessions while monitoring viscoelastic (disks, ligaments, etc.) creep and multifidus EMG. A model was fitted to the experimental data from the flexion-rest period and the 7 h recovery period. RESULTS: The creep developed in each 10 min static flexion period did not fully recovery during the following 10 min rest, resulting in a large cumulative creep at the end of the flexion-rest period. The cumulative creep did not fully recover over the following 7 h rest period. A neuromuscular disorder consisting of reduced muscular activity superimposed by spasms during static flexion periods and hyperexcitability during the 7 h recovery was evident. Comparison of the data to previous tests of continuous static flexion for 20 min reveal that the neuromuscular disorder elicited by the series of three 10 min flexion-rest was substantially attenuated when compared to a single 20 min static flexion although the overall work time was 50% larger. CONCLUSIONS: Frequent rest periods are highly beneficial in attenuating the development of a CTD, yet not able to prevent it, as viscoelastic tissues residual creep accumulates and its recovery is of extremely long duration. RELEVANCE: The data provides direct biomechanical and physiological evidence that explain the development of a CTD due to prolonged exposure to static lumbar flexion as well as confirms the epidemiological data correlating such work conditions with substantial increase in symptoms of low back disorders. The benefit of frequent rest periods in attenuating the risk of such a disorder is validated as an effective intervention.
Descriptors: back pain, cumulative trauma disorders, biomechanics, cats, elastic tissue, electromyogrphy, lumbar vertebrae.

Song, J.M., J.H. Kim, Y.H. Kim, S.W. Lee, Y.J. Yoon, J. Kim, D.H. Kang, and J.K. Song (2003). Temporal changes and histologic relation of postsystolic thickening in an animal model of acute ischemia and reperfusion. Journal of the American Society of Echocardiography 16(5): 409-14. ISSN: 0894-7317.
Abstract: BACKGROUND: We investigated the incidence and temporal changes of postsystolic thickening (PST) during myocardial ischemia and reperfusion to determine factors associated with PST. METHODS: The inferoposterior wall infarction was induced by coronary artery ligation (L) in 22 male cats. Epicardial echocardiographic examination including 2-dimensional, M-mode, and pulsed wave myocardial Doppler imaging of inferoposterior wall was performed at short-axis view before L, and regularly repeated during L until PST was not detected by myocardial Doppler image. Reperfusion (R) was done immediately after PST disappeared, and epicardial echocardiographic examination was repeated for 1 hour. Transmural extent of myocardial necrosis was morphometrically analyzed with triphenyltetrazolium chloride staining. RESULTS: PST measured by myocardial Doppler image was well correlated with that by M-mode (r = 0.63, P <.001). Immediately after L, all 22 cats showed akinesia in 2-dimensional imaging; among them PST was present in 13 cats (59%) and absent in the other 9 cats. The extent of ischemia by perimetric measurement with 2-dimensional imaging was smaller in cats with PST compared with those without (32 +/- 10% vs 47 +/- 5%, P <.001). In 13 cats with PST, the occlusion time until disappearance of PST (90-270 minutes, 160 +/- 70) and transmural extent of myocardial necrosis (0%-72%, 22 +/- 24) were quite variable. After R, PST promptly reappeared in all 13 cats. PST persisted until 1 hour after R in 5 cats, whereas it disappeared in 8 cats as systolic thickening became predominant; occlusion time was significantly longer (220 +/- 40 vs 120 +/- 40 minutes, P <.005) and transmural extent of myocardial necrosis was larger (43 +/- 17% vs 8 +/- 15%, P <.005) in cats with persistent PST until 1 hour after R. CONCLUSION: In acute ischemia and R, we observed variable patterns of PST genesis and maintenance, and different factors were related with these phenomena in each stage. PST could be used not only as a marker of acute ischemia but also as a marker of successful myocardial R, and further study is necessary to test whether PST represents different status of myocardial mechanics according to the extent of myocardial ischemia and necrosis in the clinical setting.
Descriptors: myocardial ischemia, myocardial reperfusion, myocardium, cats, animal disease models, heart, hemodynamic processes, myocardial ischemia, necrosis.

Sourvinos, G., C. Tsatsanis, and D.A. Spandidos (2000). Mechanisms of retrovirus-induced oncogenesis. Folia Biologica 46(6): 226-232. ISSN: 0015-5500.
NAL Call Number: 442.8 F712
Descriptors: molecular, feline retrovirus, infection, tumor biology, leukemia, and lymphatic disease, neoplastic disease, mammary tumor, neoplastic disease, reproductive system disease, female, skin cancer, integumentary system disease, neoplastic disease, insertional mutagenesis, retrovirus induced oncogenesis, mechanisms .

Staats, S., L. Pierfelice, C. Kim, and R. Crandell (1999). A theoretical model for human health and the pet connection. Journal of the American Veterinary Medical Association 214(4): 483-487. ISSN: 0003-1488.
NAL Call Number: 41.8 AM3
Descriptors: attitude to health, human pet bonding, health behavior, health status, adult, cats, dogs, factor analysis, likelihood functions, questionnaires.

Starr, R.M. (1998). Vaccine-associated feline sarcoma task force: a new model for problem solving in veterinary medicine. Journal of the American Veterinary Medical Association 213(10): 1428-1429. ISSN: 0003-1488.
NAL Call Number: 41.8 Am3
Descriptors: cats, vaccines, vaccination, sarcoma, side effects, medicine, advisory officers, america , immunization , immunostimulation , immunotherapy , neoplasms , north america, occupations , organic diseases, therapy , advisory committees.

Stein, R.D., S.B. Backman, B. Collier, and C. Polosa (1997). Bradycardia produced by pyridostigmine and physostigmine. Canadian Journal of Anaesthesia 44(12): 1286-1292. ISSN: 0832-610X.
Abstract: PURPOSE: The bradycardia produced by pyridostigmine and physostigmine in an animal model of acute cardiac denervation was examined according to its relation to cholinesterase inhibition and sensitivity to block by cholinergic receptor antagonists. METHODS: Cats were anaesthetised, vagotomised and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. Nicotinic and muscarinic M1 receptors were blocked with hexamethonium and pirenzepine, respectively. M2 receptors were blocked with gallamine, pancuronium and AFDX-116. RESULTS: With pyridostigmine and physostigmine the dose-response relationship for the decrease in heart rate (ED50 1.05 +/- 0.25 and 0.198 +/- 0.03 mg.kg-1, respectively) was shifted to the right of that for the inhibition of cholinesterase activity (ED50 0.094 +/- 0.03 and 0.032 +/- 0.01 mg.kg-1, respectively). The decrease in cholinesterase activity reached a plateau at a cumulative dose of 0.56 +/- 0.08 and 0.32 +/- 0.08 mg.kg-1, respectively. In contrast, there did not appear to be a plateau in the bradycardic effect. The bradycardia produced by pyridostigmine and physostigmine was blocked by hexamethonium (ED50 10 +/- 1.3 and 15.3 +/- 2.4 mg.kg-1, respectively), pirenzepine (ED50 68 +/- 16 and 138 +/- 32 micrograms.kg-1, respectively), gallamine (56 +/- 11 and 67 +/- 17 micrograms.kg-1, respectively), pancuronium (32 +/- 10 and 30 +/- 4 micrograms.kg-1, respectively), and AFDX-116 (31 +/- 4 and 28 +/- 4 micrograms.kg-1, respectively). CONCLUSION: The bradycardia produced by reversible anticholinesterase drugs containing a carbamyl group is not clearly related to the degree of cholinesterase activity, and has a low sensitivity to nicotinic and muscarinic M1 and a high sensitivity to muscarinic M2 receptor antagonists.
Descriptors: bradycardia, cholinesterase inhibitors toxicity, physostigmine toxicity, pyridostigmine bromide toxicity, bradycardia, cats, cholinesterases, drug-dose response relationship, electric stimulation, erythrocytes, erythrocytes, heart rate, muscarinic antagonists, nicotinic antagonists, vagotomy.

Steriade, M. and F. Amzica (2003). Sleep oscillations developing into seizures in corticothalamic systems. Epilepsia 44(12): 9-20. ISSN: 0013-9580.
Abstract: PURPOSE: The aim of this article is to discuss the neuronal substrates of sleep oscillations leading to seizures consisting of spike-wave (SW) complexes at 2-4 Hz, mimicking those seen in absence epilepsy, or SW and polyspike-wave (PSW) complexes at 1.5-2.5 Hz, often associated with fast runs at 10-15 Hz, as in the Lennox-Gastaut syndrome. METHODS: Extracellular recordings were done in permanently implanted animals during the natural waking-sleep cycle. Single and dual simultaneous recordings from cortical neurons, cortical and thalamic neurons, or cortical neurons and glial cells were performed in cats under ketamine-xylazine anesthesia. RESULTS: (a) The minimal substrate of SW seizures is the neocortex because such seizures may occur in thalamectomized animals, in which spindles are absent. In intact-brain animals, SW seizures are initiated in neocortex and spread to the thalamus after a few seconds. The majority of thalamocortical (TC) neurons are steadily hyperpolarized throughout the cortical SW seizures. (b) In the Lennox-Gastaut syndrome, the paroxysmal depolarizing shifts (PDSs) associated with the EEG "spike" of SW/PSW complexes contain an important inhibitory component, whereas the hyperpolarization during the EEG "wave" component is not due to gamma-aminobutryic acid (GABA)ergic inhibitory postsynaptic potentials (IPSPs) but is ascribed to a mixture of disfacilitation and K+ currents. As is also the case with seizures consisting of pure SW complexes, the majority of TC neurons are hyperpolarized during the cortical paroxysms and disinhibited after the cessation of cortical seizures. CONCLUSIONS: Seizures with SW complexes and of the Lennox-Gastaut type preferentially evolve from sleep oscillations. They are initiated in neocortex and spread to the thalamus after a few seconds. The majority of TC neurons are inhibited during these seizures.
Descriptors: cerebral cortex, seizures diagnosis, seizures, thalamus, cats, cerebral cortex, diagnosis, differential, electroencephalography, epilepsy, absence diagnosis, excitatory postsynaptic potentials, hippocampus, neural inhibition, neuroglia, neurons, seizures, sleep, thalamic nuclei, thalamic nuclei, thalamus, wakefulness, gamma aminobutyric acid.

Stetter, M., H. Bartsch, and K. Obermayer (2000). A mean-field model for orientation tuning, contrast saturation, and contextual effects in the primary visual cortex. Biological Cybernetics 82(4): 291-304. ISSN: 0340-1200.
Abstract: Orientation-selective cells in the primary visual cortex of monkeys and cats are often characterized by an orientation-tuning width that is invariant under stimulus contrast. At the same time their contrast response function saturates or even super-saturates for high values of contrast. When two bar stimuli are presented within their classical receptive field, the neuronal response decreases with the intersection angle. When two stimuli are presented inside and outside the classical receptive field, the response of the cell increases with the intersection angle. Both cats and monkeys show iso-orientation suppression, which has sometimes been reported to be combined with cross-orientation facilitation. This property has previously been described as sensitivity to orientation contrast. We address the emergence of these effects with a model that describes the processing of geniculocortical signals through cortical circuitry. We hypothesize that short intracortical fibers mediate the classical receptive field effects, whereas long-range collaterals evoke contextual effects such as sensitivity to orientation contrast. We model this situation by setting up a mean-field description of two neighboring cortical hypercolumns, which can process a nonoverlapping center and a (nonclassical) surround stimulus. Both hypercolumns interact via idealized long-range connections. For an isolated model hypercolumn, we find that either contrast saturation or contrast-invariant orientation tuning emerges, depending on the strength of the lateral excitation. There is no parameter regime, however, where both phenomena emerge simultaneously. In the regime where contrast saturation is found, the model also correctly reproduces suppression due to a second, cross-oriented grid within the classical receptive field. If two model hypercolumns are mutually coupled by long-range connections that are iso-orientation specific, nonclassical surround stimuli show either suppression or facilitation for all surround orientations. Sensitivity to orientation contrast is not observed. This property requires excitatory-to-excitatory long-range couplings that are less orientation specific than those targeting inhibitory neurons.
Descriptors: contrast sensitivity, models, neurological, neural networks computer, orientation, visual cortex, cats, computer simulation, haplorhini, photic stimulation.

Straubinger, R.K., A. Greiter, S.P. McDonough, A. Gerold, E. Scanziani, S. Soldati, D. Dailidiene, G. Dailide, D.E. Berg, and K.W. Simpson (2003). Quantitative evaluation of inflammatory and immune responses in the early stages of chronic Helicobacter pylori infection. Infection and Immunity 71(5): 2693-703. ISSN: 0019-9567.
NAL Call Number: QR1.I57
Abstract: The early consequences of Helicobacter pylori infection and the role of bacterial virulence determinants in disease outcome remain to be established. The present study sought to measure the development of host inflammatory and immune responses and their relationship to the putative bacterial virulence factors cag pathogenicity island (cagPAI), vacA allele, and oipA in combination with bacterial colonization density in a feline model of the early stages of H. pylori infection. Gastric tissues obtained from infected and uninfected cats were evaluated for H. pylori ureB, cagPAI, vacA allele, and oipA and colonization density (urease, histology, and real-time PCR). Inflammation was assessed by measuring mRNA upregulation of gamma interferon (IFN-gamma), interleukin (IL)-1 alpha, IL-1 beta, IL-4, IL-6, IL-8, IL-10, and IL-12 p40 and histopathology. The mucosal immune response was characterized by morphometric analysis of lymphoid follicles and by differentiating lymphocyte populations with antibodies against surface markers. Infecting H. pylori strains were positive for vacAs1 but lacked cagPAI and an active oipA gene. Colonization density was uniform throughout the stomach. Upregulation of IFN-gamma, IL-1 alpha, IL-1 beta, and IL-8 and increased severity of inflammatory infiltrates and fibrosis were observed in infected cats. The median number and total area of lymphoid aggregates were 5 and 10 times greater, respectively, in the stomachs of infected than uninfected cats. Secondary lymphoid follicles in uninfected cats were rare and positive for BLA.36 and B220 but negative for CD3 and CD79 alpha, whereas in infected cats they were frequent and positive for BLA.36, CD79 alpha, and CD3 but negative for B220. Upregulation of IFN-gamma, IL-1 alpha, IL-1 beta, and IL-8 and marked hyperplasia of secondary lymphoid follicles are early consequences of H. pylori infection in cats. The response appears to be similar to that of infected people, particularly children, can develop independently of the pathogenicity factors cagPAI and oipA, and is not correlated with the degree of colonization density or urease activity.
Descriptors: helicobacter infections, antigens, bacterial proteins analysis, cats, chronic disease, cytokines biosynthesis, cytokines, gastric mucosa, helicobacter infections, helicobacter pylori, helicobacter pylori pathogenicity, hyperplasia, immunopHenotyping, lymphocytes, polymerase chain reaction, RNA, messenger analysis, TH1 cells, TH2 cells.

Takauchi, Y., T. Yamazaki, and T. Akiyama (2000). Tyramine-induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats. Acta Physiologica Scandinavica 168(2): 287-93. ISSN: 0001-6772.
NAL Call Number: QP1.A2
Abstract: With the use of dialysis technique, the effects of tyramine on in situ cardiac sympathetic nerve endings were examined in anaesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and the concentration of dialysate noradrenaline (NA) served as an indicator of NA output at the cardiac sympathetic nerve ending. Locally applied tyramine (600 microM) increased dialysate NA levels from 17 +/- 1 (pg mL-1) to 3466 +/- 209 (pg mL-1). Pretreatment with reserpine (vesicle transport NA blocker 1 microM) did not affect tyramine-induced NA efflux. The tyramine-induced NA efflux was augmented by pretreatment with pargyline (1 mM) but suppressed by pargyline (10 mM). Pretreatment with alpha-methyl-tyrosine suppressed NA efflux evoked by tyramine. These pretreatments did not affect the time course of NA efflux but only altered peak height of NA efflux. The efflux of NA evoked by tyramine was not associated with any reduction of dihydroxyphenylglycol (DHPG). In contrast, in the pretreatment with reserpine, the efflux of NA was associated with a reduction of DHPG. This result suggests that NA graduation between axoplasm and stored vesicle contributes to maintaining the axoplasmic NA level during carrier-mediated outward NA transport. The tyramine-induced NA efflux provides a close reflection of the NA content at the nerve ending. With the use of dialysis, this experimental model is suitable for studying the mechanism of sympathomimetic amine-induced neurotransmitter efflux.
Descriptors: heart innervation, nerve endings, norepinephrine, sympathetic nervous system, tyramine, cats, chromatography, high pressure liquid, dialysis, electrochemistry, heart, kinetics, methoxyhydroxypHenylglycol, methoxyhydroxypHenylglycol, nerve endings, sympathetic nervous system.

Takeshima, R., J.R. Kirsch, R.C. Koehler, and R.J. Traystman (1994). Tirilazad treatment does not decrease early brain injury after transient focal ischemia in cats. Stroke 25(3): 670-6. ISSN: 0039-2499.
Abstract: BACKGROUND AND PURPOSE: We tested the hypothesis that administration of the antioxidant tirilazad mesylate improves electrophysiological recovery and decreases infarct volume after transient focal cerebral ischemia in cats. METHODS: Halothane-anesthetized cats underwent 90 minutes of left middle cerebral artery and bilateral common carotid artery occlusion followed by 180 minutes of reperfusion. Cats were assigned to receive tirilazad (1.5 mg/kg plus 0.2 mg/kg per hour IV infusion) either at the beginning (n = 9) or conclusion (n = 9) of ischemia. Control cats received an equal volume of diluent (citrate buffer, pH 3.0; n = 7) at the beginning and conclusion of ischemia in a blinded fashion. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining. RESULTS: Blood flow to the left temporoparietal cortex decreased to less than 10 mL/min per 100 g with ischemia but was minimally affected on the right side. Blood flow distribution during ischemia or reperfusion was not different in the tirilazad-treated groups. No group demonstrated postischemic hyperemia or delayed hypoperfusion. Somatosensory evoked potential recorded over the left cortex was ablated during ischemia and recovered to less than 15% of baseline amplitude at 180 minutes of reperfusion in all groups. There were no differences among groups in infarct volume of left hemisphere (pretreatment, 25 +/- 6% [mean +/- SE]; posttreatment, 33 +/- 5%; control, 28 +/- 8% of hemisphere) or caudate nucleus (pretreatment, 46 +/- 7%; posttreatment, 41 +/- 10%; control, 55 +/- 13% of hemisphere). CONCLUSIONS: In an experimental model of focal ischemia involving severe reductions of blood flow followed by reperfusion in cats, administration of tirilazad at the onset of either ischemia or reperfusion does not ameliorate infarct volume assessed during early reperfusion. Our study does not address potential efficacy of tirilazad in the setting of a different dosing strategy or duration of reperfusion.
Descriptors: ischemic attack, transient, lipid peroxidation, pregnatrienes, analysis of variance, carotid arteries surgery, cats, cerebrovascular circulation, ischemic attack, transient, ligation, random allocation, time factors.

Tamura, K., Y. Kuge, Y. Miyake, and N. Hashimoto (1999). Application of pet to verification of animal models of human disease and drug evaluation. Japanese Journal of Pharmacology 79(SUPPL. 1): 26P. ISSN: 0021-5198.
Descriptors: nervous system, neural coordination, cerebral infarction, nervous system disease, vascular disease, ischemia, middle cerebral artery occlusion, nervous system disease, positron emission tomography, high resolution imaging method, regional cerebral flow.

Tanase, D., H.A. Baghdoyan, and R. Lydic (2001). Microinjection of an adenosine a1 agonist into feline medial pontine reticular formation (mprf) increases tail flick latency (tfl) to thermal stimulation. Society for Neuroscience Abstracts 27(1): 1376. ISSN: 0190-5295.
NAL Call Number: QP351. S6
Descriptors: behavior, nervous system, thermal stimulation, stimulation method, supraspinal nociceptive behavior: modulation , tail flick latency, adenosine A1 receptor agonist, feline pontine regions , tail flick latency.

Teppema, L., E. Sarton, A. Dahan, and C.N. Olievier (2000). The neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI) and morphine act independently on the control of breathing. British Journal of Anaesthesia 84(2): 190-6. ISSN: 0007-0912.
Abstract: Inhibitors of nitric oxide synthase (NOS) have analgesic properties and reduce opioid tolerance and dependency. To investigate a possible interaction of NOS inhibitors with the respiratory depressant action of morphine, we determined the effects of the neuronal NOS inhibitor 7-nitroindazole (7-NI) on the ventilatory carbon dioxide response curve; subsequently, we studied the effects of additional morphine application. Finally, using naloxone, we investigated a possible interaction (at the opioid receptor) between the effects of 7-NI and morphine. The effects of 7-NI 50 mg kg-1 i.p., morphine 0.1 mg kg-1 i.v. and naloxone 0.1 mg kg-1 i.v. were studied using dynamic end-tidal carbon dioxide forcing in eight cats under alpha-choralose-urethane anaesthesia. Data analysis was performed using a two-compartment model comprising a fast peripheral and a slow central component characterized by carbon dioxide sensitivities and a single offset B (apnoeic threshold). 7-NI decreased the mean apnoeic threshold from 4.27 (SD 0.87) to 2.59 (1.71) kPa. Peripheral and central carbon dioxide sensitivities were reduced from 0.56 (0.22) to 0.26 (0.09) litre min-1 kPa-1 and from 0.09 (0.05) to 0.04 (0.03) litre min-1 kPa-1, respectively. Morphine increased the apnoeic threshold by 0.5 kPa and reduced carbon dioxide sensitivity by a further 35%. Naloxone reversed the ventilatory effects of morphine but not those induced by 7-NI. We conclude that the respiratory effects of 7-NI and morphine are mediated independently and that the effects of 7-NI do not result from interaction with opioid receptors.
Descriptors: analgesics, enzyme inhibitors, indazoles, morphine, nitric oxide synthase, respiration, analgesics, carbon dioxide, cats, drug interactions.

Thompson, J.T., M.S. Rackley, and T.X. O'brien (1998). Upregulation of the cardiac homeobox gene Nkx2-5 (CSX) in feline right ventricular pressure overload. American Journal of Physiology 274(5 PART 2): H1569-H1573. ISSN: 0002-9513.
NAL Call Number: 447.8 Am3
Descriptors: cardiac hypertropHy, heart disease, ventricular hypertropHy, right ventricular pressure overload, feline pulmonary artery banding model, alpha cardiac actin.

Tomita, H., U. Ito, K. Ohno, and K. Hirakawa (1994). Chronological changes in brain edema induced by experimental intracerebral hematoma in cats. Acta Neurochirurgica/ Supplementum 60: 558-60. ISSN: 0065-1419.
Abstract: To investigate the temporary profile of changing perifocal brain edema around an intracerebral hematoma (ICH), we developed an experimental ICH model using cats. The developing perifocal edema in the white matter around the hematoma was measured by means of a gravimetric technique. Edema was more severe near the ICH, and declined with increasing distance. Edema was mild 2 hours after the onset of the ICH, and was most severe in all the regions examined 3 days later. Edema decreased but still existed in all regions 7 days after the onset of the ICH. The results suggest that the mechanism of the development of edema associated with ICH seems to differ from that associated with a cold injury. This experimental ICH model proved to be useful for the study of formation, expansion, and resolution of edema associated with ICH.
Descriptors: brain edema, cerebral hemorrhage, brain barrier, cats, cerebral cortex, evans blue diagnostic use, specific gravity.

Topolnik, L., M. Steriade, and I. Timofeev (2003). Hyperexcitability of intact neurons underlies acute development of trauma-related electrographic seizures in cats in vivo. The European Journal of Neuroscience 18(3): 486-96. ISSN: 0953-816X.
Abstract: Cortical trauma can lead to development of electrographic paroxysmal activities. Current views of trauma-induced epileptogenesis suggest that chronic neuronal hyperexcitability and extensive morphological reorganization of the traumatized cortex are required for the generation of electrographic seizures. However, the mechanisms responsible for the initiation of electrographic seizures shortly after cortical injury are poorly understood. Here we show that, in the experimental model of partially deafferented (undercut) cortex, an increase in intrinsic and synaptic excitability of neurons in areas adjacent to the undercut cortex is sufficient for the generation of electrographic paroxysmal activity within few hours after partial cortical deafferentation. Locally increased and spatially restricted neuronal excitability arose from the increased incidence of intrinsically bursting neurons, enhanced intrinsic and synaptic neuronal responsiveness, and slight disinhibition. These mechanisms only operate in neurons located in the vicinity of partially deafferented sites because, after the cortical injury, partially deafferented neurons are mostly silent and hypoexcitable. Our results suggest that trauma-induced electrographic seizures first arise in cortical fields that are closest to the site of injury and such seizures do not require long-term neuronal reorganization.
Descriptors: brain injuries, cerebral cortex injuries, epilepsy, neurons, cats, denervation, electroencephalography, electrophysiology, epilepsy, neural inhibition, synapses.

Torterolo, P., J. Yamuy, S. Sampogna, F.R. Morales, and M.H. Chase (2003). Hypocretinergic neurons are primarily involved in activation of the somatomotor system. Sleep 26(1): 25-8. ISSN: 0161-8105.
Abstract: The hypocretinergic system has been implicated in the generation and/or maintenance of wakefulness. Our results challenge this hypothesis. Utilizing cats as an animal model and immunocytochemical procedures for the simultaneous detection of hypocretin and Fos, we determined that hypocretinergic neurons are activated during wakefulness but only when somatomotor activity is present. These neurons are not activated during alert or quiet wakefulness in the absence of motor activity or during quiet sleep. We conclude that the hypocretinergic system is not responsible for the generation and/or maintenance of wakefulness, per se; on the contrary, we suggest that hypocretinergic neurons are primarily involved in motor functions irrespective of the animal's behavioral state.
Descriptors: carrier proteins, intracellular signaling peptides and proteins, locomotion, neurons, neuropeptides, wakefulness, cats, electroencephalography, electromyogrphy, electrooculography, hypothalamus, sleep, rem.

Toyota, S., R. Graf, C. Dohmen, M. Valentino, M. Grond, K. Wienhard, and W.D. Heiss (2001). Elevation of extracellular glutamate in the final, ischemic stage of progressive epidural mass lesion in cats. Journal of Neurotrauma 18(12): 1349-57. ISSN: 0897-7151.
Abstract: Epidural mass lesions may cause ischemia due to progressive intracranial hypertension. In order to investigate the impact of intracranial pressure on accumulation of neuroactive substances, we gradually raised intracranial pressure in five halothane anesthetized cats by inflation of an epidural balloon. We evaluated in the parietal cortex contralateral to the site of balloon inflation, alterations of extracellular glutamate and purine catabolites and of the lactate/pyruvate ratio in relation to changes of intracranial, cerebral perfusion and mean arterial blood pressure. In a complementary experiment, regional cerebral blood flow was assessed by sequential positron emission tomography. In this simplified mass lesion model, extracellular glutamate increased in all cats at a late, critical stage after tentorial herniation, when intracranial pressure had increased to more than 90 mm Hg, cerebral perfusion pressure had decreased below 40-50 mm Hg. Positron emission tomography assessments revealed that the ischemic threshold for glutamate accumulation was in the range of 15-20 mL/100 g/min. Purine catabolites and the lactate/pyruvate ratio increased somewhat earlier than glutamate, but also after reaching the critical, terminal stage. We conclude that in this model of progressive epidural compression, glutamate-mediated excitotoxic processes at sites remote from the initial focal lesion depend on processes such as delayed ischemia in combination with tentorial herniation and systemic hypotension. These processes seem to be initiated by a decrease of cerebral perfusion pressure below a threshold of 40-50 mm Hg.
Descriptors: brain ischemia, epidural space, extracellular space, glutamic acid biosynthesis, intracranial hypertension, brain ischemia radiography, cats, epidural space, extracellular space radiography, intracranial hypertension radiography, parietal lobe supply, parietal lobe, parietal lobe radiography, tomography, emission computed statistics and numerical data.

Toyota, S., R. Graf, M. Valentino, T. Yoshimine, and W.D. Heiss (2002). Malignant infarction in cats after prolonged middle cerebral artery occlusion: glutamate elevation related to decrease of cerebral perfusion pressure. Stroke 33(5): 1383-91. ISSN: 0039-2499.
Abstract: BACKGROUND AND PURPOSE: To study the putative role and predictive significance of glutamate elevation in space-occupying ischemic stroke, we investigated the correlation between perfusional disturbances and glutamate alterations in a transient ischemia model in cats that is susceptible to secondary deterioration after reperfusion. METHODS: In 10 halothane-anesthetized cats, the left middle cerebral artery was occluded for 3 hours, followed by 6 hours of reperfusion. Laser-Doppler flowmetry (LDF) probes, microdialysis/high-performance liquid chromatography, and pressure sensors measured simultaneously regional cerebral blood flow (CBF), extracellular amino acids, mean arterial blood pressure, and intracranial pressure, respectively. Cerebral perfusion pressure (CPP) was calculated. In complementary experiments (n=2), regional CBF was assessed by sequential positron emission tomography. RESULTS: Middle cerebral artery occlusion reduced LDF-measured CBF in all animals to <25% of control. In 5 of 10 cats, glutamate rose approximately 30-fold during ischemia. LDF-measured CBF and glutamate primarily recovered after reperfusion. Glutamate rose again in the late reperfusion phase, when CPP decreased to <60 mm Hg, and symptoms of transtentorial herniation were recognized. Positron emission tomography revealed ischemic thresholds of 15 to 20 mL/100 g per minute for secondary deterioration. In the other 5 cats, ischemic elevation of glutamate was significantly smaller, and signs of secondary deterioration were not recognized. CONCLUSIONS: Glutamate determinations during ischemia predict fatal outcome, as do intracranial pressure and CPP measurements during early reperfusion. Secondary amino acid elevation during reperfusion is presumably caused by a drastic decrease of CPP to <50 mm Hg in the final stage of space-occupying, malignant focal ischemia. At this stage, a further progression of injury due to increased glutamate may be irrelevant with respect to fatal outcome.
Descriptors: blood pressure, brain, glutamic acid, flow velocity, brain supply, brain radionuclide imaging, brain edema, brain edema radionuclide imaging, cats, cerebral infarction, cerebral infarction radionuclide imaging, cerebrovascular circulation, animal disease models, disease progression, infarction, middle cerebral artery radionuclide imaging, intracranial pressure, laser doppler flowmetry, microdialysis, predictive value of tests, tomography, emission computed.

Trerotola, S.O., M.S. Johnson, and D.S. Schauwecker (1997). Like cats and dogs: no perfect animal model for thrombolysis. Radiology 202(1): 31-2. ISSN: 1527-1315.
Descriptors: animal disease models, thrombolytic therapy, thrombolytic therapy, thrombosis, cats, dogs, pulmonary embolism.

Trigo, J.A., L. Roa, A. Gruart, and J.M. Delgado Garcia (2003). A kinetic study of blinking responses in cats. The Journal of Physiology 549(Pt 1): 195-205. ISSN: 0022-3751.
NAL Call Number: 447.8 J82
Abstract: Reflexively evoked and eye-related eyelid responses were recorded using the search coil in a magnetic field technique in alert cats. The downward phase of a blink was a large (up to 21 deg), fast (up to 2000 deg s-1) eyelid displacement in the closing direction, with an almost fixed rise time duration (15-20 ms); its maximum velocity was achieved in ~10 ms. Upward eyelid motion was separated into two phases. The first phase consisted of a fast eyelid displacement, with a short duration (approximately 30 ms) and a maximum velocity up to 900 deg s-1. The second phase had an exponential-like form, lasting for 200-400 ms, and a maximum velocity ranging between 30 and 250 deg s-1. Maximum blink velocity in the downward direction was linearly related to maximum velocity of the first upward phase. The first phase in the upward direction was never observed if the eyelid stayed closed for a long period (> 50 ms) or moved slowly in the closing direction before it started to open. In these two cases, the upswing motion of the blink reflex contained only the exponential-like movement characteristic of the second upward phase, and maximum velocity in the downward direction was not related to that of the eyelid upward displacement. Mean duration of eyelid downward saccades was approximately 130 ms, and their peak velocities ranged between 50 and 440 ms. A physiological model is presented explaining the active and passive forces involved in both reflex and saccadic eyelid responses. A second-order system seems to be appropriate to describe the postulated biomechanical model.
Descriptors: blinking, eyelids, biological models, movement, air, biomechanics, cats, kinetics, magnetics, saccades.

Tsagarakis, C., T. Marchal, J.P. Magnol, C. Fournel, C. Dezutter Dambuyant, and D. Schmitt (1994). Contribution des cellules de Langerhans felines au modele du FIV feline immunodeficiency virus [Contribution of the feline Langerhans cell to the FIV model ,feline immunodeficiency virus.]. Research in Virology 145(3-4): 245-249. ISSN: 7112-2923.
Descriptors: cats, animal viruses, immunosuppression, cells, skin, mucous membrane, antigens, animal morphology, animal tissues, disease control, epithelium , immunological factors, immunotherapy , integument , therapy .

Tsorin, I.B. and G.G. Chichkanov (2004). [O protivoishemicheskom i antiaritmicheskom deistvii preperata ezafosfina] Antiischemic and antiarrhythmic effect of esafosfina. Eksperimental'Naia I Klinicheskaia Farmakologiia 67(4): 16-8. ISSN: 0869-2092.
Abstract: Esafosfina, a new preparation based on fructose 1,6-diphosphate, supported the pumping ability of the heart in experiments with a 40-min occlusion followed by 60-min reperfusion of the anterior descending branch of the left coronary artery in anesthetized cats. Esafosfina also exhibited a pronounced antifibrillatory and antiarrhythmic action in anesthetized rats with ventricular fibrillation model.
Descriptors: anti arrhythmia agents, cardiotonic agents, fructosediphosphates, myocardial reperfusion injury, ventricular fibrillation, cats, heart, heart rate, rats.
Language of Text: Russian.

Tsutsui, H., H. Tagawa, R.L. Kent, P.L. McCollam, K. Ishihara, M. Nagatsu, and G.4. Cooper (1994). Role of microtubules in contractile dysfunction of hypertrophied cardiocytes. Circulation 90(1): 533-55. ISSN: 0009-7322.
NAL Call Number: RC681 .A1C8
Abstract: Cardiac hypertrophy in response to systolic pressure overloading frequently results in contractile dysfunction, the cause for which has been unknown. Since, in contrast, the same degree and duration of hypertrophy in response to systolic volume overloading does not result in contractile dysfunction, we postulated that the contractile dysfunction of pressure hypertrophied myocardium might result from a direct effect of stress as opposed to strain loading on an intracellular structure of the hypertrophied cardiocyte. The specific hypothesis tested here is that the microtubule component of the cytoskeleton is such an intracellular structure, which, forming in excess, impedes sarcomere motion. The feline right ventricle was either pressure overloaded by pulmonary artery banding or volume overloaded by atrial septotomy. The quantity of microtubules was estimated from immunoblots and immunofluorescent micrographs, and their mechanical effects were assessed by measuring sarcomere motion during microtubule depolymerization. We show here that stress loading increases the microtubule component of the cardiac muscle cell cytoskeleton; this apparently is responsible for the entirety of the cellular contractile dysfunction seen in our model of pressure-hypertrophied myocardium. No such effects were seen in right ventricular cardiocytes from normal or volume-overloaded cats or in left ventricular cardiocytes from any group of cats. Importantly, the linked microtubule and contractile abnormalities are persistent and thus may be found to have significance for the deterioration of initially compensatory cardiac hypertrophy into the congestive heart failure state.
Descriptors: cardiomegaly, cardiomegaly, microtubules, myocardial contraction, cats, cytoskeleton, heart, motion, myocardium, sarcomeres, tubulin.

Turner, A.S. (2001). Animal models of osteoporosis--necessity and limitations. European Cells and Materials 1: 66-81. ISSN: 1473-2262.
NAL Call Number: R857.M3E97
Abstract: There is a great need to further characterise the available animal models for postmenopausal osteoporosis, for the understanding of the pathogenesis of the disease, investigation of new therapies (e.g. selective estrogen receptor modulators (SERMs)) and evaluation of prosthetic devices in osteoporotic bone. Animal models that have been used in the past include non-human primates, dogs, cats, rodents, rabbits, guinea pigs and minipigs, all of which have advantages and disadvantages. Sheep are a promising model for various reasons: they are docile, easy to handle and house, relatively inexpensive, available in large numbers, spontaneously ovulate, and the sheep's bones are large enough to evaluate orthopaedic implants. Most animal models have used females and osteoporosis in the male has been largely ignored. Recently, interest in development of appropriate prosthetic devices which would stimulate osseointegration into osteoporotic, appendicular, axial and mandibular bone has intensified. Augmentation of osteopenic lumbar vertebrae with bioactive ceramics (vertebroplasty) is another area that will require testing in the appropriate animal model. Using experimental animal models for the study of these different facets of osteoporosis minimizes some of the difficulties associated with studying the disease in humans, namely time and behavioral variability among test subjects. New experimental drug therapies and orthopaedic implants can potentially be tested on large numbers of animals subjected to a level of experimental control impossible in human clinical research.
Descriptors: cats, animals, osteoporosis models, postmenopausal, therapies, lumbar vertebrate, SERMs .

Uchiyama, T., H. Johansson, and U. Windhorst (2003). A model of the feline medial gastrocnemius motoneuron-muscle system subjected to recurrent inhibition. Biological Cybernetics 89(2): 139-51. ISSN: 0340-1200.
Abstract: Recurrent inhibition in the mammalian spinal cord is complex, and its functions are not yet well understood. Skeletomotoneurons (alpha-MNs) excite, via recurrent axon collaterals, inhibitory Renshaw cells (RCs), which in turn inhibit alpha-MNs and other neurons. The anatomical and functional structure of the recurrent inhibitory network is nonhomogeneous, and the gain and filtering characteristics of RCs are modulated by inputs circumventing alpha-MNs. This complex organization is likely to play important roles for the discharge and recruitment properties of alpha-MNs. Modeling this system is a way of investigating hypothesized roles for normal functioning including muscle fatigue and different forms of physiological pathological tremor. In this paper, a detailed model including alpha-MNs, RCs, and the muscle fibers innervated by the alpha-MNs is presented. Outlines of the experimental data underlying the model and the modeling philosophy and procedure are presented. Then the behavior of a RC model is compared with experimental data reported in the literature. Model and experimental data agree well for burst responses elicited by synchronous single-pulse activation of different numbers of motor axons. In addition, the static relation between motor-axon activation rate and RC firing rate agree fairly well in model and experiment, and the same applies to the dynamic responses to step changes in motor-axon rate. The ultimate objective is to use this model in probing the role of recurrent inhibition in the control and stability of (isometric) muscular force under normal and altered conditions occurring during fatigue and muscle pain.
Descriptors: interneurons, models, neurological, motor neurons, muscle, skeletal, neural inhibition, recruitment neurology, biofeedback psychology, cats, electric stimulation, membrane potentials, muscle contraction, numerical analysis, computer assisted, reaction time, time factors.

Ulman, L.G., E.K. Potter, and D.I. McCloskey (1994). Functional effects of a family of galanin antagonists on the cardiovascular system in anaesthetised cats. Regulatory Peptides 51(1): 17-23. ISSN: 0167-0115.
NAL Call Number: QP552 .P4
Abstract: Previous studies have shown that injection of galanin (GAL: 6.2 nmol/kg) causes prolonged inhibition of cardiac vagal action in anaesthetised cats. Stimulation of the cardiac sympathetic nerve (16 Hz for 5 min) also produces inhibition of cardiac vagal action, an effect which has been proposed to be due to the release of endogenous GAL from sympathetic nerves. In a previous study we tested galantide (M15) and in this study we compared galantide with two other GAL antagonists for their GAL antagonist activity in our experimental model. Each of these incorporate the N-terminal fragment GAL 1-13 and a C-terminal portion of another bioactive peptide and all are C-terminally amidated. GAL 1-13 Substance P 5-11 amide (galantide: M15: 62 nmol/kg and 156 nmol/kg), GAL 1-13 Spantide amide (C7: 156 nmol/kg) and GAL 1-13 NPY 24-36 amide (M32a: 62 nmol/kg) all significantly reduced the cardiac vagal inhibitory effect of exogenous GAL and also reduced the effect of sympathetic stimulation on subsequent cardiac vagal slowing, giving strong support to our hypothesis that GAL is involved in this phenomenon. No antagonist reduced the depressor effect of GAL. This study demonstrates the GAL antagonist properties of these agents on autonomic neuroeffector functions making them useful tools in elucidating further functions of endogenous GAL.
Descriptors: heart conduction system, neuropeptides, peptide fragments, peptides, peptides, substance p, analysis of variance, aortic bodies, pressure, cats, electric stimulation, galanin, heart innervation, substance p, sympathetic nervous system, vagus nerve, vagus nerve.

Usta, M.F., J. Sanabria, T.J. Bivalacqua, and W.J. Hellstrom (2004). Feline penile erection induced by topical glans penis application of combination alprostadil and SEPA (Topiglan). International Journal of Impotence Research 16(1): 73-7. ISSN: 0955-9930.
Abstract: The objective of this study was to evaluate the efficacy of topically applied prostaglandin E1 (PGE(1))+5% SEPA (soft enhancement of percutaneous absorption) on the glans penis in a feline erection model. Erectile response after glans penis administration of PGE(1)+5% SEPA cream (Topiglan, MacroChem Co., Lexington, MA, USA) was compared to the erectile response after intracavernosal administration of the triple-drug combination (1.65 mg papaverine, 25 microg phentolamine, and 0.5 microg PGE(1)). The placebo cream and increasing concentrations (0.25%, 2.5 mg/ml; 0.5%, 5 mg/ml; and 1%, 10 mg/ml) of PGE(1)+5% SEPA were applied in a total volume of 0.1 ml via a plastic needle-less syringe. The control triple-drug combination was administrated intracavernosally via a 30-gauge needle at the completion of each experiment to serve as a control reference. With each application of placebo, PGE(1)+SEPA, and the triple-drug combination, changes in intracavernosal pressure and systemic blood pressure were continuously monitored. Topical application of PGE(1)+SEPA induced increases in intracavernosal pressure in a dose-dependent manner, with minimal effects on systemic blood pressure. The increases obtained with 1% PGE(1) Topiglan cream were similar to the intracavernosal pressure values elicited by the standard intracavernosal triple-drug combination. These data demonstrate that topical glans penis application of PGE(1)+SEPA can induce an erectile response in cats with minimal systemic adverse effects. Oral pharmacological agents are the first-line treatment for male ED. Studies investigating the effectiveness of noninvasive modalities such as topical therapy should continue, because these agents have the potential to avoid the systemic effects commonly seen with oral therapies. Additionally, topical therapy may also benefit patients who are unresponsive to oral agents or have explicit contraindications. Topical PGE(1) application to the glans penis may become an important treatment option in selected patients suffering from erectile dysfunction.
Descriptors: adjuvants, pHarmaceutic, alprostadil, dioxolanes, penile erection, vasodilator agents, topical administration, pressure, cats, gels, models, animal, muscle, smooth.

Vahlenkamp, T.W., M.E. Bull, J.L. Dow, E.W. Collisson, B.J. Winslow, A.P. Phadke, W.A.F. Tompkins, and M.B. Tompkins (2004). B7+CTLA4+ T cells engage in T-T cell interactions that mediate apoptosis: a model for lentivirus-induced T cell depletion. Veterinary Immunology and Immunopathology 98(3/4): 203-214. ISSN: 0165-2427.
NAL Call Number: SF757.2. V38
Descriptors: apoptosis, disease models, immune response, lymph nodes, T lymphocytes, cats, feline immunodeficiency virus, Lentivirus.

van Gelderen, P., M.H. de Vleeschouwer, D. DesPres, J. Pekar, P.C. van Zijl, and C.T. Moonen (1994). Water diffusion and acute stroke. Magnetic Resonance in Medicine 31(2): 154-163. ISSN: 0740-3194.
Abstract: The occlusion of the middle cerebral artery was used as an experimental acute stroke model in 30 cats. The diffusion of water was followed by diffusion-sensitized MRI between 1 and 15 h after induction of stroke. It is demonstrated that images representing the trace of the diffusion tensor provide a much more accurate delineation of affected area than images representing the diffusion in one direction only. The reason is that the strong contrast caused by the anisotropy and orientation of myelin fibers is completely removed in the trace of the diffusion tensor. The trace images show a small contrast between white and gray matter. The diffusion coefficient of white matter is decreased in acute stroke to approximately the same extent as gray matter. It is further shown that the average lifetime of water in extra and intracellular space is shorter than 20 ms both for healthy and ischemic tissue indicating that myelin fibers are permeable to water. The anisotropy contrast did not change before or after induction of stroke, nor after sacrifice. Together, these observations are consistent with the view that the changes in water diffusion during acute stroke are directly related to cytotoxic oedema, i.e., to the change in relative volume of intra- and extracellular spaces. Changes in membrane permeability do not appear to contribute significantly to the changes in diffusion.
Descriptors: body water, cerebrovascular disorders, acute disease, brain edema, brain ischemia, cats, cerebral infarction, diffusion, extracellular space, intracellular fluid, magnetic resonance imaging, magnetic resonance spectroscopy, biological models, myelin sheath, permeability.

Vanzetta, I., R. Hildesheim, and A. Grinvald (2005). Compartment-resolved imaging of activity-dependent dynamics of cortical blood volume and oximetry. The Journal of Neuroscience 25(9): 2233-44. ISSN: 0270-6474.
Abstract: Optical imaging, positron emission tomography, and functional magnetic resonance imaging (fMRI) all rely on vascular responses to image neuronal activity. Although these imaging techniques are used successfully for functional brain mapping, the detailed spatiotemporal dynamics of hemodynamic events in the various microvascular compartments have remained unknown. Here we used high-resolution optical imaging in area 18 of anesthetized cats to selectively explore sensory-evoked cerebral blood-volume (CBV) changes in the various cortical microvascular compartments. To avoid the confounding effects of hematocrit and oximetry changes, we developed and used a new fluorescent blood plasma tracer and combined these measurements with optical imaging of intrinsic signals at a near-isosbestic wavelength for hemoglobin (565 nm). The vascular response began at the arteriolar level, rapidly spreading toward capillaries and venules. Larger veins lagged behind. Capillaries exhibited clear blood-volume changes. Arterioles and arteries had the largest response, whereas the venous response was smallest. Information about compartment-specific oxygen tension dynamics was obtained in imaging sessions using 605 nm illumination, a wavelength known to reflect primarily oximetric changes, thus being more directly related to electrical activity than CBV changes. Those images were radically different: the response began at the parenchyma level, followed only later by the other microvascular compartments. These results have implications for the modeling of fMRI responses (e.g., the balloon model). Furthermore, functional maps obtained by imaging the capillary CBV response were similar but not identical to those obtained using the early oximetric signal, suggesting the presence of different regulatory mechanisms underlying these two hemodynamic processes.
Descriptors: cortical blood, cats, PET, fMRI, brain, cerebral blood volume.

Villablanca, J.R. and D.A. Hovda (2000). Developmental neuroplasticity in a model of cerebral hemispherectomy and stroke. Neuroscience 95(3): 625-37. ISSN: 1471-2202.
Abstract: Cerebral hemispherectomy, a last resort treatment for childhood epilepsy, is a standard procedure which dramatically illustrates the resilience of the brain to extensive damage. If this operation, also mimicking long-term, extensive unilateral capsular stroke, is performed in postnatal cats of up to 60 days of age, there is a remarkable recovery/sparing of neurological functions that is not seen when the lesion occurs during late fetal life or in adulthood. A long-term effect at all ages is loss of neurons in bilateral brain areas remote from the resection site. This is pronounced in adult cats and shows intriguing, paradoxical features in fetal animals, but is substantially attenuated in neonatal cats. Similarly, large-scale reinnervation of subcortical sites (sprouting) by neurons of the remaining, intact hemisphere is prominent in young cats, but not in fetal or adult animals. These and other restorative processes (described herein) in young postnatal animals are matched by relatively higher rates of local cerebral glucose utilization, supporting the notion that they underlie the improved behavioral outcome. Thus, during a critical, defined stage of maturation, presumably common to higher mammals including humans, the brain entirely remodels itself in response to extensive but focal injury. Perhaps the molecular environment allowing for rescue of neurons and enhanced reinnervation at a specific developmental stage could be recreated in subjects with brain lesions at less favorable ages, thereby helping to restore circuitry and spare neurons. However, replacement via transplantation of neurons eliminated by the damage appears to be crucial in attempts to further preserve cells located remotely but yet destined to die or decrease in size. This article presents abundant evidence to show that there is a surprisingly comprehensive long-term morphological remodeling of the entire brain after extensive unilateral damage and that this occurs preferentially during a discrete period of early life. Additional evidence strongly suggests that the remodeling underlies the outstanding behavioral and functional recovery/sparing following early cerebral hemispherectomy. We argue that this period of reduced brain vulnerability to injury also exists in other higher mammals, including man, and suggest ways to enhance restorative processes after stroke/hemispherectomy occurring at other ages.
Descriptors: animals, newborn, brain surgery, cerebrovascular accident, neuronal plasticity, aging, brain embryology, brain, fetus, postoperative period.

Villablanca, J.R., T.D. Schmanke, H.A. Crutcher, A.C. Sung, and K. Tavabi (2000). The growth of the feline brain from fetal into adult life. II. A morphometric study of subcortical nuclei. Brain Research/ Developmental Brain Research 122(1): 21-33. ISSN: 0006-8993.
Abstract: As a continuation of the morphometric studies on the preceding paper, here we report on the rate of growth of the caudate nucleus (n.), thalamus, red n., and the substantia (s.) nigra using, with few exceptions, the same cohort of cats. The same previously used brains (n=64 cats) were allocated to the following age groups: fetal (E) 59 days, postnatal (P) days 1, 7, 15, 30, 45, 60, 90, 120, and 180. Sixteen additional cats, interspersed within the groups, were substituted for the red n. and s. nigra studies. There were six subjects per group (except for E59, n=4). Using a projection microscope and cytochrome oxidase-stained coronal sections, a combined (left plus right sides) total of 4693, 3822, 1636, and 1180 sections were drawn for the caudate, thalamus, s. nigra, and red n., respectively. With computer assistance, the drawings were digitized to calculate mean cross-sectional areas and then the mean volume of each structure per group. The growth time tables for the caudate n., thalamus and s. nigra were fairly synchronous. In terms of percentage of the adult volume, for the left side (both sides grew at a similar rate), the three structures grew at a fast pace between E59 and P30. Thus, at E59 their respective percentages relative to adult volume were 23.7, 29.8 and 22.6% and by P30 the percentages were within adult range (85.2, 115.1 and 87.5%, respectively). Starting at P30, for the thalamus and at P45 for the caudate n., there was a consistent tendency to an overgrow which ranged between 4.3 and 30.9% (at P180, P<0.5) for the caudate and between 0.3 and 15.1% for the thalamus. In addition, starting at P30, the right thalamus tended to be consistently larger than the left by a margin ranging between 0.5 and 11.2% (P120, P<0.05). The red n. grew at a different, slower pace. Starting from a fetal volume equivalent to an 18.6% of adult size, its volume was only a 61.0% of the adult value at P30 and came within range of adulthood size only by P60 (81. 3%). Neither the s. nigra nor the red n. showed any consistent tendency to overgrow or to asymmetry. These findings are discussed in the context of the literature. Furthermore, we discuss general conclusions and considerations pertaining to both papers as well as draw comparisons with the maturational time tables of other developmental landmarks in cats. Finally, in a comparison with growth of human brain structures, we point at the limitations and complexities involved in studying human material and, noting interspecies similarities, we propose that the present data from an advanced gyrencephalic mammal may form the bases for a model of structures maturation in humans.
Descriptors: caudate nucleus growth and development, red nucleus growth and development, substantia nigra growth and development, thalamus growth and development, cats, caudate nucleus, caudate nucleus embryology, laterality, organ size, red nucleus, red nucleus embryology, substantia nigra, substantia nigra embryology, thalamus, thalamus embryology.

Volkov, V.F., A.F. Meshcheriakov, and I.A. Fadeev (1994). Eksperimental'naia model' formirovaniia vlecheniia k priemu narkotikov u koshek na osnove pishchevoi motivatsii. [An experimental model of developing a desire for using narcotics in cats based on a food motivation]. Biulleten' Eksperimental'Noi Biologii i Meditsiny 118(8): 156-60. ISSN: 0365-9615.
NAL Call Number: 442.8 B87
Descriptors: cocaine, feeding behavior, motivation, substance related disorders, cats.
Language of Text: Russian.

Vollmer, M., R.E. Beitel, and R.L. Snyder (2001). Auditory detection and discrimination in deaf cats: psychophysical and neural thresholds for intracochlear electrical signals. Journal of Neurophysiology 86(5): 2330-43. ISSN: 0022-3077.
Abstract: More than 30,000 hearing-impaired human subjects have learned to use cochlear implants for speech perception and speech discrimination. To understand the basic mechanisms underlying the successful application of contemporary speech processing strategies, it is important to investigate how complex electrical stimuli delivered to the cochlea are processed and represented in the central auditory system. A deaf animal model has been developed that allows direct comparison of psychophysical thresholds with central auditory neuronal thresholds to temporally modulated intracochlear electrical signals in the same animals. Behavioral detection thresholds were estimated in neonatally deafened cats for unmodulated pulse trains (e.g., 30 pulses/s or pps) and sinusoidal amplitude-modulated (SAM) pulse trains (e.g., 300 pps, SAM at 30 Hz; 300/30 AM). Animals were trained subsequently in a discrimination task to respond to changes in the modulation frequency of successive SAM signals (e.g., 300/8 AM vs. 300/30 AM). During acute physiological experiments, neural thresholds to pulse trains were estimated in the inferior colliculus (IC) and the primary auditory cortex (A1) of the anesthetized animals. Psychophysical detection thresholds for unmodulated and SAM pulse trains were virtually identical. Single IC neuron thresholds for SAM pulse trains showed a small but significant increase in threshold (0.4 dB or 15.5 microA) when compared with thresholds for unmodulated pulse trains. The mean difference between psychophysical and minimum neural thresholds within animals was not significant (mean = 0.3 dB). Importantly, cats also successfully discriminated changes in the modulation frequencies of the SAM signals. Performance on the discrimination task was not affected by carrier rate (100, 300, 500, 1,000, or 1,500 pps). These findings indicate that 1) behavioral and neural response thresholds are based on detection of the peak pulse amplitudes of the modulated and unmodulated signals, and 2) discrimination of successive SAM pulse trains is based on temporal resolution of the envelope frequencies. Overall, our animal model provides a robust framework for future studies of behavioral discrimination and central neural temporal processing of electrical signals applied to the deaf cochlea by a cochlear implant.
Descriptors: auditory perception, cochlea, deafness, deafness psychology, discrimination psychology, cats, cochlear implants, differential threshold, electric stimulation, electrophysiology, inferior colliculus, inferior colliculus, neurons, afferent, psychopHysics, sensory thresholds.

Wade, T.V., D.S. Rothblat, and J.S. Schneider (2001). Changes in striatal dopamine D3 receptor regulation during expression of and recovery from MPTP-induced parkinsonism. Brain Research 905(1-2): 111-9. ISSN: 0006-8993.
Abstract: Striatal dopamine (DA) D3 receptor density (measured by quantitative receptor autoradiography) and mRNA expression (measured by reverse transcriptase-polymerase chain reaction) were analyzed in cats symptomatic for and recovered from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism. In symptomatic cats, D3 receptor density was significantly decreased in all regions of the caudate nucleus (CD) (66--77%), the nucleus accumbens (NACC) (52--83%) and the islands of calleja (IC) (67%), all of which returned to normal values in recovered cats. In contrast, D3 receptor mRNA expression was slightly elevated in symptomatic cats, and significantly increased above normal in recovered cats (45% increase in the CD and 91% in the NACC). Thus, reduction of parkinsonian signs was related to normalization of striatal D3 receptor number. These alterations in D3 receptor expression may play an important role in the recovery process observed in this model of parkinsonism.
Descriptors: down regulation, gene expression regulation, neostriatum, parkinsonian disorders, receptors, dopamine d2, receptors, dopamine d2, recovery of function, up regulation, autoradiography, base sequence, cats, DNA, complementary, DNA, complementary, dopamine, down regulation, gene expression regulation, molecular sequence data, neostriatum, neostriatum, neurons, neurons, neurons, parkinsonian disorders, parkinsonian disorders, RNA, messenger, RNA, messenger, recovery of function, reverse transcriptase polymerase chain reaction, up regulation.

Wagenaar, M., L.J. Teppema, A. Berkenbosch, C.N. Olievier, and H.T. Folgering (2000). Medroxyprogesterone acetate with acetazolamide stimulates breathing in cats. Respiration Physiology 119(1): 19-29. ISSN: 0034-5687.
NAL Call Number: QP121. A1R4
Abstract: Both medroxyprogesterone acetate (MPA) and acetazolamide (ACET) increase ventilation. Combined administration of these agents could result in an additional improvement of blood gases, for example in patients with chronic obstructive pulmonary diseases. The aim of this study in anaesthetized female (ovariohysterectomized, pre-treated with 17-beta-estradiol) cats was to compare the effects on the CO2 response curve of MPA alone (4 microg kg(-1), i.v.) with those after MPA followed by ACET (4 mg kg(-1) i.v.). We performed dynamic end-tidal CO2 forcing and analysed the data with a two-compartment model comprising a fast peripheral and slow central compartment, characterized by CO2 sensitivities (Sp and Sc, respectively) and a single offset (the apnoeic threshold B). MPA reduced Sp from 0.22 +/- 0.09 (mean +/- S.D.) to 0.13 +/- 0.06 L min(-1) kPa(-1) (P < 0.01) and Sc from 1.01 +/- 0.38 to 0.88 +/- 0.32 L min(-1) kPa(-1) (P < 0.01). B decreased from 4.02 +/- 0.27 to 3.64 +/- 0.42 kPa (P < 0.01). Subsequent administration of ACET reduced Sp and Sc further to 0.09 +/- 0.06 and to 0.70 +/- 0.49 L min(-1) kPa(-1) (P < 0.01), respectively. The apnoeic threshold decreased further to 2.46 +/- 1.50 kPa (P < 0.01). Because both treatments reduced ventilatory CO2 sensitivity, we conclude that a simulating effect on ventilation is due to a decrease in the apnoeic threshold. Combined administration of MPA and ACET may lead to larger increases in ventilation than treatment with either drugs alone.
Descriptors: acetazolamide, carbonic anhydrase inhibitors, medroxyprogesterone 17 acetate, progesterone congeners, respiration, carbon dioxide, cats, drug combinations.

Walter, J.S., M.P. Fitzgerald, J.S. Wheeler, B. Orris, A. McDonnell, and R.D. Wurster (2005). Bladder-wall and pelvic-plexus stimulation with model microstimulators: Preliminary observations. Journal of Rehabilitation Research and Development 42(2): 251-60. ISSN: 0748-7711.
Abstract: Severe urinary retention is not a common condition, but may occur following some pelvic surgeries or other medical conditions. Electrical stimulation of the bladder has been examined as a means of managing this difficult problem. We conducted preliminary investigations in cats to prove the hypothesis that pelvic-plexus (bladder-neck) stimulation would produce greater micturition response with reduced side effects, such as animal movement or discomfort, than bladder-wall stimulation with electrodes implanted higher on the bladder wall. We used model microstimulators that mimic the look and function of commercial microstimulators, but that we constructed. We instrumented four female cats during a survival surgery. Animals recovered well and studies were conducted over a 1-month period in the conscious animal and under anesthesia. We performed a variety of studies with different stimulation parameters and electrode locations to evaluate our hypothesis. In the active animal, we supplied only low currents, but two animals responded to stimulation with bladder contractions and voiding. Following anesthesia, higher stimulating currents resulted in greater bladder contractions during stimulation in two of the three animals. In two cases, pelvic-plexus (bladder-neck) stimulation induced greater micturition responses than direct bladder-wall stimulation. In conclusion, we learned from these preliminary observations that stimulation at the pelvic plexus (bladder neck) may induce a better micturition response than stimulation higher on the bladder-wall. Newly available commercial microstimulators should be further studied for the treatment of urinary retention.
Descriptors: cats, urine retention, anesthesia, electrical stimulation, micturition, bladder.

Walter, J.S., J.S. Wheeler, W. Cai, W.W. King, and R.D. Wurster (1999). Evaluation of a suture electrode for direct bladder stimulation in a lower motor neuron lesioned animal model. Institute of Electrical and Electronics Engineers Transactions on Rehabilitation Engineering 7(2): 159-66. ISSN: 1063-6528.
Abstract: The purpose of this study was to evaluate a "suture" type electrode for direct bladder stimulation in an animal model of a lower motor neuron lesion. During an initial surgery, five male cats were instrumented under anesthesia using multistranded, 316 LVM, stainless-steel, wire electrodes implanted on the bladder wall serosa above the trigone area. Electrodes were constructed with a needle attached to the end that was removed after suturing the electrode in place. Additional instrumentation included urinary bladder catheters (tubes) for pressure recording and filling, and hook type electrodes for leg and pelvic floor electromyography recording. Chronic bladder filling and stimulation studies were conducted in tethered animals three to four weeks following surgery. To test these electrodes in a spinal cord injury model, a lower motor neuron lesion was performed including the sacral cord and complete nerve roots at L6 and below. These animals were evaluated during weeks 3 and 10 after injury. Direct bladder stimulation induced active contractions and voiding both before and after spinal cord injury. Effective stimulation parameters consisted of 40 pulses per s, 300 micros to 1 ms pulse duration, a stimulation period from 3 to 4 s, and a stimulation current from 10 to 40 mA. Fluoroscopy revealed an open membranous urethra during stimulation and following stimulation. A small diameter penile urethra was observed to limit flow. Postmortem evaluation of the suture electrode revealed no abnormalities such as corrosion, migration into the bladder lumen or displacement. These findings indicate that suture electrodes are suitable and effective for short-term implantation in the lower motor neuron animal model.
Descriptors: neurogenic bladder therapy, electric stimulation therapy, spinal cord injuries therapy, neurogenic bladder, cats, animal disease models, evaluation studies, suture techniques, urodynamics.

Walter, J.S., J.S. Wheeler, M.P. Fitzgerald, A. McDonnell, and R.D. Wurster (2005). Chronic instrumentation with model microstimulators in an animal model of the lower urinary tract. The Journal of Spinal Cord Medicine 28(2): 114-20. ISSN: 1079-0268.
Abstract: BACKGROUND: Microstimulators are a new type of neuroprosthetic device that should be considered for applications such as micturition control after spinal cord injury (SCI). These devices are small (less than 25 mm by 5 mm) and the electrodes are located on the ends of the stimulator. The aim of the current study was to develop methods for chronic implantation of model microstimulators (M-Micro) on the bladder wall and pelvic plexus of female cats. A postmortem evaluation of the effects of 3 months of implantation is reported. METHODS: Techniques to produce the M-Micro are described. Four of these devices were implanted in 4 female cats and maintained after the initial instrumentation surgery and a second survival surgery for SCI (at T10). Using a single suture tied around the M-Micro, these devices were secured to the bladder wall or the fat pads adjacent to the pelvic plexus. Additional instrumentation was implanted, including 2 catheters in the bladder, 1 abdominal balloon, and electromyography electrodes in the urethral and anal sphincters. Postmortem observations of the location of the M-Micro on the bladder wall were conducted after fixation. RESULTS: The animals' conditions were good. One animal was sacrificed early because of a skin infection. A single suture was sufficient to anchor the M-Micro. However, during the surgical implantation the pelvic plexus M-Micro ended up close to the bladder neck. Extensive fibrous connective tissue formed around the M-Micro and implanted catheters on the bladder wall. This appeared to result, in part, from multiple devices implanted on or near the bladder wall. CONCLUSIONS: These pilot studies showed that the M-Micro could be easily constructed and secured to the bladder wall or fat pads close to the pelvic plexus. There was a concern that the pelvic plexus location for the M-Micro ended near the bladder neck during the surgical implantation; however, these devices did not appear to migrate over this short, 3-month implantation period. The extensive connective tissue responses of the bladder wall to the tubes, wires, and M-Micro was a major concern. The M-Micro appears to be a good device to assess the potential of commercial microstimulators for use in micturition control.
Descriptors: bladder surgery, neurogenic bladder therapy, electric stimulation therapy instrumentation, hypogastric plexus surgery, bladder, bladder, neurogenic bladder, neurogenic bladder, cats, animal disease models, electrodes, implanted, feasibility studies, follow up studies, hypogastric plexus, hypogastric plexus, spinal cord injuries, spinal cord injuries, spinal cord injuries, urodynamics.

Walter, J.S., J.S. Wheeler, R.D. Wurster, J. Sacks, and R. Dunn (2003). Preliminary observations of a synergistic bladder-sphincter relationship following spinal cord injury in a quadruped animal. The Journal of Spinal Cord Medicine 26(4): 372-9. ISSN: 1079-0268.
Abstract: BACKGROUND/OBJECTIVES: High urethral resistance or detrusor-sphincter dyssynergia (DSD) is characterized by obstructed voiding during bladder contractions. DSD is caused by an exaggerated pelvic floor reflex resulting from sensory input from elevated pressure in the bladder that produces reflex constriction of the urethral sphincter. The objective of this study was to determine whether sensory input from the bladder produced synergistic or dyssynergic pelvic floor reflexes following SCI in an animal model. METHODS: A pelvic floor reflex that shares the same motor pathway with DSD is the bulbocavernosus (BC) reflex. The BC reflex was elicited with electrical stimulation in 4 male cats with T1 spinal injury, and recorded as an anal sphincter contraction. Recordings were obtained during control and elevated bladder pressures. Increased bladder pressure was induced with either manual pressure (Crede procedure) or spontaneous contractions resulting from bladder filling. RESULTS: During the control period, the BC reflex indicated by the peak anal pressure response was 23 +/- 6 cmH2O. During elevated bladder pressure of 34 +/- 18 cmH2O, the BC response decreased to 10 +/- 3 cmH2O (not significant), showing a synergistic relationship. Anal sphincter tone between BC reflex tests showed a dyssynergic response. All 4 animals showed increased tone during elevated bladder pressures that averaged 9 +/- 5 cmH2O. Because abdominal pressure was not recorded, the significance is not clear. However, there was further support of a dyssynergic relationship based on increases in the anal and urethral electromyography recordings and some pelvic floor spasms during the elevated bladder pressure. CONCLUSIONS: Because 2 different pelvic floor activities were observed during increased bladder pressures, this animal model may be described best as a mixed model. This model shows both synergistic and dyssynergic relationships between the bladder and the BC contractions. Although observed changes were not significant, the unique observations of synergistic bladder-sphincter activity shown by the inhibited BC reflex is in marked contrast to the strictly dyssynergic bladder-sphincter relationship seen in SCI patients.
Descriptors: anus innervation, neurogenic bladder, motor neurons, muscle hypertonia, pelvic floor innervation, reflex, abnormal, spinal cord injuries, urethra innervation, urodynamics, bladder innervation, cats, hydrostatic pressure, isometric contraction, neural inhibition.

Walter, J.S., P. Zaszczurynski, W. Cai, J.S. Wheeler, L. Riedy, and V.E. Scarpine (1995). Direct bladder stimulation with percutaneous electrodes and impedance monitoring of volume in an SCI animal model. The Journal of Spinal Cord Medicine 18(2): 98-102. ISSN: 1079-0268.
Abstract: Bladder responses to percutaneous electrodes were investigated with stimulation in three male spinal cats. The animals had been spinalized (T1 level lesion) 10 weeks prior to these studies and had been instrumented with chronic bladder had been spinalized (T1 level lesion) 10 weeks prior to these studies and had been instrumented with chronic bladder wall electrodes and suprapubic bladder catheters for filling and pressure recording. percutaneous stimulation in tethered animals was conducted wit hook electrodes inserted with a needle in the abdomen bilaterally adjacent to the bladder trigone. Stimulation was conducted with 40 Hz pulse trains of 10 to 30 mA for three seconds. Stimulation with both percutaneous and chronic electrodes induced high bladder pressures and voiding. In addition, with chronically implanted electrodes, impedance monitoring of bladder volume was found to be an effective recording technique.
Descriptors: bladder, electric stimulation therapy, spinal cord injuries, spinal cord injuries therapy, cats, electric impedance, electrodes, implanted, electrophysiology, monitoring, physiologic, transcutaneous electric nerve stimulation.

Wang, F., Y. Seta, G. Baumgarten, D.J. Engel, N. Sivasubramanian, and D.L. Mann (2001). Functional significance of hemodynamic overload-induced expression of leukemia-inhibitory factor in the adult mammalian heart. Circulation 103(9): 1296-1302. ISSN: 0009-7322.
NAL Call Number: RC681 .A1C8
Descriptors: feline heart, molecular biophysics, Leukemia inhibitory factor, apoptosis, hemodynamic overloading, ex vivo, cardiac myocyte, mRNA.

Wang, Z., T.P. O'Connor, S. Heshka, and S.B. Heymsfield (2001). The reconstruction of Kleiber's law at the organ-tissue level. Journal of Nutrition 131(11): 2967-70. ISSN: 0022-3166.
NAL Call Number: 389.8 J82
Abstract: The relationship between resting energy expenditure (REE) (kJ/d) and body mass (M) (kg) is a cornerstone in the study of energy physiology. By expressing REE as a function of body mass observed across mammals, Kleiber formulated the now classic equation: REE = 293M(0.75). The biological processes underlying Kleiber's law have been a topic of long-standing interest and speculation. In the present report we develop a new perspective of Kleiber's law by developing an organ-tissue level REE model consisting of five components: liver, brain, kidneys, heart and remaining tissues. The resting thermal output of each component is the product of the component's specific resting metabolic rate (K) and mass (T). With increasing body size, the K values for all five components had negative exponents and were directly proportional to M(-0.08--0.27), and all component T values were directly proportional to M(0.76-1.01). The resulting exponents of the product (K x T) were M(0.60-0.86) for the five components. Although the (K x T) values of individual components do not scale equally, their combined formula (286M(0.76)) is similar to that observed by Kleiber on the whole-body level. Modeling mammalian REE at the organ-tissue level provides new insights and pathways for future mechanistic explorations of REE-body composition relationships.
Descriptors: basal, biological models, body composition, brain, cats, dogs, kidney, liver, myocardium, rabbits, rats, species specificity.

Ward, C.R., S.E. Achenbach, D. Holt, M.E. Peterson, and J.L. Meinkoth (2005). Thyrotropin-stimulated DNA synthesis and thyroglobulin expression in normal and hyperthyroid feline thyrocytes in monolayer culture. Thyroid 15(2): 114-120. ISSN: 1050-7256.
Abstract: Feline hyperthyroidism is a common, spontaneous disease in older cats that is similar clinically and histopathologically to human toxic multinodular goiter (TNG). In this study, the functional response of feline normal thyroid (NT) and hyperthyroid (HT) cells grown in monolayer culture to thyrotropin (TSH) was determined. Basal levels of DNA synthesis were similar in NT and HT cells. TSH stimulated concentration-dependent DNA synthesis in NT and HT cells, with maximal stimulation seen at 1 and 10 mU/mL TSH in NT and HT cells, respectively. HT cells had higher basal levels of thyroglobulin (Tg) expression. TSH stimulated Tg expression in NT and HT cells in a concentration-dependent fashion, with maximal activity at 0.5 and 5 mU/mL TSH, respectively. These results demonstrate that NT and HT cells in monolayer culture exhibit growth and functional responses to TSH. HT cells have higher basal Tg expression than NT cells and require higher TSH concentrations to stimulate DNA synthesis and Tg expression, two measures of thyroid cell activation. These data support the idea that feline hyperthyroidism is caused by cell abnormalities, resulting in dysregulated growth and hormone synthesis, and emphasize its importance as an animal model for TNG.
Descriptors: Feline hyperthyroidism, aged cats, human toxic multinodular goiter (TNG), thyrotropin, animal model for TNG.

Watson, J.C., E.M. Doppenberg, M.R. Bullock, A. Zauner, M.R. Rice, D. Abraham, and H.F. Young (1997). Effects of the allosteric modification of hemoglobin on brain oxygen and infarct size in a feline model of stroke. Stroke 28(8): 1624-30. ISSN: 0039-2499.
Abstract: BACKGROUND AND PURPOSE: Cerebral ischemia and stroke are leading causes of morbidity and mortality. An approach to protecting the brain during ischemia is to try to increase the delivery of oxygen via the residual blood flow through and around ischemic tissue. To test this hypothesis, we used a novel oxygen delivery agent, RSR-13 (2-[4-[[(3,5-dimethylanilino)-carbonyl]-methyl]phenoxy]-2-methylpr opionic acid). Intravenous administration of RSR-13 increases oxygen delivery through allosteric modification of the hemoglobin molecule, resulting in a shift in the hemoglobin/oxygen dissociation curve in favour of oxygen delivery. METHODS: We studied RSR-13 in a feline model of permanent middle cerebral artery occlusion to assess its effects on cerebral oxygenation and infarct size. A randomized, blinded study of RSR-13 (n = 6) versus 0.45% saline (n = 12) was conducted, after an RSR-13 dose-escalation study (n = 4). Drug was administered as a preocclusion bolus followed by a continuous infusion for the duration of the experiment (5 hours). Brain oxygen was measured continuously with the use of a Clark oxygen electrode. Infarct size was measured at 5 hours after occlusion with computer-assisted volumetric analysis. RESULTS: The drug treatment group had consistently higher mean brain oxygen tension than controls (33 +/- 5 and 27 +/- 6 mm Hg, respectively) and significantly smaller infarcts (21 +/- 9% versus 33 +/- 9%, respectively, P < .008). We observed an inverse relationship between the dose response of RSR-13 (the shift in the hemoglobin/oxygen dissociation curve) and infarct size. CONCLUSIONS: These results are evidence that allosteric hemoglobin modification is protective to the brain after acute focal ischemia, providing a new opportunity for neuroprotection and raising the possibility of enhancing the protective effect of thrombolysis and ion channel blockade.
Descriptors: brain, cerebral infarction, cerebrovascular disorders, aniline compounds, biological availability, cats, hemoglobins, oxygen, propionic acids, time factors.

Webb, C.B., D.C. Twedt, M.J. Fettman, and G. Mason (2003). S-adenosylmethionine (SAMe) in a feline acetaminophen model of oxidative injury. Journal of Feline Medicine and Surgery 5(2): 69-75. ISSN: 1098-612X.
NAL Call Number: SF985 .J68
Descriptors: cats, adenosylmethionine, acetaminophen, glutathione, oxidative stress.

Wesche, D.L., B.G. Schuster, W.X. Wang, and R.L. Woosley (2000). Mechanism of cardiotoxicity of halofantrine. Clinical Pharmacology and Therapeutics 67(5): 521-9. ISSN: 0009-9236.
Abstract: OBJECTIVES AND METHODS: To further evaluate the scope and mechanism of potential cardiotoxicity associated with the antimalarial drug halofantrine, case reports submitted to the US Food and Drug Administration Spontaneous Reporting System were examined. Because halofantrine was associated with electrocardiographic prolongation of the QT interval and ventricular arrhythmias, in vitro cardiac electrophysiologic studies (isolated perfused cardiac model and isolated ventricular myocytes) were conducted to test the hypothesis that halofantrine or its metabolite is responsible for cardiotoxicity. RESULTS: Although it is difficult to ascertain causality and to estimate overall incidence, a significant number of adverse events related to the cardiovascular system were reported, including QT interval prolongation, life-threatening arrhythmias, and sudden death. The effect of halofantrine and its active metabolite (N-desbutylhalofantrine) on repolarization were examined in an isolated perfused heart model. Results indicate that halofantrine was able to prolong the QT interval, whereas N-desbutylhalofantrine had minimal effect on the QT interval relative to baseline. In an attempt to further elucidate the mechanism of QT interval prolongation, the effects of racemic halofantrine, its stereoisomers, and N-desbutylhalofantrine on repolarizing currents in isolated ventricular myocytes were studied with use of patch-clamp techniques. Halofantrine produced a stereoselective block of the delayed rectifier potassium channel in isolated feline myocytes. CONCLUSIONS: These results indicate that halofantrine is similar to quinidine and class III antiarrhythmics in its ability to prolong repolarization. We conclude that high plasma concentrations of halofantrine should be avoided, especially in women, and that N-desbutylhalofantrine may have potential as a safer antimalarial drug.
Descriptors: antimalarials, heart conduction system, myocardium, phenanthrenes, adolescent, adult, adverse drug reaction reporting systems, aged, cardiovascular diseases, cats, child, child, preschool, disease models, animal, infant, middle aged.

Weyrich, A.S., M. Buerke, K.H. Albertine, and A.M. Lefer (1995). Time course of coronary vascular endothelial adhesion molecule expression during reperfusion of the ischemic feline myocardium. Journal of Leukocyte Biology 57(1): 45-55. ISSN: 0741-5400.
NAL Call Number: QP185 .R4
Abstract: The time course of endothelial P-selectin, ICAM-1, and E-selectin expression was studied in a feline model of myocardial ischemia and reperfusion. Cats were subjected to 90 min of myocardial ischemia followed by 0, 10, 20, 60, 150, or 270 min of reperfusion. At the end of reperfusion, the coronary vasculature was examined immunohistochemically to localize monoclonal antibodies (mAbs) PB1.3, RR1/1, and Cy1787 directed against P-selectin, ICAM-1, and E-selectin, respectively. Immunohistochemical localization for P-selectin, recognized by mAb PB1.3, was maximally expressed 20 min after reperfusion in 60 +/- 6% of coronary venules (P < 0.05 compared to non-reperfused controls), and covered 59 +/- 3% of the endothelial cell perimeter of immunostained coronary venules. Immunolocalization of mAb PB1.3 gradually declined at 60, 150, and 270 min of reperfusion. Immunohistochemical localization of mAb RR1/1 (anti-ICAM-1) in endothelial cells of coronary venules was observed to a modest extent in non-ischemic myocardium and at 10, 20, and 60 min of reperfusion, but was significantly increased following 150 and 270 min of reperfusion (P < 0.05 compared non-reperfused controls). At 270 min post-reperfusion, mAb RR1/1 was seen in 50 +/- 4% of coronary venules. Endothelial immunolocalization of mAb Cy1787 (anti-E-selectin) was only observed in 13 +/- 1 and 14 +/- 3% of coronary venules after 150 and 270 min of reperfusion, respectively, suggesting that pronounced expression of E-selectin does not occur within 270 min after reperfusion. These results demonstrate sequential expression of three major endothelial cell adherence molecules in situ following myocardial ischemia and reperfusion. The timing of endothelial cell expressed P-selectin and ICAM-1 could coordinate neutrophil trafficking during the early stages of reperfusion.
Descriptors: cell adhesion molecules biosynthesis, intercellular adhesion molecule 1 biosynthesis, myocardial ischemia, myocardial reperfusion injury, platelet membrane glycoproteins biosynthesis, antibodies, monoclonal, cats, cell adhesion molecules analysis, creatine kinase, E selectin, endothelium, vascular, endothelium, vascular, endothelium, vascular, immunohistochemistry, intercellular adhesion molecule 1 analysis, myocardial ischemia, myocardial reperfusion injury, myocardium, neutrophils, p selectin, platelet membrane glycoproteins analysis, time factors.

Whang, C.J. and Y. Kwon (1994). Cerebral energy metabolism following ESWL brain injury model and effects of cerebral protective drugs. Journal of Korean Medical Science 9(2): 123-34. ISSN: 1011-8934.
Abstract: The goal of this study was to introduce a new method inducing an experimental brain injury model using ESWL(Extracorporeal Shock Wave Lithotripsy) and to evaluate findings of localized lesions on 1H MR imaging and the response of cerebral energy metabolism using a 31P MR spectroscope to the ESWL brain injury in cats. This study also examined effects of cerebral protective drugs. 1) There were no statistically significant changes in pH at all measurement points. 2) In the trauma group, initial decrease of PCr/Pi was seen at 30 to 60 minutes with return to control levels by 2 hours after injury(P < 0.05), followed by a second decline at 4 hours which lasted until 8 hours after injury. 3) Significant recovery in PCr/Pi(P < 0.05) was observed in both the THAM and dexamethasone treated groups at all measurement points and in the mannitol treated group only temporary recovery at 30 and 60 minutes (P < 0.05). 4) High intensity signals were seen on 1H MR imaging in traumatized animals. This study demonstrated the immediate and persistent recovery of cerebral energy metabolism using THAM or dexamethasone and an immediate but transient effect with mannitol in traumatized animals.
Descriptors: brain, brain injuries, dexamethasone, animal disease models, energy, lithotripsy, tromethamine, adenosine triphosphate, brain, brain injuries, brain injuries, cats, hydrogen ion concentration, magnetic resonance spectroscopy, phosphates, phosphocreatine, random allocation.

Widdison, A.L. (1996). Pathogenesis of pancreatic infection. Annals of the Royal College of Surgeons of England 78(4): 350-3. ISSN: 0035-8843.
Abstract: John Hunter studied comparative anatomy of the pancreas but was unaware of pancreatic infection which is now the leading cause of mortality in pancreatitis. This was investigated using a feline model of pancreatitis. Pathogens spread to the healthy and inflamed gland from many sources including colon, gallbladder, or a septic focus and by various routes including the circulation, reflux into the pancreatic duct or by transmural migration from the colon. Colonisation risk was proportional to necrosis and inflammation, confirming clinical observations. These studies showed that pathogens frequently colonised the pancreas, but infection developed only in animals with pancreatitis. In cats with pancreatitis, phagocytic function was reduced by 28%. This was probably owing to phagocytic capacity being overwhelmed by protease-antiprotease complexes because, in humans, granulocyte and lymphocyte function was normal. These experiments suggested that it would be difficult to prevent pancreatic colonisation, but indicated some types of therapy may have potential. These were investigated using this animal model of pancreatic infection. Treatment with either cefotaxime or levamisole (an immunostimulant) were effective. However, the anti-inflammatory drug dopamine, which reduced inflammation, did not eradicate all pathogens.
Descriptors: bacterial infections, opportunistic infections, pancreatitis microbiology, acute disease, bacterial infections, bacterial infections, cats, animal disease models, escherichia coli infections, escherichia coli infections, escherichia coli infections, opportunistic infections, opportunistic infections, pancreatitis, pancreatitis, phagocytosis, risk factors.

Widdison, A.L., C. Alvarez, Y.B. Chang, N.D. Karanjia, and H.A. Reber (1994). Sources of pancreatic pathogens in acute pancreatitis in cats. Pancreas 9(4): 536-41. ISSN: 0885-3177.
Abstract: The source(s) of pancreatic pathogens is uncertain, although the colon is usually implicated. We studied whether pathogens may spread from different sites in a feline model of the disease. Acute pancreatitis was induced using a standard technique and a distinctive clinical strain of Escherichia coli as the marker bacterium. E. coli were placed in the colon, gall bladder, main pancreatic duct, or obstructed renal pelvis of control cats (no pancreatitis) and acute pancreatitis cats. Pancreases were colonized from each source, whether or not pancreatitis was present. The pancreatic colonization rate was greater in acute pancreatitis only when E. coli had been placed in the colon. In conclusion, E. coli may spread to the pancreas from different sources. The high rate of pancreatic colonization in both control and inflamed glands suggested that, clinically, bacteria may spread to the pancreas more frequently than is currently thought.
Descriptors: escherichia coli infections microbiology, pancreas microbiology, pancreatitis microbiology, acute disease, cats, colon microbiology, escherichia coli, gallbladder microbiology, kidney microbiology, pancreatic ducts microbiology.

Widdison, A.L., N.D. Karanjia, and H.A. Reber (1994). Antimicrobial treatment of pancreatic infection in cats. The British Journal of Surgery 81(6): 886-9. ISSN: 0007-1323.
Abstract: An investigation examined the efficacy of antibiotics in a novel feline model of pancreatic infection in acute pancreatitis. Acute pancreatitis was induced in cats using an established technique. In control animals (no pancreatitis) and cats with pancreatitis, Escherichia coli (10(4) in 0.1 ml) was placed in the pancreatic duct. Reoperation was performed after 24 h in six controls and six cats with pancreatitis. E. coli was cultured from the pancreas in five control animals and five cats with pancreatitis. Reoperation was performed after 1 week in ten controls, in 11 cats with pancreatitis and in nine with pancreatitis that were treated with cefotaxime (50 mg/kg intramuscularly three times daily) started 12 h after the induction of pancreatitis and administration of E. coli. Pancreatic infection developed in eight cats with pancreatitis compared with none of the cefotaxime-treated animals and none of the controls (P < 0.05). Cefotaxime reached bactericidal levels in pancreatic tissue and juice. In conclusion, ductal administration of E. coli caused pancreatic infection only in cats with acute pancreatitis. Early administration of an appropriate antibiotic was effective in treating pancreatic infection in acute pancreatitis.
Descriptors: cefotaxime, escherichia coli infections, opportunistic infections, pancreatitis, acute disease, cats, animal disease models, Escherichia coli, pancreas microbiology, pancreatitis microbiology.

Widdison, A.L., N.D. Karanjia, and H.A. Reber (1994). Routes of spread of pathogens into the pancreas in a feline model of acute pancreatitis. Gut 35(9): 1306-10. ISSN: 0017-5749.
NAL Call Number: RC799 G8
Abstract: The routes of spread of pathogens into the pancreas in acute pancreatitis were investigated. Four experiments were performed: (1) cats with and without acute pancreatitis were given 10(7) Escherichia coli (E coli) intravenously, (2) in cats with acute pancreatitis 10(8) E coli was placed in the colon. In half of them the colon was then enclosed in an impermeable bag to prevent transmural spread. (3) E coli (10(4)) was placed in the pancreatic duct in cats with and without acute pancreatitis. (4) In cats with acute pancreatitis 10(5) E coli was placed in the gall bladder. In half of them the common bile duct was ligated to prevent biliary-pancreatic reflux. After 24 hours, intravenous E coli infected the pancreas in six of nine cats with acute pancreatitis and three of 10 controls. After 72 hours E coli spread to the pancreas from the colon in six of nine cats with acute pancreatitis. This was prevented by enclosing the colon in an impermeable bag (p = 0.02). In five of six cats with acute pancreatitis and five of six controls E coli placed in the pancreatic duct colonised the pancreas within 24 hours. Pancreatic colonisation from the gall bladder occurred in five of six cats with a patent common bile duct and in three of six with an obstructed common bile duct. In conclusion, in cats E coli can spread to the pancreas by the blood stream, transmurally from the colon, and by reflux into the pancreatic duct.
Descriptors: Escherichia coli infections microbiology, pancreas microbiology, pancreatitis microbiology, acute disease, bile reflux microbiology, cats, colitis microbiology, colon microbiology, animal disease models.

Willey, C.D., S. Balasubramanian, M. Rodriguez Rosas, R.S. Ross, and D. Kuppuswamy (2003). Focal complex formation in adult cardiomyocytes is accompanied by the activation of beta3 integrin and c-Src. Journal of Molecular and Cellular Cardiology 35(6): 671-83. ISSN: 0022-2828.
Abstract: In pressure-overloaded myocardium, our recent study demonstrated cytoskeletal assembly of c-Src and other signaling proteins which was partially mimicked in vitro using adult feline cardiomyocytes embedded in three-dimensional (3D) collagen matrix and stimulated with an integrin-binding Arg-Gly-Asp (RGD) peptide. In the present study, we improved this model further to activate c-Src and obtain a full assembly of the focal adhesion complex (FAC), and characterized c-Src localization and integrin subtype(s) involved. RGD dose response experiments revealed that c-Src activation occurs subsequent to its cytoskeletal recruitment and is accompanied by p130Cas cytoskeletal binding and focal adhesion kinase (FAK) Tyr925 phosphorylation. When cardiomyocytes expressing hexahistidine-tagged c-Src via adenoviral gene delivery were used for RGD stimulation, the expressed c-Src exhibited relocation: (i) biochemical analysis revealed c-Src movement from the detergent-soluble to the -insoluble cytoskeletal fraction and (ii) confocal microscopic analysis showed c-Src movement from a nuclear/perinuclear to a sarcolemmal region. RGD treatment also caused sarcolemmal co-localization of FAK and vinculin. Characterization of integrin subtypes revealed that beta3, but not beta1, integrin plays a predominant role: (i) expression of cytoplasmic domain of beta1A integrin did not affect the RGD-stimulated FAC formation and (ii) both pressure-overloaded myocardium and RGD-stimulated cardiomyocytes exhibited phosphorylation of beta3 integrin at Tyr773/785 sites but not beta1 integrin at Thr788/789 sites. Together these data indicate that RGD treatment in cardiomyocytes causes beta3 integrin activation and c-Src sarcolemmal localization, that subsequent c-Src activation is accompanied by p130Cas binding and FAK Tyr925 phosphorylation, and that these events might be crucial for growth and remodeling of hypertrophying adult cardiomyocytes.
Descriptors: integrin beta3, myocardium, proteins, src family kinases, adenoviridae, antigens, cd29, Western blot, cats, cell nucleus, cells, cultured, collagen, cytoplasm, cytoskeleton, dose response relationship, drug, histidine, hypertrophy, integrins, microscopy, confocal, myocardium, oligopeptides, phosphoproteins, phosphorylation, protein binding, protein tyrosine kinase, signal transduction, time factors, tyrosine, vinculin.

Woodman, R.C., D. Teoh, D. Payne, and P. Kubes (2000). Thrombin and leukocyte recruitment in endotoxemia. American Journal of Physiology: Heart and Circulatory Physiology 279(3): H1338-45. ISSN: 0002-9513.
NAL Call Number: 447.8 AM3
Abstract: Because thrombin has been implicated in sepsis, it has been proposed that antithrombin III (AT III) is beneficial due to its anticoagulatory and antiadhesive effects. Using intravital microscopy, we visualized leukocyte-endothelium interactions in postcapillary venules of the feline mesentery exposed to lipopolysaccharide (LPS). At a concentration of AT III that blocks leukocyte adhesion in postischemic mesentery, we found no role for thrombin in LPS-induced rolling, adhesion and emigration, or microvascular dysfunction. Furthermore, AT III did not attenuate leukocyte-endothelial interactions after tumor necrosis factor-alpha superfusion of the mesentery. In contrast, fucoidan, a selectin inhibitor, prevented almost all LPS-induced rolling and reduced adhesion, emigration, and microvascular dysfunction. In a model of endotoxemia, leukocyte recruitment into mesentery or lungs was unaffected by AT III. Finally, in a human cell system that mimics the flow conditions in vivo, human neutrophils rolled, adhered, and emigrated similar to the feline postcapillary microvessels, and AT III had no effect on leukocyte recruitment induced by LPS. If AT III has beneficial effects in endotoxemia, it is not due to a direct effect upon leukocyte rolling, adhesion, or emigration in postcapillary venules in vivo.
Descriptors: antithrombin III, endotoxemia, leukocytes, thrombin, capillary permeability, cats, cell adhesion, cell movement, cells, cultured, chemotaxis, leukocyte, diffusion chambers, culture, dose response relationship, drug, endotoxemia, hemodynamic processes, leukocytes, lipopolysaccharides, lymphatic system, mesentery supply, mesentery, neutrophil infiltration, selectins, thrombin, tumor necrosis factor alpha.

Xie, R., F. Stapleton, and D.F. Sweeney (2001). Confocal microscopy of feline cornea implanted with synthetic onlays: preliminary in vivo observations. Investigative Ophthalmology and Visual Science 42(4): S271. ISSN: 0146-0404.
Descriptors: sense organs, feline cornea, sensory reception, confocal microscopy, feasibility, imaging method, light microscopy, simplified epikeratophakia technique, therapeutic method, synthetic onlay implantation, inflammatory response .
Notes: Meeting Information: Annual Meeting of the Association for Research in Vision and Ophthalmology, Fort Lauderdale, Florida, USA; April 29-May 4, 2001.

Yamamoto, J.K. (Inventor) Feline lymphoid cell lines capable of producing FIV for FIV diagnostics and vaccines. 2000). Official Gazette of the United States Patent and Trademark Office Patents, 1237 (4). ISSN: 0098-1133
NAL Call Number: T223. A21
Descriptors: infection, FIV detection, detection method, FIV vaccine, polynucleotide probes, viral genome, HIV model.

Yang FaZhu, Huang XiaoHong, Tu ZhaoPing, and Zhang YingZhen (2000). Establishment of an animal model of Capillaria hepatica. Chinese Journal of Parasitology and Parasitic Diseases 18(4): 229-231. ISSN: 1000-7423.
Descriptors: animal models, disease models, experimental infections, laboratory animals, Capillaria hepatica, cats, rats.
Language of Text: Chinese; Summary in English.

Yang, T.D., J.S. Pei, S.L. Yang, Z.Q. Liu, and R.L. Sun (2002). Medical prevention of space motion sickness--animal model of therapeutic effect of a new medicine on motion sickness. Advances in Space Research 30(4): 751-755. ISSN: 0273-1177.
Descriptors: antiemetics, cholinergic antagonists, models, animal, space motion sickness, space motion sickness, acceleration, cats, clinical trials, dose response relationship, drug, drugs, chinese herbal, oxotremorine, rabbits, rats, scopolamine.

Yinon, U. (1994). Visual hemispheric dominance induced in split brain cats during development: a model of deficient interhemispheric transfer derived from physiological evidence in single visual cortex cells. Behavioural Brain Research 64(1-2): 97-110. ISSN: 0166-4328.
Abstract: The effects of cancellation of both interhemispheric callosal transfer and interocular interactions, were studied in early monocularly deprived cats. The main purpose of this study was therefore to prove whether unilateral hemispheric dominance would result under these conditions and to what extent each hemisphere will be functionally independent. Secondly, we have attempted to establish such an experimental model physiologically, on the single cell level. Interhemispheric transfer was surgically canceled by sagittal transection of the corpus callosum. In addition, the ocular projections were separated by sagittal transection of the optic chiasm in the transbuccal approach. This condition had practically induced visual split brain condition in these cats. These manipulations were carried out concurrently with monocular deprivation (SBDK group) which was surgically done by eye closure during the critical period of development of the visual system. Thus, the hemisphere ipsilaterally to the visually deprived eye had developed under conditions of deficient visual experience while the hemisphere ipsilaterally to the normal eye had developed under conditions of unaltered visual experience. A group of cats (SBK) similarly operated but equally binocularly exposed during development was served as controls. In addition, adult cats similarly operated during adulthood either chronically or acutely were studied to evaluate the effects of interhemispheric and interocular separation. Other groups of cats were also studied for comparison, and included sham operated and normal adult cats. At adulthood, electrophysiological studies were done on these cats, in which action potentials were extracellularly recorded from single cells in the visual cortex (area 17-18 boundary) following anesthesia and paralysis. Stimulation was carried out manually and by a computer driven optical system, presenting on a tangent screen light bars at various spatial positions, orientations and directions. Receptive fields were thus mapped for all neurons and their dimensions and eccentricities were measured. The responsiveness, ocular dominance and other parameters were also studied for these cells. The results in the early deprived cats and in their controls, had shown a full separation between the two hemispheres, as reflected in the almost absolute ipsilateral eye responsiveness (> 97.0% cells). In comparison, in the sham operated and in the normal control cats only minor proportions of cells (13.0-18.7%) have been found as ipsilaterally and monocularly driven, showing almost full interhemispheric and interocular interaction. The main difference, however, in the results between the early monocularly deprived cats and their controls is that in the first group the two hemispheres were asymmetric concerning the amount of visual activation and in the second one they were very symmetric.(ABSTRACT TRUNCATED AT 400 WORDS)
Descriptors: attention, corpus callosum, dominance, cerebral, neuronal plasticity, sensory deprivation, vision, monocular, visual cortex, animals, newborn, brain mapping, cats, evoked potentials, visual, neurons, optic chiasm, vision, binocular, visual fields.

Zauner, A., T. Clausen, O.L. Alves, A. Rice, J. Levasseur, H.F. Young, and R. Bullock (2002). Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model. Journal of Neurosurgery 97(3): 643-9. ISSN: 0022-3085.
Abstract: Currently, there are no good clinical tools to identify the onset of secondary brain injury and/or hypoxia after traumatic brain injury (TBI). The aim of this study was to evaluate simultaneously early changes of cerebral metabolism, acid-base homeostasis, and oxygenation, as well as their interrelationship after TBI and arterial hypoxia. METHODS: Cerebral biochemistry and O2 supply were measured simultaneously in a feline model of fluid-percussion injury (FPI) and secondary hypoxic injury. After FPI, brain tissue PO2 decreased from 33 +/- 5 mm Hg to 10 +/- 4 mm Hg and brain tissue PCO2 increased from 55 +/- 2 mm Hg to 81 +/- 9 mm Hg, whereas cerebral pH fell from 7.1 +/- 0.06 to 6.84 +/- 0.14 (p < 0.05 for all three measures). After 40 minutes of hypoxia, brain tissue PO2 and pH decreased further to 0 mm Hg and 6.48 +/- 0.28, respectively (p < 0.05), whereas brain tissue PCO2 remained high at 83 +/- 13 mm Hg. Secondary hypoxic injury caused a drastic increase in cerebral lactate from 513 +/- 69 microM/L to 3219 +/- 490 microM/L (p < 0.05). The lactate/glucose ratio increased from 0.7 +/- 0.1 to 9.1 +/- 2 after hypoxia was introduced. The O2 consumption decreased significantly from 18.5 +/- 1.1 microl/mg/hr to 13.2 +/- 2.1 microl/mg/hr after hypoxia was induced. CONCLUSIONS: Cerebral metabolism, O2 supply, and acid-base balance were severely compromised ultra-early after TBI, and they declined further if arterial hypoxia was present. The complexity of pathophysiological changes and their interactions after TBI might explain why specific therapeutic attempts that are aimed at the normalization of only one component have failed to improve outcome in severely head injured patients.
Descriptors: brain, brain injuries, hypoxia, brain, acid base equilibrium, brain, carbon dioxide, cats, animal disease models, mitochondria, mitochondria ultrastructure, mitochondrial swelling, oxygen.

Zimmer, H.G. (2001). Perfusion of isolated organs and the first heart-lung machine. Canadian Journal of Cardiology 17(9): 963-969. ISSN: 0828-282X.
Descriptors: cardiovascular system, cats, equipment, apparatus, devices and instrumentation, embolism, vascular disease, cardiopulmonary bypass, surgical method, therapeutic method, heart lung machine, open heart surgery, isolated organ perfusion, oxygen consumption.