Animal Models of Disease Animal Welfare Information Center United States Department of Agriculture National Agricultural Library

Compiled By:
Tim Allen
Animal Welfare Information Center, Information Centers Branch
National Agricultural Library, Agricultural Research Service, U. S. Department of Agriculture
10301 Baltimore Ave., Beltsville, Maryland 20705-2351

National Agricultural Library Cataloging Record:

 Allen, Tim
   Animal models of disease : January 1988-January 1995.
   (Quick bibliography series ; 95-14)
   1. Diseases--Animal models--Bibliography. 2. Animal models
 in research--Bibliography. 3. Laboratory animals--
 Bibliography. I. Title.
 aZ5071.N3 no.95-14
 

Search Strategy

   Line Description
   ---- -----------
   1.   animal(W)model?
   2.   disease? or disorder? or syndrome?
   3.   S1 and S2
   4.   S3 and PY=1988:1995
 
 

 1                                     NAL Call. No.: 381 J8282
 Aberrant hypothalamic-pituitary-ovarian axis in the Watanabe
 heritable hyperlipidemic rabbit.
 Robins, E.D.; Nelson, L.M.; Hoeg, J.M.
 Bethesda, Md. : Lipid Research, inc., 1959-; 1994 Jan.
 Journal of lipid research v. 35 (1): p. 52-59; 1994 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Rabbits; Hyperlipemia; Animal models; Disease
 models; Hypercholesterolemia; Hypothalamus; Pituitary;
 Ovaries; Pituitary-gonadal axis; Low density lipoprotein;
 Receptors; Fsh; Lh; Progesterone; Estradiol; Gonadotropins;
 Cholesterol; Blood lipids
 
 Abstract:  The WHHL rabbit has a defective low density
 lipoprotein receptor and is a model for familial
 hypercholesterolemia. WHHL rabbits are less fecund than NZW
 rabbits, the strain into which the defect has been inbred.
 This lower fecundity could be related to impaired ovarian
 steroidogenesis due to reduced intracellular availability of
 cholesterol. Here we compare the WHHL and NZW rabbits with
 regard to oocyte morphology and fertilization rates after
 stimulation with equine chorionic gonadotropin. We also
 compare hypothalamic-pituitary-ovarian axis function by
 measuring baseline and gonadotropin releasing hormone-
 stimulated plasma estradiol, progesterone, and gonadotropin
 levels, both before and after simvastatin inhibition of de
 novo cholesterol synthesis. WHHL rabbit oocytes remained
 encased in cumulus and had a lowered fertilization rate (9/50
 vs. 83/87, P < 0.05). WHHL rabbits had lower baseline
 estradiol levels (7.1 +/- 0.72 vs. 10.2 +/- 0.94, P < 0.05)
 and had higher baseline follicle stimulating hormone (P <
 0.05) and luteinizing hormone (P < 0.05) levels. Simvastatin
 lowered luteal progesterone concentrations only in WHHL
 rabbits (P < 0.05). We conclude that the hypothalamic-
 pituitary-ovarian axis in WHHL rabbits is abnormal. The
 reduced availability of intracellular cholesterol for
 progesterone synthesis by inhibition of de novo cholesterol
 biosynthesis leads to a significant reduction in plasma
 progesterone concentrations in the WHHL. These findings have
 implications for women with familial hypercholesterolemia,
 particularly regarding treatment with inhibitors of de novo
 cholesterol synthesis.
 
 
 2                                      NAL Call. No.: 500 N21P
 Abnormal class I assembly and peptide presentation in the
 nonobese diabetic mouse.
 Li, F.; Guo, J.; Fu, Y.; Yan, G.; Faustman, D.
 Washington, D.C. : National Academy of Sciences,; 1994 Nov08.
 Proceedings of the National Academy of Sciences of the United
 States of America v. 91 (23): p. 11128-11132; 1994 Nov08. 
 Includes references.
 
 Language:  English
 
 Descriptors: Mice; Diabetes; T lymphocytes; Major
 histocompatibility complex; Histocompatibility antigens;
 Autoimmunity; Autoimmune diseases; Structural genes; Alleles;
 Gene expression; Animal models
 
 Abstract:  Presentation of self-antigens by major
 histocompatibility compatibility complex (MHC) class I
 molecules requires the function MHC class II-linked genes
 Tap-1 and Tap-2. Evidence suggests that interruption of self-
 peptide presentation results in reduced cell surface
 expression of MHC class I molecules and the interruption
 correlates with progression to diabetic autoimmunity in
 nonobese diabetic (NOD) mice and humans. NOD mice possess a
 rare Tap-1 allele (Tap-1b); this is associated with reduced
 Tap-1 mRNA abundance in lymphocytes from diabetes-prone
 females and decreased conformationally correct class I
 molecules on the cell surface. In this study, we demonstrate
 that, similar to lymphoma cell lines with mutations in Tap-1
 or Tap-2, the reduced expression of class I molecules on the
 surface of lymphocytes from diabetes-prone female NOD mice was
 normalized by incubation at low temperatures or by exposure to
 class I allele-specific peptides. As would be expected for
 cells that express surface class I molecules not associated
 with peptide, female NOD lymphocytes were resistant to lysis
 by class I-restricted, peptide-specific cytotoxic T
 lymphocytes. Furthermore, the rate of class I exit from the
 endoplasmic reticulum of lymphocytes from female NOD mice was
 delayed as demonstrated by delayed glycosylation. Male NOD
 mice, which are not prone to diabetes, lacked these functional
 defects in class I assembly and had near-normal levels of
 Tap-1 mRNA and exhibited normal density of class I epitopes
 that were peptide filled. These results are consistent with
 the possibility that the rare Tap-1b allele is associated with
 a quantitative defect in Tap-1 expression that influences
 disease course.
 
 
 3                                    NAL Call. No.: RC628.A1O2
 Abnormalities of plasma lipoproteins in a new genetically
 obese rat with non-insulin-dependent diabetes mellitus (Wistar
 fatty rat). Jiao, S.; Matsuzawa, Y.; Matsubara, K.; Kubo, M.;
 Tokunaga, K.; Odaka, H.; Ikeda, H.; Matsuo, T.; Tarui, S.
 Basingstoke, Hampshire : The Macmillan Press Ltd; 1991 Jul.
 International journal of obesity v. 15 (7): p. 487-495; 1991
 Jul.  Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Diabetes mellitus; Insulin; Cholesterol
 acyltransferase; Lipoproteins; Apolipoproteins; Blood plasma;
 Diet; Intestinal absorption; Rats
 
 Abstract:  We investigated plasma lipoprotein profiles and the
 activities of tissue cholesterol regulating enzymes in Wistar
 fatty rats, an animal model for non-insulin-dependent diabetes
 mellitus (NIDDM). Wistar fatty rats were made by transfer of
 the fa gene to the Wistar Kyoto rats by backcross-breeding.
 Wistar fatty and control non-diabetic littermates were given a
 laboratory chow or an atherogenic diet containing 1 percent
 (weight percent) cholesterol, 0.5 percent cholic acid, and 5
 percent lard. Under the chow diet, plasma fasting glucose and
 immunoreactive insulin concentrations in Wistar fatty rats
 were 1.5- and 6-fold higher than controls, respectively.
 Plasma cholesterol was significantly increased in Wistar fatty
 rats compared with controls. Elevated plasma cholesterol
 levels in Wistar fatties was accounted for by the increases of
 cholesterol content in the d < 1.006 g/ml lipoprotein and
 high-density lipoproteins. Under the atherogenic diet, plasma
 cholesterol levels in Wistar fatties were further increased by
 129 percent compared with controls. The diet-induced increase
 of cholesterol contents was shown in all lipoprotein classes
 for Wistar fatty rats. The activities of regulatory enzymes
 for cholesterol biosynthesis or absorption were measured in
 Wistar fatty rats. Both hepatic and intestinal 3-hydroxy-3-
 methylglutaryl (HMG)-CoA reductase activities were
 significantly higher in Wistar fatty rats than those in
 controls (P < 0.05 and P < 0.01, respectively). ACAT
 activities in Wistar fatties were significantly increased in
 the intestine (P < 0.05) and decreased in the liver in
 comparison with controls (P < 0.01). Cholesterol loading
 caused suppression of HMG-CoA reductase activities and
 enhancement of ACAT activities of both tissues in Wistar fatty
 rats as much as in controls. These data suggest that
 hypercholesterolemia in the NIDDM rats might be attributed to
 the increases in both de novo synthesis and intestinal
 absorption of cholesterol. Magnified response of
 
 
 4                                    NAL Call. No.: RA784.A1I5
 Activity-induced anorexia in rats does not affect hypothalamic
 neuropeptide gene expression chronically.
 Wong, M.L.; Licinio, J.; Gold, P.W.; Glowa, J.
 New York, N.Y. : John Wiley & Sons; 1993 May.
 The International journal of eating disorders v. 13 (4): p.
 399-405; 1993 May.  Includes references.
 
 Language:  English
 
 Descriptors: Physical activity; Anorexia; Hypothalamus;
 Neuropeptides; Gene expression; Rats
 
 Abstract:  Hypothalamic neuropeptides are thought to
 contribute to the pathophysiology of eating disorders. In an
 animal model with chronic abnormalities of energy expenditure,
 appetitive behavior, and body weight, without acute food
 restriction, we found alterations in peripheral levels of
 adrenocorticotropic hormone and corticosterone, but no
 alterations in the expression of neuropeptides genes that are
 known to regulate ingestive behavior and food intake acutely.
 Our data suggest that activation of hypothalamic-pituitary-
 adrenal function in activity anorexia may not be due to
 increased transcription of corticotropin-releasing hormone
 gene, but might be related to posttranscriptional events or to
 other neuropeptides, such as arginine vasopressin.
 Furthermore, we suggest that abnormalities in neuropeptides
 observed in eating disorders may be caused by acute food
 restriction, rather than by chronic hyperactivity, anorexia,
 and low weight.
 
 
 5                                      NAL Call. No.: 381 J824
 Adipose cell hyperplasia and enhanced glucose disposal in
 transgenic mice overexpressing GLUT4 selectively in adipose
 tissue.
 Shepherd, P.R.; Gnudi, L.; Tozzo, E.; Yang, H.; Leach, F.;
 Kahn, B.B. Baltimore, Md. : American Society for Biochemistry
 and Molecular Biology; 1993 Oct25.
 The Journal of biological chemistry v. 268 (30): p.
 22243-22246; 1993 Oct25. Includes references.
 
 Language:  English
 
 Descriptors: Mice; Transgenic animals; Animal proteins;
 Glucose; Active transport; Plasma membranes; Adipocytes;
 Hyperplasia; Adipose tissue; Carbohydrate metabolism; Brown
 fat; Body fat; Glucose tolerance
 
 Abstract:  To gain insight into the molecular pathogenesis of
 obesity and specifically the role of nutrient partitioning in
 the development of obesity, we overexpressed the insulin-
 responsive glucose transporter (GLUT4) in transgenic mice
 under the control of the fat-specific aP2 fatty acid-binding
 protein promoter/enhancer. Two lines of transgenic mice were
 generated, which overexpressed GLUT4 6-9-fold in white fat and
 3-5-fold in brown fat with no overexpression in other tissues.
 In vivo glucose tolerance was enhanced in transgenic mice. In
 isolated epididymal, parametrial, and subcutaneous adipose
 cells from transgenic mice, basal glucose transport was 20-34-
 fold greater than in nontransgenic littermates. Insulin-
 stimulated glucose transport was 2-4-fold greater in cells
 from transgenic mice. Total body lipid was increased 2-3-fold
 in transgenic mice overexpressing GLUT4 in fat. Surprisingly,
 fat cell size was unaltered and fatcell number was increased
 >2-fold. This is the first animal model in which increased fat
 mass results solely from adipocyte hyperplasia and it will be
 a valuable model for understanding the mechanisms responsible
 for fat cell replication and/or differentiation in vivo.
 
 
 6                                      NAL Call. No.: 421 J828
 Aedes (Gymnometopa) mediovittatus (Diptera: Culicidae) as an
 experimental vector of Brugia pahangi and B. malayi
 (Spirurida: Filariidae). Trpis, M.
 Lanham, Md. : The Entomological Society of America; 1994 May.
 Journal of medical entomology v. 31 (3): p. 442-444; 1994 May. 
 Includes references.
 
 Language:  English
 
 Descriptors: Aedes mediovittatus; Brugia malayi; Brugia
 pahangi; Disease vectors; Experimental infection;
 Susceptibility; Animal models; Filariasis
 
 Abstract:  To test the susceptibility of Aedes (Gymnometopa)
 mediovittatus to infection with Brugia pahangi and Brugia
 malayi, females originating from the suburbs of San Juan,
 Puerto Rico, were fed on infected gerbils (Meriones
 unguiculatus). On average, 39.2% of the Ae. mediovittatus
 females became infected with L3 larvae of B. pahangi and 47.4%
 with B. malayi. The average number of infective L3 larvae of
 B. pahangi and B. malayi dissected from mosquitoes was 2.6 +/-
 1.2 and 2.9 +/- 1.0, respectively. The largest number of in a
 single mosquito was 16. After 10 d of development in the
 mosquitoes, L3 larvae of both Brugian species were found in
 greatest number in the thorax, in lesser number in the
 head/proboscis, and in least number in the abdomen. Ae.
 mediovittatus may, serve as a useful laboratory model for the
 study of genetic susceptibility and refractoriness of mosquito
 vectors to filarial parasites.
 
 
 7                                      NAL Call. No.: 41.8 P27
 Age-related changes in the prostate and testes of the beagle
 dog. Lowseth, L.A.; Gerlach, R.F.; Gillett, N.A.; Muggenburg,
 B.A. Lawrence, Kan. : American College of Veterinary
 Pathologists; 1990 Sep. Veterinary pathology v. 27 (5): p.
 347-353; 1990 Sep.  Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Prostate; Weight; Testes; Histology; Blood
 serum; Testosterone; Aging; Age differences; Animal models
 
 
 8                                     NAL Call. No.: TX345.B74
 Alcoholism and folate homeostasis.
 Halsted, C.H.
 San Diego, Calif. : Academic Press; 1989.
 Bristol-Myers Squibb/Mead Johnson nutrition symposia v. 7: p.
 249-266. charts; 1989.  In the series analytic: Nutrition and
 the Origins of Disease / edited by G.H. Halsted and R.B.
 Rucker.  Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Folic acid; Alcoholism; Vitamin deficiencies;
 Nutrition physiology; Liver; Nutrient balance; Literature
 reviews
 
 Abstract:  This chapter examines a variety of issues relating
 to folate deficiency and alcoholism: 1) incidence; 2) clinical
 significance (anemia, intestinal mucosa, hepatic injury and
 regeneration); 3) pathogenesis (dietary inadequacy, intestinal
 malabsorption; hepatobiliary metabolism, urinary excretion);
 and 4) animal models.
 
 
 9                                     NAL Call. No.: SF601.J65
 Alterations in carbohydrate metabolism in canine lymphoma.
 Vail, D.M.; Ogilvie, G.K.; Wheeler, S.L.; Fettman, M.J.;
 Johnston, S.D.; Hegstad, R.L.
 Hagerstown, Md. : American College of Veterinary Medicine;
 1990 Jan. Journal of veterinary internal medicine v. 4 (1): p.
 8-11; 1990 Jan.  Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Lymphoma; Carbohydrate metabolism
 disorders; Blood sugar; Glucose tolerance; Blood serum; Lactic
 acid; Insulin; Cachexia; Disease models; Animal models
 
 
 10                                     NAL Call. No.: 41.8 AM3
 Alternatives to the use of conventional research animals in
 neoplasia research.
 Ladiges, W.C.
 Schaumburg, Ill. : The Association; 1992 Mar01.
 Journal of the American Veterinary Medical Association v. 200
 (5): p. 674-676; 1992 Mar01.  Paper presented at the symposium
 "Animal welfare and alternatives to animals--current knowledge
 and research needs", July 31, 1991, Seattle, Washington. 
 Includes references.
 
 Language:  English
 
 Descriptors: Animal testing alternatives; Medical research;
 Neoplasms; Animal models; Disease models
 
 
 11                                     NAL Call. No.: 41.8 Am3
 Alternatives to the use of conventional research animals in
 neoplasia research.
 Ladiges, W.C. \u University of Washington, Seattle, WA
 Schaumburg, Ill. : The Association; 1992 Mar01.
 Journal of the American Veterinary Medical Association v. 200
 (5): p. 674-676; 1992 Mar01.  Corrects AGRICOLA accession
 number IND92017402 in which the publication year was
 incorrectly entered as 1991.  Paper presented at the symposium
 "Animal welfare and alternatives to animals--current knowledge
 and research needs", July 31, 1991, Seattle, Washington. 
 Includes references.
 
 Language:  English
 
 Descriptors: Animal testing alternatives; Medical research;
 Neoplasms; Animal models; Disease models
 
 
 12                                  NAL Call. No.: QP141.A1J68
 Amino acid availability and brain development: effects of
 nutritional and metabolic inadequacies.
 Huether, G.
 Basingstoke : The Macmillan Press Ltd; 1989.
 European journal of clinical nutrition v. 43 (suppl.1): p.
 19-25; 1989. Includes 25 references.
 
 Language:  English
 
 Descriptors: Amino acids; Bioavailability; Brain disorders;
 Hyperphenylalaninemia; Child development; Protein metabolism;
 Protein synthesis; Malnutrition; Neurotransmitters; Serotonin;
 Animal models; Man
 
 Abstract:  Inadequacies of the brain's amino acid supply are
 relevant to the processes of protein accretion and transmitter
 synthesis during brain development. Experimental
 hyperphenylalaninaemia has demonstrated the consequences of
 rather severe imbalances of the brain's amino acid supply. An
 inadequate supply of essential amino acids has been shown to
 influence a variety of developmental processes.
 
 
 13                                  NAL Call. No.: QP141.A1A63
 Amino acid metabolism in human cancer cachexia.
 Pisters, P.W.T.; Brennan, M.F.
 Palo Alto, Calif. : Annual Reviews, Inc; 1990.
 Annual review of nutrition v. 10: p. 107-132. charts; 1990. 
 Includes 138 references.
 
 Language:  English
 
 Descriptors: Amino acid metabolism; Carcinoma; Cachexia;
 Nitrogen balance; Kinetics; Men; Women
 
 Abstract:  Cancer cachexia is a complex syndrome that occurs
 with variable incidence in patients with solid tumors and
 those with hematologic malignancies. It is associated with
 characteristic physical and laboratory findings, and at a more
 fundamental level, with significant abnormalities in
 carbohydrate, lipid, and protein metabolism. These alterations
 in intermediary metabolism are demonstrable early in the
 syndrome, even before the onset of weight loss, when the more
 characteristic features of cancer cachexia are evident.
 Progressive wasting of peripheral protein stores is a major
 feature of cancer cachexia and often one of the most graphic
 realities of malignancy for patients and their families.
 Unfortunately, significant problems with the animal models of
 cancer cachexia make conclusions derived from animal studies
 difficult to extrapolate to humans. Data from human studies
 indicate that human cancer cachexia is associated with minimal
 aberrations in circulating free amino acid concentrations;
 increased whole-body protein turnover, synthesis, and
 catabolism; reduced rates of skeletal muscle protein
 synthesis; and increased rates of hepatic protein synthesis.
 Whether or not these alterations represent pathologic
 responses or physiologic adaptation by the host to the
 presence of malignancy remains to be seen. Future
 investigations must focus on more careful evaluation of
 interorgan amino acid metabolism, investigation of skeletal
 muscle protein catabolic rates in cancer cachexia, and
 definition of the roles of altered hormonal and cytokine
 regulation of these processes. Such studies will more
 precisely define the level at which amino acid metabolism is
 altered significantly and, we hope, permit more specific
 therapeutic intervention designed to reverse the debilitating
 effects of cancer cachexia.
 
 
 14                                     NAL Call. No.: QP501.C6
 An animal model of systemic carnitine deficiency produced by
 haemodialysis of sheep.
 Snoswell, A.M.; Fishlock, R.C.; Runciman, W.B.; Carapetis, R.
 Oxford : Pergamon Press; 1989.
 Comparative biochemistry and physiology : B : Comparative
 biochemistry v. 93 (4): p. 741-745; 1989.  Includes
 references.
 
 Language:  English
 
 Descriptors: Sheep; Models; Deficiency diseases; Carnitine;
 Hemodialysis
 
 
 15                                     NAL Call. No.: TD172.J6
 An animal model to assess the potential for viral disease
 transmission from lawns irrigated with wastewater.
 Deming, E.J.; Mote, C.R.; Von Bernuth, R.D.; Potgieter, L.N.D.
 New York, N.Y. : Marcel Dekker; 1992 Dec.
 Journal of environmental science and health : Part A :
 Environmental science and engineering v. 27 (8): p. 2199-2211;
 1992 Dec.  Includes references.
 
 Language:  English
 
 Descriptors: Lawns and turf; Irrigation; Waste water;
 Contamination; Porcine enterovirus; Pigs; Disease
 transmission; Animal models; Disease models; Human diseases;
 Infection; Risk
 
 
 16                                    NAL Call. No.: SF95.A1C6
 Animal models for studies of relationships between diet and
 diabetes. Herberg, L.
 Basel : Karger; 1988.
 Comparative animal nutrition v. 6: p. 111-148; 1988.  In the
 series analytic: Use of Animal Models for Research in Human
 Nutrition / edited by A.C. Beynen and C.E. West.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Diabetes mellitus; Pancreas; Insulin; Pituitary
 hormones; Rats; Blood sugar; Dietary carbohydrate; Dietary
 fat; Animal models; Feed intake; Cricetulus barabensis;
 Hyperinsulinemia; Insulin secretion; Literature reviews
 
 
 17                                   NAL Call. No.: QR180.3.D4
 Animal models for the evaluation of drugs and vaccines for HIV
 infection and AIDS: report of a WHO working group.
 Esparza, J.
 Basel : S. Karger; 1990.
 Developments in biological standardization v. 72: p. 367-372;
 1990.  In the series analytic: Progress in animal retroviruses
 / edited by D. Gaudry and W. Hennessen. Meeting held on Oct
 4-6, 1989, Annecy, France.
 
 Language:  English
 
 Descriptors: Disease models; Human immunodeficiency virus;
 Acquired immune deficiency syndrome
 
 
 18                            NAL Call. No.: RC607.A26I63 1989
 Animal models in AIDS.
 Schellekens, Huub; Horzinek, Marian C.
 Nederlandse Centrale Organisatie voor Toegepast-
 Natuurwetenschappelijk Onderzoek
 International TNO Meeting 1989 : Maastricht, Netherlands.
 Amsterdam ; New York : Elsevier ; New York, NY, USA : Sole
 distributors for the USA and Canada, Elsevier Science Pub.
 Co.,; 1990.
 xxii, 380 p. : ill. ; 25 cm.  Includes index.  Includes
 bibliographical references.
 
 Language:  English
 
 Descriptors: AIDS (Disease)
 
 
 19                               NAL Call. No.: QL55.A53  1988
 Animal models in biomedical research proceedings of symposium,
 20-21 January 1988.
 Laboratory Animals Information Service Centre (India)
 Hyderabad, India : Laboratory Animals Information Service
 Centre, National Institute of Nutrition, Indian Council of
 Medical Research, [1988?]; 1988. 79 p., [7] p. of plates :
 ill. ; 25 cm.  Symposium held in New Delhi, India. Includes
 bibliographical references.
 
 Language:  English
 
 Descriptors: Animal models in research; Diseases
 
 
 20                                NAL Call. No.: QL55.F43 1987
 Animal models in hemostasis and thrombosis.
 Rowsell, H.C.
 Dordrecht : M. Nijhoff; 1988.
 New developments in biosciences : their implications for
 laboratory animal science : proceedings of the Third
 Symposium, Amsterdam, The Nethrlands, 1-5 June 1987 / edited
 by Anton C. Beyneen and Henk A. Solleveld. p. 289-294; 1988. 
 Includes references.
 
 Language:  English
 
 Descriptors: Laboratory animals; Disease models; Thrombosis;
 Blood flow; Hemorrhage; Blood coagulation
 
 
 21                                      NAL Call. No.: 475 EX7
 Animal models in interferon research: some current trends.
 Schellekens, H.
 Basel : Birkhauser; 1989 Jun15.
 Experientia v. 45 (6): p. 558-562; 1989 Jun15.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Animal experiments; Animal research; Interferon;
 In vivo; Disease models; Bacterial diseases; Protozoal
 infections; Parasites
 
 
 22                               NAL Call. No.: 41.8  Ad9 v.37
 Animal models in liver research.
 Cornelius, Charles E.
 San Diego : Academic Press,; 1993.
 xx, 479 p. : ill. ; 24 cm. (Advances in veterinary science and
 comparative medicine ; v.37).  Includes bibliographical
 references and index.
 
 Language:  English
 
 Descriptors: Diseases
 
 
 23                                       NAL Call. No.: QR1.F4
 Animal models in the study of pathogenesis.
 Adlam, C.
 Amsterdam : Elsevier Science Publishers; 1988.
 FEMS symposium - Federation of European Microbiological
 Societies v. 40: p. 159-167; 1988.  Includes references.
 
 Language:  English
 
 Descriptors: Animals; Models; Pathogenesis; Bovine mastitis;
 Rhinitis; Lymphadenitis; Sheep; Respiratory diseases
 
 
 24                                   NAL Call. No.: QP141.A1C8
 Animal models of appetitive behavior: interaction of
 nutritional factors and drug seeking behavior.
 Kanarek, R.B.; Marks-Kaufman, R.
 New York, N.Y. : Wiley; 1988.
 Current concepts in nutrition v. 16: p. 1-5; 1988.  Includes
 references.
 
 Language:  English
 
 Descriptors: Feeding behavior; Appetite; Models; Nutrition;
 Drug effects; Interactions
 
 
 25                                    NAL Call. No.: QP601.M49
 Animal models of chronic ethanol toxicity.
 Lieber, C.S.; DeCarli, L.M.
 New York : Academic Press, 1955-; 1994.
 Methods in enzymology. p. 585-594; 1994.  In the series
 analytic: Oxygen radicals in biological systems (Part C) /
 edited by L. Packer.  Includes references.
 
 Language:  English
 
 Descriptors: Ethanol; Toxicity; Chronic course; Diet; Liquid
 diets; Liver; Animal models; Papio; Rats
 
 
 26                                    NAL Call. No.: SF95.A1C6
 Animal models of diet-induced atherosclerosis.
 Clarkson, T.B.; Shively, C.A.; Weingand, K.W.
 Basel : Karger; 1988.
 Comparative animal nutrition v. 6: p. 56-82; 1988.  In the
 series analytic: Use of Animal Models for Research in Human
 Nutrition / edited by A.C. Beynen and C.E. West.  Includes
 references.
 
 Language:  English
 
 Descriptors: Animal models; Experimental atherosclerosis;
 Atherogenic diet; Rabbits; Pigeons; Pigs; Primates;
 Pathogenesis
 
 
 27                                    NAL Call. No.: aZ5071.N3
 Animal models of disease 1979-August 1988.
 Swanson, J.C.
 Beltsville, Md. : The Library; 1988 Nov.
 Quick bibliography series - U.S. Department of Agriculure,
 National Agricultural Library (U.S.). (89-07): 25 p.; 1988
 Nov.  Bibliography.
 
 Language:  English
 
 Descriptors: Animals; Disease models; Animal welfare;
 Bibliographies
 
 
 28                                    NAL Call. No.: aZ5071.N3
 Animal models of disease, January 1979-August 1989.
 Swanson, J.; Clingerman, K.
 Beltsville, Md. : The Library; 1989 Dec.
 Quick bibliography series - U.S. Department of Agriculure,
 National Agricultural Library (U.S.). (90-09): 27 p.; 1989
 Dec.  Updates QB 89-07. Bibliography.
 
 Language:  English
 
 Descriptors: Animals; Laboratory animals; Animal diseases;
 Disease models; Bibliographies
 
 
 29                                    NAL Call. No.: aZ5071.N3
 Animal models of disease, January 1988-January 1994.
 Smith, C.P.; Larson, J.A.
 Beltsville, Md., National Agricultural Library; 1994 Mar.
 Quick bibliography series - National Agricultural Library
 (94-19): 83 p.; 1994 Mar.  Updates QB 92-61.
 
 Language:  English
 
 Descriptors: Animal models; Disease models; Bibliographies
 
 
 30                                    NAL Call. No.: aZ5071.N3
 Animal models of disease--January 1979-December 1990.
 Smith, C.P.
 Beltsville, Md. : The Library; 1991 Feb.
 Quick bibliography series - U.S. Department of Agriculture,
 National Agricultural Library (U.S.). (91-42): 38 p.; 1991
 Feb.  Updates QB 90-09. Bibliography.
 
 Language:  English
 
 Descriptors: Animal models; Diseases; Bibliographies
 
 
 31                                    NAL Call. No.: aZ5071.N3
 Animal models of disease--January 1981-July 1992.
 Smith, C.P.
 Beltsville, Md. : The Library; 1992 Aug.
 Quick bibliography series - U.S. Department of Agriculture,
 National Agricultural Library (U.S.). (92-61): 59 p.; 1992
 Aug.  Updates QB 91-42.
 
 Language:  English
 
 Descriptors: Animal diseases; Disease models; Bibliographies
 
 
 32                           NAL Call. No.: QR201.A37A55  1993
 Animal models of HIV and other retroviral infections.
 Racz, Paul; Letvin, Norman L.; Gluckman, J. C.
 Basel ; New York : Karger,; 1993.
 viii, 200 p. : ill. (some col.) ; 25 cm.  Includes
 bibliographical references and index.
 
 Language:  English
 
 Descriptors: HIV infections; Retrovirus infections
 
 
 33                                     NAL Call. No.: 500 N484
 Animal models of human eating disorders.
 Smith, G.P.
 New York, N.Y. : The Academy; 1989.
 Annals of the New York Academy of Sciences v. 575: p. 63-74;
 1989.  In the series analytic: The psychology of human eating
 disorders: preclinical and clinical perspectives / edited by
 L.H. Schneider, S.J. Cooper, and K.A. Halmi.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Nutritional disorders; Human nutrition research;
 Animal experiments; Anorexia nervosa; Bulimia nervosa; Models
 
 
 34                                     NAL Call. No.: 41.8 Ad9
 Animal models of liver fibrosis.
 Rojkind, M. \u Albert Einstein College of Medicine, Bronx, NY;
 Greenwel, P. San Diego, Calif. : Academic Press; 1993.
 Advances in veterinary science and comparative medicine v. 37:
 p. 333-355; 1993.  In the series analytic: Animal models in
 liver research / edited by Charles E. Cornelius.  Includes
 references.
 
 Language:  English
 
 Descriptors: Liver diseases; Animal models; Alcoholism;
 Schistosomiasis; Carbon tetrachloride
 
 
 35                                     NAL Call. No.: 41.8 P27
 Animal models of retrovirus-associated malignancies.
 Cremer, K.J.; Gruber, J.
 Lawrence, Kan. : American College of Veterinary Pathologists;
 1992 Nov. Veterinary pathology v. 29 (6): p. 572-578; 1992
 Nov.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Retroviridae
 
 
 36                                    NAL Call. No.: QH301.N32
 Animal studies of iodized oils: iodine disposition and
 physiological effects. Chambon, C.; Chastin, I.
 New York, N.Y. : Plenum Press; 1993.
 NATO ASI series : Series A : Life sciences v. 241: p. 159-167;
 1993.  In the series analytic: Iodine deficiency in Europe: a
 continuing concern / edited by F. Delange, J.T. Dunn, and D.
 Glioner. Proceedings of an International Workshop, April
 24-28, 1992, Brussels, Belgium. Includes a discussion, p.
 166-167.  Includes references.
 
 Language:  English
 
 Descriptors: Cooking oils; Deficiency diseases; Goiter; Human
 diseases; Iodine; Physiopathology; Rats; Animal models;
 Livestock
 
 
 37                                     NAL Call. No.: 41.8 Am3
 Animals as a source of Escherichia coli pathogenic for human
 beings. Whipp, S.C.; Rasmussen, M.A.; Cray, W.C. Jr
 Schaumburg, Ill. : The Association; 1994 Apr15.
 Journal of the American Veterinary Medical Association v. 204
 (8): p. 1168-1175; 1994 Apr15.  Includes references.
 
 Language:  English
 
 Descriptors: Cattle; Escherichia; Escherichia coli;
 Pathogenicity; Man; Disease prevalence; Animal models; Human
 diseases; Gastrointestinal diseases
 
 
 38                                   NAL Call. No.: 389.1 W892
 Antiarrhythmic effects of fish oils.
 Charnock, J.S.
 Basel : S. Karger; 1991.
 World review of nutrition and dietetics v. 66: p. 278-291;
 1991.  In the series analytic: Health effects of omega 3
 polyunsaturated fatty acids in seafoods / edited by A.P.
 Simopoulos, R.R. Kifer, Martin, R.E. and S.M. Barlow. 
 Includes references.
 
 Language:  English
 
 Descriptors: Fish oils; Heart rate; Supplements; Animal
 models; Polyenoic fatty acids; Dietary fat; Muscle
 contraction; Animal experiments; Literature reviews
 
 
 39                                    NAL Call. No.: QH426.T74
 Atherosclerosis in mice: getting to the heart of a polygenic
 disorder. Rubin, E.M.; Smith, D.J.
 Cambridge, U.K. : Elsevier Trends Journals; 1994 Jun.
 Trends in genetics v. 10 (6): p. 199-203; 1994 Jun.  Includes
 references.
 
 Language:  English
 
 Descriptors: Mice; Atherosclerosis; Animal models; Transgenic
 animals; Genetic engineering; Apolipoproteins; High density
 lipoprotein; Literature reviews; Low density lipoprotein;
 Induced mutations
 
 Abstract:  The mouse is being increasingly used as a model
 system for understanding the common and complex polygenic
 condition of atherosclerosis. Mice have been created in which
 genes involved in this condition have been overexpressed or
 have been altered by gene targeting. Here, we concentrate on
 recent experiments that use transgenic and gene knockout mice
 as an in vivo assay system to unravel the interactions between
 various genes involved in atherogenesis. We focus in
 particular on examples in which unique insights into the human
 condition have been derived from studies in mice.
 
 
 40                                  NAL Call. No.: SF910.T8A86
 Atlas of tumor pathology of the Fischer rat..  Fischer rat
 Stinson, Sherman F.,_1946-; Schuller, Hildegard M.; Reznik,
 Gerd Boca Raton, Fla : CRC Press,; 1990.
 546 p. : ill. ; 27 cm.  Includes bibliographical references
 and index.
 
 Language:  English
 
 Descriptors: Tumors in animals; Atlases; Rats as laboratory
 animals; Atlases; Rats; Diseases; Atlases; Tumors; Animal
 models; Atlases
 
 
 41                                    NAL Call. No.: 447.8 Am3
 Atrial natriuretic peptide and glomerular hyperfiltration
 during onset of spontaneous diabetes mellitus.
 Okwueze, M.I.; Opgenorth, T.J.; Von Geldern, T.W.; Vari, R.C.
 Bethesda, Md. : American Physiological Society, 1898-; 1994
 Feb. American journal of physiology v. 266 (2,pt.2): p. R572-
 R577; 1994 Feb. Includes references.
 
 Language:  English
 
 Descriptors: Diabetes mellitus; Glomerular filtration rate;
 Peptides; Receptors; Antagonists; Hemodynamics; Kidneys; Rats
 
 Abstract:  The mechanisms responsible for the elevation of
 glomerular filtration rate (GFR) in early stages of insulin-
 dependent diabetes mellitus (IDDM) are undefined. The
 objectives of this study were to define the temporal pattern
 of onset of glomerular hyperfiltration in the spontaneously
 diabetes-prone (BB/DP) rat and to evaluate the possible role
 of atrial natriuretic peptide (ANP) as the primary mediator of
 the observed alterations in renal hemodynamics. GFR was
 significantly higher (1.38 +/- 0.07 ml.min-1.g-1; n = 5) in
 moderately hyperglycemic BB/DP rats (blood glucose > 270
 mg/dl) 14 days after the onset of IDDM compared with age-
 matched diabetes-resistant rats (BB/DR), which averaged 1.03
 +/- 0.07 ml.min-1.g-1 (n = 7). Circulating ANP levels in
 moderately hyperglycemic BB/DP rats 1, 7, and 14 days after
 onset of IDDM were within the normal range, averaging 100 +/-
 21, 57 +/- 12, and 65 +/- 6 pg/ml, respectively, and were not
 significantly different (P > 0.05) from ANP levels in age-
 matched normoglycemic BB/DR rats. To further test the role of
 ANP in glomerular hyperfiltration, an ANP receptor antagonist
 was infused into anesthetized BB/DP rats (n = 10) 14 days
 after onset of IDDM, after baseline measurements of mean
 arterial pressure, renal hemodynamics, and renal fluid and
 electrolyte excretions. ANP receptor antagonism caused a
 significant reduction in mean arterial pressure from 120 +/- 3
 to 103 +/- 2 mmHg; however, there were no significant effects
 of ANP receptor blockade on GFR. These results indicate that
 1) glomerular hyperfiltration occurs within the first 2 wk
 after onset of IDDM in the moderately hyperglycemic BB/DP rat
 and 2) ANP is not the primary mediator of glomerular
 hyperfiltration during the onset of diabetes in this animal
 model of spontaneous IDDM.
 
 
 42                                    NAL Call. No.: 448.8 V81
 Attenuating mutations in the E2 glycoprotein gene of
 Venezuelan equine encephalitis virus: construction of single
 and multiple mutants in a full-length cDNA clone.
 Davis, N.L.; Powell, N.; Greenwald, G.F.; Willis, L.V.;
 Johnson, B.J.B.; Smith, J.F.; Johnston, R.E.
 Duluth, Minn. : Academic Press; 1991 Jul.
 Virology v. 183 (1): p. 20-31; 1991 Jul.  Includes references.
 
 Language:  English
 
 Descriptors: Venezuelan equine encephalitis virus; Mutants;
 Mutations; Clones; Phenotypes; Live vaccines; Attenuation;
 Glycoproteins; Genes; Virulence; Immune response; Pathogenesis
 
 Abstract:  Attenuated mutants of Venezuelan equine
 encephalitis virus (VEE) were isolated by selection for rapid
 penetration of cultured cells (R.E.Johnston and J.F. Smith,
 1988, Virology 162, 437-443). Sequence analysis of these
 mutants identified candidate attenuating mutations at four
 loci in the VEE E2 glycoprotein gene: a double mutation at E2
 codons 3 and 4, and single substitutions at E2 76, 120, and
 209. Each candidate mutation was reproduced in an isogenic
 recombinant VEE strain using site-directed mutagenesis of a
 full-length cDNA clone of VEE. Characterization of these
 molecularly cloned mutant viruses showed that mutation at each
 of the four loci in the E2 gene was sufficient to confer both
 the accelerated penetration and attenuation phenotypes.
 Inoculation of the molecularly cloned viruses into rodent
 models that differ in their response to VEE suggested that
 individual mutations affected different aspects of VEE
 pathogenesis. Full-length clones containing multiple mutations
 were produced by combining independently attenuating
 mutations. Molecularly cloned viruses carrying two or three
 mutations were more attenuated in sensitive animal models than
 viruses which contained any single mutation alone. However,
 these highly attenuated strains still retained the ability to
 induce an immune response sufficient to protect against a high
 dose challenge with virulent VEE. These results indicate that
 production of a molecularly cloned live virus vaccine for VEE
 is feasible.
 
 
 43                                     NAL Call. No.: 41.8 Ad9
 Avian fatty liver hemorrhagic syndrome: a comparative review.
 Hansen, R.J. \u University of California, Davis, CA; Walzem,
 R.L. San Diego, Calif. : Academic Press; 1993.
 Advances in veterinary science and comparative medicine v. 37:
 p. 451-468; 1993.  In the series analytic: Animal models in
 liver research / edited by Charles E. Cornelius.  Includes
 references.
 
 Language:  English
 
 Descriptors: Hens; Fatty liver; Fatty liver hemorrhagic
 syndrome; Animal models; Lipid metabolism; Transport;
 Pathogenesis; Man; Cows; Cats; Literature reviews
 
 
 44                                   NAL Call. No.: HV5285.A43
 Behavioral animal models in alcohol abuse research.
 Grant, K.A.
 Washington, D.C. : U.S. Department of Health and Human
 Services; 1990. Alcohol health and research world - National
 Institute on Alcohol Abuse and Alcoholism v. 14 (3): p.
 187-192; 1990.  Includes references.
 
 Language:  English
 
 Descriptors: Alcoholism; Drinking behavior; Animal
 experiments; Laboratory animals; Animal models
 
 
 45                                     NAL Call. No.: 500 N21P
 beta-Cell lipotoxicity in the pathogenesis of non-insulin-
 dependent diabetes mellitus of obese rates: Impairment in
 adipocyte-beta-cell relationships. Lee, Y.; Hirose, H.;
 Ohneda, M.; Johnson, J.H.; McGarry, J.D.; Unger, R.H.
 Washington, D.C. : National Academy of Sciences,; 1994 Nov08.
 Proceedings of the National Academy of Sciences of the United
 States of America v. 91 (23): p. 10878-10882; 1994 Nov08. 
 Includes references.
 
 Language:  English
 
 Descriptors: Rats; Diabetes mellitus; Pancreas islets;
 Pathogenesis; Blood lipids; Fatty acids; Hyperglycemia;
 Insulin secretion; Lipid metabolism disorders; Animal models;
 Obesity; Experimental diabetes
 
 Abstract:  Hyperinsulinemia, Ioss of glucose-stimulated
 insulin secretion (GSIS), and peripheral insulin resistance
 coexist in non-insulin-dependent diabetes mellitus (NIDDM).
 Because free fatty acids (FFA) can induce these same
 abnormalities, we studied their role in the pathogenesis NIDDM
 of obese Zucker diabetic fatty (ZDF-drt) rats from 5 weeks of
 age (before the onset of hyperglycemia) until 14 weeks. Two
 weeks prior to hyperglycemia, plasma FFA began to rise
 progressively, averaging 1.9 + 0.06 mM at the onset of
 hyperglycemia (P < 0.001 vs. controls). At this time GSIS was
 absent and beta-cell GLUT-2 glucose transporter was decreased.
 The triacylglycerol content of prediabetic islets rose to 10
 times that of controls and was correlated with plasma FFA (r =
 0.825; P < 0.001), which, in turn. was correlated with the
 plasma glucose concentration (r = 0.873; P < 0.001). Reduction
 of hyperlipacidemia to 1.3 +/- 0.07 mM by pair feeding with
 lean littermates reduced all beta-cell abnormalities and
 prevented hyperglycemia. Normal rat islets that had been
 cultured for 7 days in medium containing 2 mM FFA exhibited
 increased basal insulin secretion at 3 mM glucose, and first-
 phase GSIS was reduced by 68%; in prediabetic islets, first-
 phase GSIS was reduced by 69% by FFA. The results suggest a
 role for hyperlipacidemia in the pathogenesis of NIDDM:
 resistance to insulin-mediated antilipolysis is invoked to
 explain the high FFA despite hyperinsulinemia, and sensitivity
 of beta cells to hyperlipacidemia is invoked to explain the
 FFA-induced loss of GSIS.
 
 
 46                                     NAL Call. No.: 41.8 Ad9
 Biliary atresia in lampreys.
 Youson, J.H. \u University of Toronto, Ontario, Canada
 San Diego, Calif. : Academic Press; 1993.
 Advances in veterinary science and comparative medicine v. 37:
 p. 197-255; 1993.  In the series analytic: Animal models in
 liver research / edited by Charles E. Cornelius.  Includes
 references.
 
 Language:  English
 
 Descriptors: Liver diseases; Atresia; Liver; Lampreys; Bile
 ducts; Life cycle; Animal models; Literature reviews
 
 
 47                         NAL Call. No.: TP248.2.B55126  1993
 Biotechnology and safety assessment.
 Thomas, J. A._1933-; Myers, Laurie A.
 New York : Raven Press,; 1993.
 ix, 270 p. : ill. ; 25 cm.  Includes bibliographical
 references and index.
 
 Language:  English
 
 Descriptors: Biotechnology; Health risk assessment
 
 
 48                                NAL Call. No.: QL55.F43 1987
 Blastomere karyotyping: a direct method for producing mouse
 trisomy 16 less than leads to diploid aggregation chimeras as
 an animal model of human down's syndrome.
 Bacchus, C.; Buselmaier, W.
 Dordrecht : M. Nijhoff; 1988.
 New developments in biosciences : their implications for
 laboratory animal science : proceedings of the Third
 Symposium, Amsterdam, The Nethrlands, 1-5 June 1987 / edited
 by Anton C. Beyneen and Henk A. Solleveld. p. 405-408. ill;
 1988.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Blastomere; Karyotypes; Trisomy; Diploidy;
 Chimeras; Disease models; Down's syndrome
 
 
 49                                     NAL Call. No.: QR360.J6
 Borna disease virus in mice: host-specific differences in
 disease expression. Rubin, S.A.; Waltrip, R.W. II; Bautista,
 J.R.; Carbone, K.M. Washington, D.C. : American Society for
 Microbiology; 1993 Jan. Journal of virology v. 67 (1): p.
 548-552; 1993 Jan.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Bo RNAdisease virus; Animal models;
 Experimental infections; Immunopathology; Antibody formation;
 Inflammation; Strain differences; Encephalitis; Abnormal
 behavior
 
 Abstract:  We developed a mouse model of Borna disease to
 facilitate immunopathogenesis research by adaptation of Borna
 disease virus to mice through serial passage in mouse brain
 tissue. Borna disease virus replication, antibody production,
 inflammation, and Borna disease expression in several
 different strains of mice were examined.
 
 
 50                                     NAL Call. No.: QR360.J6
 Bovine leukemia virus, an animal model for the study of
 intrastrain variability.
 Willems, L.; Thienpont, E.; Kerkhofs, P.; Burny, A.;
 Mammerickx, M.; Kettmann, R.
 Washington, D.C. : American Society for Microbiology; 1993
 Feb. Journal of virology v. 67 (2): p. 1086-1089; 1993 Feb. 
 Includes references.
 
 Language:  English
 
 Descriptors: Sheep; Bovine oncovirus; Genetic variation;
 Structural genes; Viral proteins; Repetitive  DNA; Nucleotide
 sequences; Strain differences; Mutations
 
 Abstract:  Intradermal injection of a cloned bovine leukemia
 virus (BLV) provirus (pV344) into sheep allowed direct
 evaluation of intrastrain variability. A sheep was injected
 with pV344 DNA mixed with DEAE-dextran and became persistently
 infected with BLV strain 344. After 18 months, DNA was
 extracted from peripheral blood leukocytes from a single 0.5-
 ml blood sample. The long terminal repeat (LTR) and the env
 gene were amplified by using the polymerase chain reaction,
 cloned, and sequenced. Nineteen independent LTR clones (0.6-kb
 inserts) and 16 env clones (1-kb inserts) were analyzed. The
 in vivo rate of nucleotide change was 0.009%/year (two
 mutations out of 14,464 bp in 1.5 years), corresponding to
 only one amino acid change in the env gene. Five point
 mutations (all transitions), corresponding to a modification
 rate of 0.034%/year (five mutations out of 9,709 bp in 1.5
 years), were identified in the LTR. As a control for Taq DNA
 polymerase errors, the same procedure using pV344 plasmid DNA
 was carried out. Out of 9,944 bp sequenced, three point
 mutations were found (i.e., one misincorporation in 3,315
 nucleotides). These data demonstrate the extremely low level
 (or absence) of intrastrain variability of BLV in vivo.
 Consequently, BLV persistence in the infected host does not
 seem to result from an escape mutant strategy, in sharp
 contrast with the high mutation rates observed in the
 lentivirus family. The lack of genetic variation supports the
 possibility of successful vaccine against BLV and probably
 against the related human T-cell leukemia viruses.
 
 
 51                                    NAL Call. No.: SF601.C66
 Bovine leukemia virus. III. Zoonotic potential, molecular
 epidemiology, and an animal model.
 Johnson, R.
 Trenton, N.J. : Veterinary Learning Systems Company, Inc; 1991
 Oct. The Compendium on continuing education for the practicing
 veterinarian v. 13 (10): p. 1631-1640; 1991 Oct.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Dairy cattle; Bovine oncovirus; Zoonoses; Risk;
 Molecular biology; Epidemiology; Disease models; Animal
 models; Human diseases; Leukemia; Literature reviews
 
 
 52                                  NAL Call. No.: QP141.A1P72
 Brain iron: location and function.
 Beard, J.L.; Connor, J.D.; Jones, B.C.
 Tarrytown, N.Y. : Pergamon Press; 1993 Jul.
 Progress in food & nutrition science v. 17 (3): p. 183-221;
 1993 Jul. Includes references.
 
 Language:  English
 
 Descriptors: Iron; Brain; Nutrition physiology; Mental
 ability; Mineral deficiencies; Tissues; Mineral content; Blood
 picture; Central nervous system; Animal models; Ferritin;
 Transferrin; Multiple sclerosis; Alzheimer's disease;
 Parkinson's disease; Neurotransmitters; Human behavior;
 Neuroleptics; Literature reviews
 
 Abstract:  This review has a focus on the distribution and
 function of iron in human brain and appropriate animal models.
 Data are presented on the consequences of abnormalities of
 iron status with regard to neural development,
 neurotransmitter metabolism, and cognition.
 
 
 53                                   NAL Call. No.: RC628.O294
 BSB: a new mouse model of multigenic obesity.
 Fisler, J.S. \u University of California, Los Angeles, CA;
 Warden, C.H.; Pace, M.J.; Lusis, A.J.
 Baton Rouge, LA : North American Association for the Study of
 Obesity, c1993-; 1993 Jul.
 Obesity research v. 1 (4): p. 271-280; 1993 Jul.  Includes
 references.
 
 Language:  English
 
 Descriptors: Obesity; Multiple genes; Phenotypes; Genetic
 models; Animal models; Mice
 
 
 54                                      NAL Call. No.: QR1.I57
 BvgAS-mediated signal transduction: analysis of phase-locked
 regulatory mutants of Bordetella bronchiseptica in a rabbit
 model.
 Cotter, P.A.; Miller, J.F.
 Washington, D.C., American Society for Microbiology; 1994 Aug.
 Infection and immunity v. 62 (8): p. 3381-3390; 1994 Aug. 
 Includes references.
 
 Language:  English
 
 Descriptors: Bordetella bronchiseptica; Mutants; Phenotypes;
 Animal models; Bacterial proteins; Transduction; Strain
 differences; Virulence; Colonizing ability
 
 Abstract:  Members of the Bordetella genus alternate between
 two distinct phenotypic phases in response to changes in their
 environment. This switch, termed phenotypic modulation, is
 mediated by the BvgAS sensory transduction system. We
 developed an animal model based on the interaction of
 Bordetella bronchiseptica with one of its natural hosts, the
 rabbit. To investigate the importance of BvgAS signal
 transduction, we constructed constitutive (RB53) and Bvg-
 (RB54) phase-locked derivatives of a wild-type strain, RB50.
 RB50 and RB53, but not RB54, established respiratory
 infections in B. bronchiseptica-free rabbits with an
 intranasal 50% infective dose of less than 200 organisms, and
 the course of the infection closely resembled that observed
 with naturally infected rabbits. Bacteria were recovered from
 the nasal cavity, larynx, trachea, and lungs in similar
 numbers from RB50- and RB53-infected rabbits, yet no pathology
 was detected by histological examination of lung and tracheal
 sections. The antibody responses in rabbits inoculated with 50
 or RB53 were quantitatively and qualitatively
 indistinguishable, high titers of antibodies were generated
 primarily against Bvg+ -phase-specific antigens. No response
 against flagella, a Bvg- phase factor, was detected.
 Assessment of bacteria associated with alveolar macrophages
 indicated that only a small percentage of bacteria, if any,
 appear to be residing within lung macrophages. We also tested
 the ability of these strains to survive in a nutrient poor
 environment, conditions which may be encountered within
 certain niches in the host or in an environmental reservoir.
 The Bvg- phase was advantageous for growth under these
 conditions. Our results indicate the Bvg+ phase is sufficient
 for establishment of respiratory tract infection in the rabbit
 and the normal BvgAS-mediated response to environmental
 signals is not required during initial colonization. The Bvg-
 phase may play a role at later stages of infection, including
 persistence, transmission, or survival in the environment.
 
 
 55                                    NAL Call. No.: 410.9 P94
 Canine models of bone marrow transplantation.
 Ladiges, W.C.; Storb, R.; Thomas, E.D.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1990 Jan. Laboratory animal science v. 40 (1): p.
 11-15; 1990 Jan.  Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Bone marrow transplant; Models; Human
 diseases
 
 Abstract:  Progress in experimental bone marrow
 transplantation in dogs has provided for the direct transfer
 of research data to the clinical setting and the therapeutic
 application of marrow grafting to a variety of human diseases.
 Animal models of total body irradiation, engraftment and
 graft-versus-host disease are still needed to solve the
 existing clinical problems of marrow transplantation.
 Therefore, work in various canine model systems continues to
 be of interest. Pet dogs with spontaneously occurring
 lymphomas are used to study the clinical parameters necessary
 for applying the technique of transplanting their own marrow
 (autologous), in conjunction with high dose radiation and/or
 chemotherapy, to human patients with cancer. A major
 consideration in the successful transplantation of donor bone
 marrow (allogeneic) is overcoming histocompatibility barriers
 to assure engraftment and the prevention of graft-versus-host
 disease, a major limiting aspect of clinical marrow
 transplantation. Chemicals, radiation, radiotherapeutic
 techniques, antisera and monoclonal antibodies have been and
 continue to be developed in laboratory bred dogs. These
 approaches suppress the immune system either nonspecifically
 by ablation of immune reactive tissue, or specifically by
 affecting certain types of immune reactive cells. Parameters
 such as clinical effectiveness (engraftment or prevention of
 graft-versus-host disease), immune reconstitution and
 undesirable side affects in long-term survivors are all used
 to determine whether new technology can be transferred from
 preclinical canine studies to human bone marrow
 transplantation protocols.
 
 
 56                                     NAL Call. No.: 500 N21P
 Canine X chromosome-linked hereditary nephritis: a genetic
 model for human X-linked hereditary nephritis resulting from a
 single base mutation in the gene encoding the alpha-5 chain of
 collagen type IV.
 Zheng, K.; Thorner, P.S.; Marrano, P.; Baumal, R.; McInnes,
 R.R. Washington, D.C. : National Academy of Sciences,; 1994
 Apr26. Proceedings of the National Academy of Sciences of the
 United States of America v. 91 (9): p. 3989-3993; 1994 Apr26. 
 Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Hereditary diseases; Nephritis; Structural
 genes; Collagen; Mutations; Nucleotide sequences; Exons; Sex
 linkage; X chromosome; Animal models; Kidneys; Amino acid
 sequences
 
 Abstract:  Many families with X-chromosome linked hereditary
 nephritis (HN) have mutations in the gene on the X chromosome
 that codes for the alpha5 chain of collagen type IV. Canine X-
 linked HN is an animal model for human X-linked HN. To study
 the alpha5(IV) gene in this model, we used the nucleotide
 sequence published for the human alpha5(IV) cDNA to construct
 sets of primers covering approximately equal 95% of the
 complete cDNA. cDNA from both affected and normal dog kidneys
 was amplified by PCR in nine overlapping regions. The
 nucleotide sequence encoding the noncollagenous domain NC1
 hybridized to the human X chromosome and was 93% identical at
 the DNA level and 97% identical at the protein level to the
 human alpha 5(IV) NC1 domain, confirming that the canine alpha
 5(IV) cDNA had been amplified. Sequence analysis of the alpha
 5(IV) cDNA detected a single nucleotide substitution, G leads
 to T, in affected dogs, changing a codon for a conserved
 glycine residue (GGA) to a stop codon (TGA). When genomic DNA
 was amplified, the same abnormality was found in exon 35.
 Using the canine NC1 domain cDNA as a probe for Northern
 analysis, two transcripts of approximately equal to 8.6 kb and
 approximately equal to 6.7 kb were identified in both normal
 and affected male dog kidney RNA. However, the abundance of
 both transcripts was decreased by a factor of approximately
 equal 10 in the affected dog. These results establish at the
 molecular level that canine X-linked HN is a model for human
 X-linked HN. This model provides an opportunity to determine
 the efficacy of new therapies and to investigate the role of
 the alpha5(IV) chain in type IV collagen assembly.
 
 
 57                                    NAL Call. No.: 442.8 L62
 Cardiovascular abnormalities associated with human and rodent
 obesity. Paulson, D.J.; Tahiliani, A.G.
 Tarrytown, N.Y. : Pergamon Press Inc; 1992.
 Life sciences v. 51 (20): p. 1557-1569; 1992.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Diet; Weight reduction; Cardiovascular
 diseases; Heart; Animal models; Rats; Man; Literature reviews
 
 Abstract:  Obesity is a major risk factor for cardiovascular
 disease. However, a direct link between these two states is
 difficult to establish, since obesity frequently occurs with
 other disease states such as diabetes, hypertension and
 atherosclerosis. Clinical studies have clearly shown that
 uncorrected obesity is associated with cardiac hypertrophy and
 compromised ventricular function. A number of rodent models of
 obesity have been studied in terms of cardiovascular
 adaptations. Cardiac function of the obese Zucker rat appears
 to be normal at a younger age. Only after several months is
 depression in cardiac function discernable. These animals are
 mildly hypertensive, but do not exhibit the characteristic
 increase in cardiac output associated with human obesity. A
 unique characteristic of JCR:LA-cp rat is that they develop
 atherosclerotic and myocardial lesions. Hearts from these
 animals will maintain normal function when perfused with
 physiological levels of calcium. At higher calcium
 concentrations, however, mechanical function becomes impaired.
 Dietary-induced obese rats exhibit many of the hemodynamic
 alterations associated with human obesity, but there is no
 evidence to-date that these animals will develop severe
 cardiac depression. Short-term weight reduction apparently has
 beneficial cardiovascular effects, but weight cycling may be
 harmful. Given the widespread occurrence of obesity, further
 studies are warranted to characterize the cardiac
 manifestations of this condition.
 
 
 58                                       NAL Call. No.: QP1.C6
 Carnitine prolongs the half-life of ethanol in broilers.
 Smith, M.O.; Cha, Y.S.; Sachan, D.S.
 Oxford : Pergamon Press Ltd; 1994 Sep.
 Comparative biochemistry and physiology. A: Comparative
 physiology v. 109A (1): p. 177-180; 1994 Sep.  Includes
 references.
 
 Language:  English
 
 Descriptors: Ethanol; Metabolism; Carnitine; Supplements;
 Broilers; Animal models
 
 Abstract:  The object was to determine if carnitine attenuated
 ethanol metabolism in broilers similar to that reported in the
 rats. Two groups (n = 5) of 5-week-old broilers were given for
 10 days the feed with or without 0.5% L-carnitine supplement.
 A single oral dose of ethanol on day 8 was followed by serial
 blood samples which were analysed for ethanol. Another dose of
 ethanol was given on day 10 and 2 hr later, plasma and liver
 were collected and analysed for ethanol, total lipid,
 triglycerides and carnitine. The carnitine supplemented diet
 prolonged the half-life of ethanol due to attenuation of
 ethanol metabolism which is similar to that reported earlier
 in rodents. The increases in plasma and hepatic acylcarnitines
 indicate that supplementary carnitine lessens the load of free
 acyl groups in the liver by eventual oxidation or excretion.
 
 
 59                                    NAL Call. No.: 389.8 J82
 The carnitine-deprived newborn rabbit: a potential model to
 study carnitine deficiency.
 Penn, D.; Schmidt-Sommerfeld, E.
 Bethesda, Md. : American Institute of Nutrition; 1988 Dec. The
 Journal of nutrition v. 118 (12): p. 1535-1539; 1988 Dec. 
 Includes 34 references.
 
 Language:  English
 
 Descriptors: Nutrient deficiencies; Carnitine; Neonates;
 Rabbits
 
 Abstract:  This report describes the novel development of an
 animal model for neonatal carnitine deficiency using the
 artificially fed newborn rabbit. Each litter was separated
 from the mother following the first colostrum feeding and
 divided into 2 groups, one of which was fed a purified rabbit
 formula that was essentially free of carnitine; the other
 received the same formula supplemented with L-carnitine (100
 mg/l). At 9-13 d of age, rabbit pups receiving the carnitine-
 free formula had lower concentrations of total, free and
 acylcarnitine in plasma and urine, as well as lower total acid
 soluble carnitine concentrations in liver, muscle, heart and
 brown adipose tissue than those receiving the same formula
 supplemented with L-carnitine. Their plasma and tissue levels
 were also lower, but their urinary carnitine concentrations
 were higher than those in naturally-raised pups. The findings
 suggest that the described animal model may prove to be a
 useful tool for the investigation of certain aspects of
 neonatal carnitine deficiency.
 
 
 60                                    NAL Call. No.: 389.8 J82
 Carotenoids and cancer in animal models.
 Krinsky, N.I.
 Bethesda, Md. : American Institute of Nutrition; 1989 Jan. The
 Journal of nutrition v. 119 (1): p. 123-126; 1989 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Diet; Carotenoids; Carcinoma; Disease prevention
 
 Abstract:  As evidence accumulated from epidemiological
 studies that beta-carotene acts as a chemopreventive agent
 with respect to inhibiting the appearance of certain types of
 tumors in humans, attention focused on animal models as a
 means of extending our understanding of carotenoid function.
 Unfortunately, most animals used in research are "white fat"
 animals, and require large amounts of carotenoids in their
 diets to obtain significant blood and tissue levels. Even with
 these limitations, beta-carotene, a provitamin A carotenoid,
 as well as canthaxanthin, a nonprovitamin A carotenoid, have
 been shown to protect animals against UV-induced skin tumors,
 UV and carcinogen-induced tumors, and carcinogen treatment
 alone. Similar observations have been made in cell and organ
 cultures where carotenoids have been shown to prevent
 malignant transformation and nuclear damage. Although the
 mechanism of this protection is still unclear, the evidence
 continues to accumulate that carotenoids may possess intrinsic
 chemopreventive action with respect to tumor formation.
 
 
 61                                    NAL Call. No.: 410.9 P94
 Cataracts in a laboratory colony of ferrets.
 Miller, P.E.; Marlar, A.B.; Dubielzig, R.R.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1993 Dec. Laboratory animal science v. 43 (6): p.
 562-568; 1993 Dec.  Includes references.
 
 Language:  English
 
 Descriptors: Ferrets; Cataract; Disease prevalence;
 Histopathology; Animal models; Disease models
 
 Abstract:  Cataracts were found by use of slit-lamp
 biomicroscopy in two genetically unrelated ferret populations
 (A and B). When they were initially examined at the age of 11
 to 12 months, 34 of 73 ferrets (46.6%) in population A had
 lens opacities, which could be categorized into one of three
 groups. Group-1 ferrets (n = 25) manifested a continuum of
 lens changes ranging from fine, multifocal, punctate
 opacification of the superficial posterior lens cortex (n =
 3), to changes in both the anterior and posterior cortex (n =
 13), to immature (n = 1), or mature/hypermature cataracts (n =
 8). Group-2 ferrets (n = 7) had bilateral microphthalmia and
 cataracts. Group-3 ferrets (n = 2) had minor lens changes
 involving the nucleus or cortex that were not typical of
 either group 1 or 2. By the age of 18 months, 41 of the
 remaining 42 animals in population A had developed fine,
 multifocal, punctate opacities of the posterior cortex. In
 group-1 animals, histologic changes in the lens ranged from
 several 80 X 40-micrometers, punctate, spheroidal lesions in
 the posterior cortex, to posterior migration of the lens
 epithelium, Morganian granules, and a complete
 mature/hypermature cataract. One group-2 ferret had
 microphthalmia, filling of the lens capsule with a cell-poor,
 periodic acid-Schiff stain-positive membranous material, and
 retinal detachment. Population B consisted of 15 adult and 47
 6-month-old juvenile ferrets. Eleven adults had multifocal,
 fine, punctate, posterior cortical opacities, and one adult
 had a nuclear cataract. Ten juveniles had nuclear cataracts
 (often in a multifocal punctate pattern); two had fine,
 multifocal, punctate, posterior cortical opacities; one had
 multifocal nuclear and posterior cortical opacities; and three
 had multifocal nuclear opacities that also involved both the
 anterior and posterior cortices. The ferret may be a
 potentially useful new animal model for studying mechanisms of
 cataractogenesis and microphthalmia. Caution should be used
 when interpreting the ocular toxicity of test compounds in
 this species.
 
 
 62                                  NAL Call. No.: QR188.3.C45
 Cellular aspects of autoimmunity.
 Cruse, Julius M.,_1937-; Lewis, R. E.
 Basel ; New York : Karger,; 1988.
 200 p. : ill. ; 25 cm. (Concepts in immunopathology ; vol. 6). 
 Includes bibliographies and index.
 
 Language:  English
 
 Descriptors: Autoimmunity; Autoimmune diseases; Animal models;
 Cellular immunity
 
 
 63                                    NAL Call. No.: 410.9 P94
 Changes in platelet-activating factor, catecholamine, and
 serotonin concentrations in brain, cerebrospinal fluid, and
 plasma of pichinde virus-infected guinea pigs.
 Guo, Z.M.; Qian, C.G.; Peters, C.J.; Liu, C.T.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1993 Dec. Laboratory animal science v. 43 (6): p.
 569-574; 1993 Dec.  Includes references.
 
 Language:  English
 
 Descriptors: Pichinde virus; Animal models; Epinephrine;
 Norepinephrine; Immunological factors; Serotonin; Brain;
 Cerebrospinal fluid; Blood plasma; Physiopathology; Guinea
 pigs
 
 Abstract:  Brain concentrations of platelet-activating factor
 (PAF), catecholamines, and serotonin were measured in control
 and Pichinde virus-infected strain 13 guinea pigs on
 postinoculation day (PID) 12. After virus inoculation, PAF
 concentrations increased 81% in cerebrum, 147% in
 diencephalon-brain stem, and 110% in cerebellum from baseline
 values of 2.6 +/- 0.3, 4.3 +/- 0.2, and 6.1 +/- 0.5 (ng/g wet
 tissue), respectively. Dopamine concentrations in the infected
 cerebrum and diencephalon-brain stem increased significantly,
 whereas norepinephrine concentration increased only in
 cerebrum. However, serotonin concentrations in all three
 regions of infected brain decreased significantly as compared
 with control values. There were no significant changes in
 epinephrine concentrations of infected brain. Norepinephrine
 and epinephrine concentrations in plasma and cerebrospinal
 fluid on PID 7 and 12 increased significantly as compared with
 control values, while plasma dopamine concentration increased
 significantly on PID 7. Increased brain PAF, dopamine, and
 norepinephrine concentrations with decreased brain serotonin
 concentrations may mediate the hyperactivity of the
 hypothalamic-pituitary-adrenal axis and involve some unknown
 pathophysiologic processes of arenaviral infection.
 Furthermore, increased plasma catecholamine concentrations are
 associated with stress and may be partially responsible for
 the development of cardiovascular dysfunction and pulmonary
 edema during this viral disease.
 
 
 64                                   NAL Call. No.: 47.8 Am33P
 Changes in the frequency and size of smooth muscle tumors in
 Japanese quail lines differing in body weight.
 Nestor, K.E.; Bacon, W.L.
 Champaign, IL : Poultry Science Association, 1921-; 1994 Jul.
 Poultry science v. 73 (7): p. 947-952; 1994 Jul.  Includes
 references.
 
 Language:  English
 
 Descriptors: Japanese quails; Smooth muscle; Neoplasms;
 Weight; Incidence; Line differences; Body weight; Laying
 performance; Selection responses; Oviducts; Ligaments
 
 Abstract:  The purpose of this investigation was to study the
 incidence and size of smooth muscle tumors in several Japanese
 quail lines and to report recent correlated changes in mature
 BW and egg production. Laying females from lines selected
 solely (HW) or partly (HW-HP; HW-LP) for increased 4-wk BW or
 for decreased 4-wk BW (LW) and from the corresponding
 randombred control (R1) were used. Lines HW-HP and HW-LP were
 sublines of Line HW in which males were selected for increased
 4-wk BW and females were selected for high or low level of
 total plasma phosphorus, respectively. Laying hens were
 examined for the presence of smooth muscle tumors after about
 170 d of egg production (240 d of age). During Generations 19
 through 26, mature BW was increasing in the HW line and
 decreasing in the LW line. Selection for either increased or
 decreased 4-wk BW resulted in decreased egg production, but
 the only significant change with generations was a decrease of
 2.7 eggs per hen for a 120-d laying period in the LW line.
 Frequency and weight of the smooth muscle tumors were greater
 for females from the large-bodied lines than females from Line
 R1. No tumors were detected in LW females. Based on the linear
 regression of response on generations, tumor frequency was
 increasing in Line HW-LP but tumor weight was decreasing in
 this line. Tumor weight was increasing in the HW line. No
 other changes in tumor frequency or size were noted across
 generations. Weight of the tumors was not correlated with egg
 production. The presence of tumors did not seem to affect
 mortality during the laying period. The Japanese quail lines
 may serve as a useful animal model for the study of smooth
 muscle tumors in humans, chickens, and turkeys.
 
 
 65                                    NAL Call. No.: SF95.A1C6
 The changing role of animal models in human nutrition
 research. West, C.E.; Beynen, A.C.
 Basel : Karger; 1988.
 Comparative animal nutrition v. 6: p. 1-13; 1988.  In the
 series analytic: Use of Animal Models for Research in Human
 Nutrition / edited by A.C. Beynen and C.E. West.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Laboratory animals; Animal models; Nutrition
 physiology; Human nutrition research; Vitamins; Nutrient
 requirements; Species differences; Literature reviews
 
 
 66                                    NAL Call. No.: QL55.A1L3
 Characteristics of mutant mice (ICGN) with spontaneous renal
 lesions: a new model for human nephrotic syndrome.
 Ogura, A.; Asano, T.; Matsuda, J.; Takano, K; Nakagwa, M.;
 Fukui, M. London : Royal Society of Medicine Services; 1989
 Apr.
 Laboratory animals v. 23 (2): p. 169-174. ill; 1989 Apr. 
 Includes references.
 
 Language:  English
 
 Descriptors: Mice; Mutants; Disease models; Nephrotic
 syndrome; Glomerulonephritis; Histopathology
 
 Abstract:  Spontaneous nephrotic mice (ICGN mice), a new
 mutant strain of mouse from outbred ICR, were clinically,
 macroscopically, histologically and immunohistochemically
 studies to establish their value as a model for human
 nephrotic syndrome. Most of the affected mice developed
 proteinuria, hypoproteinaemia and hypercholesterolaemia, and
 some of them developed systemic oedema. A high concentration
 of blood urea nitrogen (BUN) and a low haematocrit value were
 also observed. The kidneys of severe cases showed a decrease
 in size and had a yellowish granular surface. These findings
 indicated that the mice were terminally affected by chronic of
 renal insufficiency. Histopathology demonstrated glomerular
 lesions consisting of thickened basement membranes of the
 capillary loops with irregular spike-like protrusions and
 enlargement of the mesangium unaccompanied by cellular
 proliferation. The immunofluorescence technique revealed
 positive granular staining for IgA, IgG and IgM and to a
 lesser extent for C3 along the capillary loops in affected
 mice. The similarity between this spontaneous disease and
 human nephrotic syndrome caused by idiopathic glomerular
 lesions is discussed. ICGN mice may be a useful animal model
 for this human disease.
 
 
 67                                    NAL Call. No.: QL55.A1L3
 Characterization of acute and latent herpes simplex virus
 infection of dorsal root ganglia in rats.
 Blondeau, J.M.; Aoki, F.Y.; Glavin, G.B.; Nagy, J.I.
 London : Royal Society of Medicine Services; 1991 Apr.
 Laboratory animals v. 25 (2): p. 97-105; 1991 Apr.  Includes
 references.
 
 Language:  English
 
 Descriptors: Rats; Herpes simplex virus; Ganglia; Acute
 infections; Latent infections; Animal models; Experimental
 infections; Subcutaneous injection; Feet
 
 Abstract:  The characteristics of HSV type-1 infection
 following subcutaneous inoculation in the dorsum of one hind
 paw of Sprague-Dawley rats were studied to determine whether
 infection in rats might more closely parallel the infection in
 man than is seen in other animals. The serologic and virologic
 characteristics of acute and latent ganglion infection
 conformed to those of human infection. Immunohistochemical
 studies suggested that sensory ganglion infection arose via
 centripetal axonal migration of virus as is hypothesized in
 man. In rat, small type B neuronal cell bodies appeared
 central to the maintenance of latent infection and
 reactivation observed during cocultivation of lumbar ganglia.
 Acute and latent lumbar sensory ganglion infection in rats
 after subcutaneous hind paw injection of HSV-1 appears to be
 another suitable model of this infection in man.
 
 
 68                                     NAL Call. No.: 41.8 J82
 Chediak-Higashi syndrome in rats: light and electron
 microscopical characterization of abnormal granules in beige
 rats.
 Ozaki, K.; Maeda, H.; Nishikawa, T.; Nishimura, M.; Narama, I.
 London : Academic Press; 1994 May.
 Journal of comparative pathology v. 110 (4): p. 369-379; 1994
 May.  Includes references.
 
 Language:  English
 
 Descriptors: Chediak-higashi syndrome; Histopathology; Cell
 ultrastructure; Granules; Rats; Animal models
 
 
 69                                    NAL Call. No.: QL55.A1L3
 Chest roentgenographic techniques for demonstrating human lung
 tumour xenografts in nude rats.
 Zeligman, B.E.; Howard, R.B.; Marcell, T.; Chu, H.; Rossi,
 R.P.; Mulvin, D.; Johnston, M.R.
 London : Royal Society of Medicine Services; 1992 Apr.
 Laboratory animals v. 26 (2): p. 100-106; 1992 Apr.  Includes
 references.
 
 Language:  English
 
 Descriptors: Rats; Animal models; Disease models; Neoplasms;
 Lungs; Radiography; Monitoring
 
 Abstract:  Roentgenographic techniques were investigated for
 imaging orthotopic tung tumours in anaesthetized nude rats
 endobronchially implanted with human lung cancer cells. A
 conventional radiographic unit with a dual-screen, double-
 emulsion film mammographic receptor produced images preferable
 to those from a mammographic unit because of superior
 resolution. Typical exposure factors were 300 mA, 29 kVp, and
 17 ms at a focus-film distance of 76 cm with a 2.11 by 2.41 mm
 effective focal spot and inherent filtration of 1.2 mm
 aluminium. Sensitivity for tumour detection was 0.93 for 59
 animals with pathologically proved tumours and 0.96 for 54
 animals with tumours larger than 4 mm or 50 mg. For 24
 pathologically tumour-free animals, specificity was 1-00. For
 55 animals radiographically judged to have tumours, positive
 predictive value was 1.00. For all 83 animals, accuracy was
 0.95. This technique effectively demonstrates orthotopic human
 lung tumours in nude rats and should be useful for noninvasive
 monitoring of tumour presence, location, size, and changes in
 size.
 
 
 70                                     NAL Call. No.: 47.8 B77
 Chicken neoplasia--a model for cancer research.
 Calnek, B.W.
 Oxfordshire : Carfax Publishing Company; 1992 Mar.
 British poultry science v. 33 (1): p. 3-16; 1992 Mar. 
 Literature review. Includes references.
 
 Language:  English
 
 Descriptors: Fowls; Neoplasms; Animal models
 
 
 71                                    NAL Call. No.: RA1190.A7
 Chlorpyrifos-induced delayed polyneuropathy.
 Capodicasa, E.; Scapellato, M.L.; Moretto, A.; Caroldi, S.;
 Lotti, M. Berlin, W. Ger. : Springer; 1991.
 Archives of toxicology v. 65 (2): p. 150-155; 1991.  Paper
 presented at the International Symposium on "Biochemical and
 Cellular Indices of Toxicity in Occupational and Environmental
 Medicine," June 1986, Milan, Italy, at a meeting held March
 1986, New Orleans, LA, and at a meeting held Aug/Sept 1989,
 Praglia, Italy.  Includes references.
 
 Language:  English
 
 Descriptors: Chlorpyrifos; Nervous system diseases;
 Neurotoxins; Acetylcholinesterase; Esterases;
 Pharmacokinetics; Brain; Man; Fowls; Hens
 
 Abstract:  Chlorpyrifos [0,0-diethyl 0-(3,5,6-trichloro-
 pyridyl) phosphorothioate] caused delayed polyneuropathy in
 man. Contrary to previous studies, we report here that it also
 causes delayed polyneuropathy in the hen, the animal model for
 this toxicity. The minimal neuropathic dose was 60-90 mg/kg
 p.o., corresponding to 4-6 times the estimated LD50.
 Consequently, pralidoxime (2-PAM) in conjunction with atropine
 was necessary to reverse acetylcholinesterase AChE) inhibition
 and cholinergic toxicity in hens given high enough doses of
 chlorpyrifos to cause neuropathy. Chlorpyrifos was slowly
 absorbed after single oral doses and the threshold of
 inhibition (>70%) of neuropathy target esterase (NTE), the
 putative target for delayed neuropathy, was reached within 5-6
 days. High AChE inhibition (>90%), however, was measured
 within hours after dosing because of the higher potency of
 chlorpyrifos to inhibit this enzyme. In vitro studies showed
 that chlorpyrifos-oxon, the active metabolite of chlorpyrifos,
 was 10-20 times more active against AChE than against NTE,
 confirming the clinical observation. No differences were seen
 between human and hen enzymes in this respect. Hen and human
 brain homogenates contain A-esterases which hydrolysed
 chlorpyrifos to about the same extent in both species. In
 conclusion, chlorpyrifos causes delayed polyneuropathy in the
 hen, as was reported in man. The reasons for previous negative
 data in the hen are probably due to the relatively lower doses
 which were used. Judging from in vitro studies with hen and
 human enzymes, there are no differences in the two species as
 far as their relative sensitivity to delayed polyneuropathy.
 It is likely that delayed polyneuropathy would develop in both
 species only after severe cholinergic toxicity requiring
 aggressive antidotal treatment.
 
 
 72                                   NAL Call. No.: 389.8 B773
 The cholesterol-raising effect of coffee in the Syrian
 hamster. Sanders, T.A.B.; Sandaradura, S.
 Cambridge : Cambridge University Press; 1992 Sep.
 The British journal of nutrition v. 68 (2): p. 431-434; 1992
 Sep.  Includes references.
 
 Language:  English
 
 Descriptors: Diet; Coffee; Blood plasma; Cholesterol; Hamsters
 
 Abstract:  Adult male Syrian hamsters were fed on a high-fat
 diet with or without access to boiled coffee. Plasma total,
 low-density-lipoprotein- and high-density-lipoprotein-
 cholesterol and triacylglycerol concentrations were increased
 by the coffee and very-low-density-lipoprotein-cholesterol
 concentrations were lowered. It is concluded that the Syrian
 hamster is a suitable animal model in which to study the
 hypercholesterolaemic effect of coffee.
 
 
 73                                    NAL Call. No.: QH301.N32
 Chronic alcoholism, malnutrition, and folate deficiency.
 Halsted, C.H.
 New York, N.Y. : Plenum Press; 1991.
 NATO ASI series : Series A : Life sciences v. 206: p. 237-251;
 1991.  In the series analytic: Alcoholism a molecular
 perspective / edited by T.N. Palmer. Literature review. 
 Includes references.
 
 Language:  English
 
 Descriptors: Alcoholism; Chronic course; Deficiency diseases;
 Folic acid; Malabsorption; Malnutrition; Metabolism;
 Physiopathology; Veterans; Animal models; Literature reviews
 
 
 74                                     NAL Call. No.: SF601.A5
 Clinical evaluation of cyclosporine in animal models with
 cutaneous immune-mediated disease and epitheliotropic
 lymphoma.
 Rosenkrantz, W.S.; Griffin, C.E.; Barr, R.J.
 Golden, Colo. : The Association; 1989 Jul.
 The Journal of the American Animal Hospital Association v. 25
 (4): p. 377-384. ill; 1989 Jul.  Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Cat; Epithelium; Lymphoma; Treatment;
 Immunological diseases; Drug therapy; Immunosuppressive agents
 
 
 75                                  NAL Call. No.: QP141.A1A63
 Cobalamin deficiency and the pathogenesis of nervous system
 disease. Metz, J.
 Palo Alto, Calif. : Annual Reviews, Inc; 1992.
 Annual review of nutrition v. 12: p. 59-79. ill; 1992. 
 Literature review. Includes references.
 
 Language:  English
 
 Descriptors: Vitamin b12; Vitamin deficiencies; Demyelination;
 Animal models; Nitrous oxide; Biochemistry; Methylation;
 Toxicity; Literature reviews
 
 
 76                                   NAL Call. No.: RA421.P684
 Colon cancer: dietary modifications required for a balanced
 protective diet. McIntosh, G.H.
 Orlando, Fla. : Academic Press; 1993 Sep.
 Preventive medicine v. 22 (5): p. 767-774; 1993 Sep.  Paper
 presented at the Fourth International Conference on Prevention
 of Human Cancer: Nutrition and Chemoprevention Controversies,
 June 3-6, 1992, Tucson, Arizona.  Includes references.
 
 Language:  English
 
 Descriptors: Carcinoma; Colon; Disease prevention; Diet;
 Animal models; Fiber; Dietary protein; Dietary fat; Vitamin e;
 Calcium; Nutrient nutrient interactions; Animal fat; Animal
 protein; Rats
 
 Abstract:  Background. There is increasing support of the view
 that our diet is too calorie dense, with its high animal fat,
 sugar, and alcohol content. Food processing has helped to
 create this situation as well as the desire to eat sugar- and
 fat-rich foods. By examining the influence of these dietary
 effects on colon cancer, experimental animal studies can help
 dissect the influences not readily assessable by
 epidemiological means. Methods. The Sprague Dawley rat model
 of colon cancer induced by dimethylhydrazine provides a means
 of assessing dietary influences with the use of a semipurified
 diet and varying a single factor at a time. We have examined
 the influence of Ca vitamin E, protein type, and cereal
 dietary fiber sources on tumor burden and incidence in rats on
 a standardized experimental protocol. Results. A significant
 interactive effect has been seen with high Ca and low vitamin
 E intake in protecting rats from tumors. When comparing
 differing protein sources, whey protein concentrate was found
 to be very protective relative to red meat and other protein
 sources. Spent barley grain was also shown to be very
 protective relative to wheat bran and commercial barley bran.
 Conclusions. There are several potentially useful strategies
 for protection from colon cancer by varying diet composition.
 Protein sources such as whey protein concentrate, insoluble
 dietary fiber from barley grain, and high calcium intake seem
 to be very promising. These need further detailed examination
 as to whether they can combine to reduce risk further and to
 understand better the mechanisms responsible for protection.
 They may provide greater potential than attempts to lower the
 fat in the human diet.
 
 
 77                                    NAL Call. No.: QR180.C62
 Comparative features of retroviral infections of livestock.
 Evermann, J.F.
 Exeter : Pergamon Press; 1990.
 Comparative immunology, microbiology and infectious diseases
 v. 13 (3): p. 127-136; 1990.  Literature review.  Includes
 references.
 
 Language:  English
 
 Descriptors: Livestock; Man; Lentivirinae; Oncovirinae;
 Disease transmission; Spread; Pathogenesis; Host specificity;
 Viral diseases; Disease models; Literature reviews; Animal
 models
 
 Abstract:  Retrovial infections of livestock have become of
 increasing importance due to their usefulness as comparative
 models for human retroviral infections and their effects upon
 animal health and marketability of animals and animal products
 nationally and internationally. This paper presents a
 perspective on the retroviruses of economic concern in
 veterinary medicine with emphasis on the importance of
 understanding the modes of virus transmission and the species
 specificity of the viruses. The retroviruses reviewed include
 the oncovirus, bovine leukosis virus, and the lentiviruses,
 equine infectious anemia virus; maedi/visna virus, caprine
 arthritis-encephalitis virus and bovine visna-like virus. The
 comparative features amongst these animal retroviruses and
 those of humans must be recognized by the veterinary and
 medical professions since the similarities in virus
 replication and spread by blood transfer can provide important
 clues in controlling and perhaps preventing human retroviruses
 infections, such as the human immunodeficiency virus.
 
 
 78                                    NAL Call. No.: 41.8 AM3A
 Comparative virulence of Haemophilus parasuis serovars 1 to 7
 in guinea pigs. Rapp-Gabrielson, V.J.; Gabrielson, D.A.;
 Schamber, G.J.
 Schaumburg, Ill. : American Veterinary Medical Association;
 1992 Jun. American journal of veterinary research v. 53 (6):
 p. 987-994; 1992 Jun. Includes references.
 
 Language:  English
 
 Descriptors: Haemophilus; Virulence; Serotypes; Strain
 differences; Guinea pigs; Intraperitoneal injection;
 Application methods; Morbidity; Mortality; Disease models
 
 Abstract:  Reference strains for Haemophilus parasuis serovars
 1 to 7 were examined for virulence by inoculation of guinea
 pigs. Guinea pig response to intraperitoneal inoculation was
 similar for the 7 reference strains. However, apparent
 differences in virulence were detected after intratracheal
 inoculation. Cells of the reference strains for serovars 1 and
 5 were most invasive, causing moribundity or death at higher
 doses and a persistent septicemia at lower doses. Haemophilus
 parasuis could be isolated from respiratory and systemic
 sites; purulent bronchopneumonia, pericarditis, and pleuritis
 were apparent in infected guinea pigs. Inoculation of cells of
 the reference strains for serovars 2 and 6 also resulted in
 bronchopneumonia and moribundity or death in some guinea pigs;
 however, reisolation of H parasuis and microscopic lesions at
 necropsy were less pronounced than those observed with
 serovars 1 and 5. Inoculation of cells of serovars 3, 4, and 7
 induced only transient clinical signs and minimal evidence of
 H parasuis infection at necropsy. The data from intratracheal
 inoculation of guinea pigs are similar to data from other
 investigations in swine, indicating differences in the
 pathogenic potential of H parasuis strains. Thus, guinea pigs
 may be useful as a laboratory animal model for examining
 cellular factors associated with virulence and immunogenicity
 of H parasuis.
 
 
 79                                    NAL Call. No.: 410.9 P94
 Comparison of hematologic parameters in normal and
 streptozotocin-induced diabetic rats.
 Alder, V.A.; Yu, D.Y.; Su, E.N.; Cringle, S.J.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Apr. Laboratory animal science v. 42 (2): p.
 170-173; 1992 Apr.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Diabetes; Animal models; Hematology; Normal
 values; Blood sugar; Hemoglobin; Glycerate 2,3-bis(phosphate)
 
 Abstract:  Hematologic values are compared for normal and
 streptozotocin-induced diabetic rats after 6 weeks of induced
 diabetes. Most hematologic parameters were the same in the two
 groups except for blood glucose, glycated hemoglobin, and 2,3
 diphosphoglycerate, all of which were elevated in the
 streptozotocin group. However the P50 (the P02 at which the
 oxygen-carrying capacity of blood is 50% of maximal) remained
 normal. We hypothesize that a left shift in the oxyhemoglobin
 dissociation curve caused by the glycation of a small
 percentage of the hemoglobin is compensated by elevation in
 the 2,3-diphosphoglycerate which returns the P50 to normal
 values. This compensatory mechanism also occurs in some stages
 of human diabetes.
 
 
 80                                  NAL Call. No.: QP141.A1N88
 Comparison of the effect of dietary casein and cottonseed
 protein on food intake and growth in normal tumor-bearing
 rats.
 Radcliffe, J.D.
 Elmsford, N.Y. : Pergamon Press; 1991 Sep.
 Nutrition research v. 11 (9): p. 1055-1066; 1991 Sep. 
 Includes references.
 
 Language:  English
 
 Descriptors: Dietary protein; Casein; Cottonseed protein; Food
 intake; Growth rate; Neoplasms; Rats
 
 Abstract:  Male Fischer 344 rats with (tumor-bearers) and
 without (controls) a transplantable methylcholanthrene sarcoma
 were fed isonitrogenous, isoenergetic diets containing either
 casein or cottonseed protein (CSP) so as to compare the
 effects of these two proteins on the development of cancer-
 induced anorexia and cachexia. For both diets, tumor growth
 was associated with depressed food intake, decreased body
 weight, hypoalbuminemia and hyperlipidemia. Diet had no effect
 on food intake, weight gain or serum albumin for either
 controls or tumor-bearers; tumor weight was unaffected by type
 of dietary protein. Liver weights were lower for animals fed
 CSP than for those fed casein. Dietary CSP exerted a
 hypolipidemic effect in normal rats, but this differential
 effect of protein quality on serum lipids was abolished by
 tumor growth, as were differences in serum fatty acid profile
 associated with consumption of CSP. Tumor growth itself was
 associated with altered fatty acid profiles in serum, with the
 percentages of fatty acids as stearic and arachidonic acids
 being decreased and the percentages as oleic and linoleic
 acids being increased. Thus, dietary CSP has similar effects
 to casein on the development of cancer anorexia and cachexia
 in this animal model. The effects of protein quality on serum
 lipids, however, can be altered by tumor growth.
 
 
 81                                   NAL Call. No.: SF757.8.A4
 Computed tomography of rambouillet sheep affected with
 neuronal ceroid lepofuscinosis.
 Woods, P.R.; Walker, M.A.; Weir, V.A.; Storts, R.W.; Menzies,
 C.; Shelton, M. Raleigh, NC : American College of Veterinary
 Radiology; 1994 Jul. Veterinary radiology & ultrasound : the
 official journal of the American College of Veterinary
 Radiology and the International Veterinary Radiology
 Association v. 34 (4): p. 259-262; 1994 Jul.  Includes
 references.
 
 Language:  English
 
 Descriptors: Sheep; Computed tomography; Neurons;
 Degeneration; Brain; Ceroid; Thalamus; Diagnosis; Postmortem
 examinations; Animal models
 
 
 82                                   NAL Call. No.: QL55.A1I43
 The contribution of nonhuman primates to understanding
 coronary artery atherosclerosis in humans.
 Clarkson, R.B.; Klumpp, S.A.
 Washington, D.C. : Institute of Laboratory Animal Resources,
 National Research Council; 1990.
 I.L.A.R. news v. 32 (2): p. 4-8; 1990.  Includes references.
 
 Language:  English
 
 Descriptors: Monkeys; Animal models; Disease models;
 Atherosclerosis; Cholesterol; Blood plasma; Tobacco smoking;
 Stress; Sex differences; Oral contraceptives
 
 
 83                                  NAL Call. No.: RC620.A1N47
 Control of hypoallergenicity by animal models.
 Pahud, J.J.; Schwarz, K.; Granato, D.
 New York, N.Y. : Raven Press; 1988.
 Nestle nutrition workshop series v. 17: p. 199-207; 1988. 
 Includes references.
 
 Language:  English
 
 Descriptors: Food allergies; Immune response; Allergens;
 Hypersensitivity; Models; Breast feeding
 
 
 84                                   NAL Call. No.: RA421.P684
 Controversial issues of dietary fat and experimental mammary
 carcinogenesis. Ip, C.
 Orlando, Fla. : Academic Press; 1993 Sep.
 Preventive medicine v. 22 (5): p. 728-737; 1993 Sep.  Paper
 presented at the Fourth International Conference on Prevention
 of Human Cancer: Nutrition and Chemoprevention Controversies,
 June 3-6, 1992, Tucson, Arizona.  Includes references.
 
 Language:  English
 
 Descriptors: Mammary gland neoplasms; Dietary fat; Linoleic
 acid; Diet; Caloric intake; Risk; Pregnancy; Lactation;
 Carcinogenesis; Literature reviews
 
 Abstract:  Epidemiological evidence from different countries
 worldwide has suggested a positive association between the
 availability of fat in the diet and variations in breast
 cancer mortality rate. A voluminous amount of information is
 also available in the literature linking increased fat
 consumption, particularly polyunsaturated fat, and stimulation
 of mammary tumorigenesis in animal models. In the past few
 years, our laboratory has been studying the impact of several
 confounding factors that could modulate the enhancing effect
 of fat on neoplastic development of the mammary gland in
 female rats which are treated with a carcinogen. It is our
 conclusion that fat promotes mammary carcinogenesis only under
 a very stringent set of conditions which might not be
 duplicated in the arena of fat intake and human breast cancer
 risk. Previous studies on fat and mammary cancer in
 experimental models have used young virgin rats which are
 given a dose of carcinogen at a particular age. The question
 arises as to whether the promoting effect of fat might be a
 consequence of the characteristics of the model. We have
 supportive evidence showing that the following criteria must
 be satisfied in order for fat enhancement of mammary
 carcinogenesis to be manifested: (a) carcinogen administered
 at a time when the mammary gland is exquisitely susceptible to
 tumor induction, (b) animals maintained on a semipurified
 diet, (c) ad libitum feeding necessary, and (d) unusually high
 requirement of linoleic acid for tumor development. On the
 other hand, the stimulatory effect of fat is attenuated or
 sometimes even negated by (a) feeding of a natural ingredient
 diet, (b) submaximal calorie intake, and (c) previous history
 of pregnancy and lactation. Given the spectrum of confounders
 that are inherent in epidemiological studies linking fat
 intake and breast cancer, including differences in lifestyle,
 reproductive history, eating habits, as well as complexity of
 the total diet, our findings suggest that there may be a need
 to reevaluate the validity of extrapolating animal data that
 are obtained under a highly defined set of conditions to the
 etiological significance of dietary fat in human breast
 cancer.
 
 
 85                                    NAL Call. No.: 410.9 P94
 Convulsions in senescence-accelerated mice (SAM-R/1/Eis).
 Yamazaki, K.; Kumazawa, A.; Ito, K.; Kurihara, K.; Nakayama,
 M.; Wakabayashi, T.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Aug. Laboratory animal science v. 42 (4): p.
 378-381; 1992 Aug.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Animal models; Convulsions; Aging
 
 Abstract:  Senescence-accelerated mice (SAM) are one of the
 animal models used for studying senescence, which consist of
 several substrains such as SAM-R/1, R/2, P/1, P/2. SAM-R/1/Eis
 maintained in Eisai Tsukuba Research Laboratories, Ibaraki,
 Japan, was originally introduced as a substrain of a normal
 control SAM-R/1 from Kyoto University, Japan. We have noted
 signs of convulsions in SAM-R/1/Eis mice during routine animal
 care, particularly while changing cages. We identified the
 clinical signs and determined the concentrations of glucose
 and immunoreactive insulin in plasma of SAM-R/1/Eis mice.
 There were no differences in the male:female ratios of mice
 showing prodrome only, grand mal, or no-signs. The ages at
 which prodrome and grand mal were first noted peaked between
 20 and 25 weeks. Concentrations of glucose and immunoreactive
 insulin in plasma did not indicate the mice were in insulin
 hypoglycemia, which is one cause of convulsions. AKR strain
 mice, some of which originated with the SAM strain are known
 to become convulsive by repeated "throwing" stimulations.
 Conversely, in SAM-R/1/Eis, throwing stimuli are not needed to
 cause convulsive signs. Thus it is likely that in SAM-R/1/Eis
 mice the signs are triggered by repeating mild environmental
 changes, such as changing cages. The results of this study
 show that SAM-R/1/Eis is neither a normal control strain, nor
 an original SAM-R/1 strain. But it is possible that SAM-
 R/1/Eis is another useful animal model for studying
 spontaneous convulsion.
 
 
 86                                    NAL Call. No.: 410.9 P94
 Coronary arterial abnormalities in hyperlipidemic rats with
 renal failure. Yamasaki, K.; Yoshikawa, Y.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1994 Apr. Laboratory animal science v. 44 (2): p.
 125-130; 1994 Apr.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Hyperlipemia; Renal failure; Coronary
 vessels; Arteries; Disease course; Heart; Kidneys;
 Histopathology; Cholesterol; Triacylglycerols; Phospholipids;
 Urea; Nitrogen; Blood pressure; Weight
 
 Abstract:  Hyperlipidemic rats, which have been described as a
 useful animal model for focal glomerulosclerosis in humans,
 were examined at the ages of 17, 20, 24, and 27 weeks for
 evaluation of spontaneously developed coronary arterial
 lesions. The mean concentrations of cholesterol, triglyceride,
 phospholipid, and urea nitrogen were greater than the
 respective control concentrations at and after the age of 17
 weeks. No abnormalities were detected in the blood pressure
 values. Starting from the age of 24 weeks, the rats had
 disseminated white spots in the ventricles and septum of the
 heart. Mean renal weights of hyperlipidemic rats were higher
 than those of control rats at the ages of 17 and 20 weeks, and
 the surface of the kidney appeared irregular when rats were 27
 weeks old. Histologic examination revealed atrophy of the
 coronary artery, a decrease in the number of smooth muscle
 cells, and thinning of the wall, resulting in loss of the
 normal wall structure. A homogenous eosinophilic substance,
 the nature and cause of which were unknown, was also seen in
 the affected arterial walls. Furthermore, white spots observed
 macroscopically were found to represent myocardial
 degeneration and necrosis with reactive histiocytic cells and
 lymphocytes, adventitial fibrosis, and edema associated with
 the affected arteries. These arterial lesions became evident
 in rats at and after the age of 24 weeks. Electron microscopic
 examination of coronary arteries revealed enlargement of the
 subendothelial space and spaces between the smooth muscle
 cells containing cell debris in rats at the age of 20 weeks,
 and degeneration and necrosis of the endothelial cells, smooth
 muscle cells in the media, and striated muscle cells adjacent
 to the affected arteries in rats at the age of 27 weeks.
 Histologic examination of affected kidneys revealed focal
 glomerulosclerosis, accompanied by the dilatation of the
 tubules, which contained eosinophilic casts and infiltrating
 lymphocytes in the interstitium together with edema, at and
 after the age of 17 weeks.
 
 
 87                                    NAL Call. No.: RC927.C73
 CRC handbook of animal models for the rheumatic diseases.. 
 Handbook of animal models for the rheumatic diseases
 Greenwald, Robert A.,_1943-; Diamond, Herbert S.,
 Boca Raton, Fla. : CRC Press,; 1988.
 2 v. : ill. ; 26 cm.  Includes bibliographies and index.
 
 Language:  English
 
 Descriptors: Rheumatism; Animal models; Handbooks, manuals,
 etc; Arthritis; Animal models; Handbooks, manuals, etc; Animal
 welfare
 
 
 88                                    NAL Call. No.: RC756.H28
 CRC handbook of animal models of pulmonary disease..  Handbook
 of animal models of pulmonary disease
 Cantor, Jerome O.
 Boca Raton, Fla. : CRC Press,; 1989.
 2 v. : ill. ; 26 cm.  Includes bibliographies and indexes.
 
 Language:  English
 
 Descriptors: Lungs
 
 
 89                                     NAL Call. No.: 381 J824
 Defective glucose-dependent endoplasmic reticulum Ca2+
 sequestration in diabetic mouse islets of Langerhans.
 Roe, M.W.; Philipson, L.H.; Frangakis, C.J.; Kuznetsov, A.;
 Mertz, R.J.; Lancaster, M.E.; Spencer, B.; Worley, J.F. III;
 Dukes, I.D. Bethesda, Md. : American Society for Biochemistry
 and Molecular Biology; 1994 Jul15.
 The Journal of biological chemistry v. 269 (28): p.
 18279-18282; 1994 Jul15. Includes references.
 
 Language:  English
 
 Descriptors: Mice; Experimental diabetes; Diabetes mellitus;
 Calcium ions; Endoplasmic reticulum; Glucose;
 Pyrophosphatases; Enzyme activity; Pancreas islets; Insulin
 secretion
 
 Abstract:  Non-insulin-dependent diabetes mellitus (NIDDM) is
 a metabolic disease associated with abnormal insulin
 secretion, the underlying mechanisms of which are unknown.
 Glucose-dependent signal transduction pathways were
 investigated in pancreatic islets derived from the db/db
 mouse, an animal model of NIDDM. After stimulation with
 glucose (4-12 mM), the changes in intracellular Ca2+
 concentration (Ca2+]i) were different; unlike control islets,
 db/db islets lacked an initial reduction of [Ca2+]i and the
 subsequent [Ca2]i oscillations following stimulation with 12
 mM glucose. The severity of these defects in Ca2+ signaling
 correlated with the age-dependent development of
 hyperglycemia. Similarly defective glucose-induced Ca2+
 signaling were reproduced in control islets by pre-exposure to
 thapsigargin, a selective inhibitor of endoplasmic reticulum
 (ER) Ca2+-ATPase. Estimation of ATPase activities from rates
 of ATP hydrolysis and by immunoblot hybridization with an
 antiserum directed against the sacro/endoplasmic reticulum
 Ca2+-ATPase both demonstrated that the ER Ca2+-ATPase was
 almost entirely absent from db/db islets. The effects of
 inhibition of ER Ca2+-ATPase on insulin secretion were also
 examined; a 4-day exposure of control islets to 1 micromolar
 thapsigargin resulted in basal and glucose-stimulated insulin
 secretion levels similar to those found in db/db islets. These
 results suggest that aberrant ER Ca2+ sequestration underlies
 the impaired glucose responses in the db/db mouse and may play
 a role in defective insulin secretion associated with NIDDM.
 
 
 90                                    NAL Call. No.: 41.8 V643
 The development of a vaccine against feline immunodeficiency
 virus. Hosie, M.J.
 London : Bailliere Tindall; 1994 Jan.
 The British veterinary journal v. 150 (1): p. 25-39; 1994 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Cats; Vaccines; Feline immunodeficiency virus;
 Infection; Vaccine development; Vaccination; Disease
 prevention; Literature reviews
 
 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.
 
 
 91                                    NAL Call. No.: RC628.O22
 Development of insulin resistance during the course of
 obesity: lessons from animal models.
 Penicaud, L.; Ferre, P.
 New York, N.Y. : Human Sciences Press; 1988.
 Journal of obesity and weight regulation v. 7 (2): p. 91-109;
 1988. Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Diabetes; Obesity; Insulin; Adipose tissue;
 Glucose tolerance; Animal models; Genetic markers;
 Experimental diets; Hypothalamic lesions; Metabolism; Lipids;
 Literature reviews; Rats
 
 
 92                               NAL Call. No.: RC628.N48 1987
 The development of the SHR/N- and LA/N-cp (Corpulent) congenic
 rat strains. Hansen, C.T.
 Bethesda, Md. : National Institutes of Health; 1988.
 New models of genetically obese rats for studies in diabetes,
 heart disease, and complications of obesity : NIH workshop,
 June 18-19, 1987, summaries of workshop papers and current
 bibliography. p. 7-11; 1988.
 
 Language:  English
 
 Descriptors: Obesity; Animal breeding; Animal models; Rats
 
 
 93                                    NAL Call. No.: 381 J8282
 Development of unesterified cholesterol-rich lipid particles
 in atherosclerotic lesions of WHHL and cholesterol-fed NZW
 rabbits. Chao, F.F.; Blanchette-Mackie, E.J.; Dickens, B.F.;
 Gamble, W.; Kruth, H.S. Bethesda, Md. : Lipid Research, inc.,
 1959-; 1994 Jan.
 Journal of lipid research v. 35 (1): p. 71-83; 1994 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Rabbits; Experimental atherosclerosis;
 Cholesterol; Lipids; Animal models; Disease models;
 Hyperlipemia; Phosphatidylcholines; Sphingomyelins
 
 Abstract:  Previously, we isolated and characterized
 unesterified cholesterol-rich lipid particles (UCLP) that
 accumulate in extracellular spaces of atherosclerotic lesions
 of humans and cholesterol-fed rabbits. In the present study,
 we examined early developing atherosclerotic lesions to
 determine when UCLP appear and when they become enriched in
 cholesterol and sphingomyelin. Cholesterol-fed NZW rabbits,
 which rapidly develop atherosclerotic lesions, and genetically
 hyperlipidemic WHHL rabbits, which develop lesions over a
 longer period of time, were studied. UCLP of peak density 1.04
 g/ml appear as early as 4 weeks after the onset of cholesterol
 feeding and progressively accumulate during atherosclerotic
 lesion development. Beginning with their appearance and
 afterwards, UCLP contain a saturating level (2:1 molar ratio)
 of cholesterol relative to phospholipid. Whereas, early UCLP
 are enriched in phosphatidylcholine, with time UCLP become
 enriched with sphingoymelin. Another UCLP population having a
 peak density of 1.09 g/ml was present in control aortas and
 increased in amount more slowly than the d 1.04 g/ml UCLP
 during cholesterol feeding. The d 1.09 g/ml particles were
 predominantly unilamellar vesicles, the majority between 100
 and 200 nm in diameter. They contained > 90% of their
 cholesterol in unesterified form and their ratio of
 unesterified cholesterol to phospholipid progressively
 increased from 0.6 to 1.7 during cholesterol feeding. Liposome
 resistance to solubilization by high density lipoproteins is
 known to be increased by enrichment with unesterified
 cholesterol and sphingomyelin. Sphingomyelin enrichment of
 unesterified cholesterol-rich lipid particles (UCLP) could
 stabilize cholesterol in a form that does not readily
 crystallize. However, at the same time, the early and
 progressive accumulation of UCLP in developing atherosclerotic
 lesions may limit reverse cholesterol transport and accelerate
 disease progression.
 
 
 94                                     NAL Call. No.: QP501.E8
 Developmental changes of 6-phosphofructo-1-kinase subunit
 levels in erythrocytes from normal dogs and dogs affected by
 glycogen storage disease type VII.
 Mhaskar, Y.; Harvey, J.W.; Dunaway, G.A.
 New York, NY : Springer-Verlag New York Inc; 1992 Mar.
 European journal of biochemistry v. 101 (3): p. 303-307; 1992
 Mar.  Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Glycogenosis; Phosphofructokinase;
 Isoenzymes; Enzyme activity; Erythrocytes; Age differences;
 Animal models
 
 Abstract:  1. The subunit proportions (L:M:C) of the PFK
 isozymes from normal adult erythrocytes were 2:86:12. Affected
 adult erythrocyte 6-phosphofructo-1-kinase (PFK) isozymes
 contained normal L-type (31%) and C-type (61%) subunits as
 well as a small amount (8%) of truncated M-type subunit. 2.
 When measured within 24 hr of birth, both normal and affected
 dog erythrocytes contained high PFK activities due to elevated
 levels of the L-type subunit. As the dogs matured, PFK
 activity decreased due to a greater than 99% loss of the L-
 type subunit. 3. By 2 weeks of age, the M-type and C-type
 subunits in normal dog PFK isozymes increased severalfold and
 attained near adult levels. 4. During post-natal development,
 the L-type subunit from affected dog erythrocytes decreased
 more rapidly than from normal dog erythrocytes; but it was
 maintained at a higher level in the affected adult
 erythrocytes. Also, in the affected dog erythrocytes,
 truncated M-type subunits were detected; and the initially
 high levels of the C-type subunit decreased approximately 50%
 after 4 weeks.
 
 
 95                                  NAL Call. No.: QP141.A1P72
 Diabetes mellitus. What have we learned from animals?.
 Berdanier, C.D.
 Tarrytown, N.Y. : Pergamon Press; 1993 Jul.
 Progress in food & nutrition science v. 17 (3): p. 261-285;
 1993 Jul. Includes references.
 
 Language:  English
 
 Descriptors: Diabetes mellitus; Animal models; Animal
 experiments; Insulin; Obesity; Incidence; Pancreas islets;
 Autoimmune diseases; Viral diseases; Blood sugar; Glucose;
 Nutrient transport; Carbohydrate metabolism; Literature
 reviews
 
 Abstract:  Progress in our understanding of the
 pathophysiology of diabetes mellitus has been made possible
 because of the availability of animal analogs of the various
 human diseases. Diabetes mellitus can be mild, moderate or
 severe depending on the genetic error that is responsible for
 the disease. Present estimates of errors that result in
 diabetes range from 20 to 100. Because similar errors have
 been found in spontaneously diabetic animals scientists have
 been able to identify the sequence of metabolic events and
 subsequent tissue change in many of these phenotypes. Studies
 of the efficacy of various drugs, diets and lifestyle choices
 on disease development and management thus were made possible.
 
 
 96                                   NAL Call. No.: QL55.A1I43
 Diabetes-prone and diabetes-resistant BB rats: animal models
 of spontaneous and virally induced diabetes mellitus,
 lymphocytic thyroiditis, and collagen-induced arthritis.
 Guberski, D.L.
 Washington, Institute of Laboratory Animal Resources, National
 Research Council; 1993.
 ILAR news v. 35 (2): p. 29-37; 1993.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Disease models; Diabetes; Strain
 differences
 
 
 97                                  NAL Call. No.: QP801.H7H65
 Diabetic embryopathy and fuel-mediated organ teratogenesis:
 lessons from animal models.
 Freinkel, N.
 Stuttgart, W. Ger. : Georg Thieme; 1988 Aug.
 Hormone and metabolic research; Hormon- und
 Stoffwechselforschung; Hormones et metabolisme v. 20 (8): p.
 463-475. ill; 1988 Aug.  Includes references.
 
 Language:  English
 
 Descriptors: Diabetes; Pregnancy; Maternal effects; Models;
 Abnormalities
 
 
 98                                    NAL Call. No.: SF95.A1C6
 Dietary effects in experimental carcinogenesis: animal models.
 Kritchevsky, D.
 Basel : Karger; 1988.
 Comparative animal nutrition v. 6: p. 174-185; 1988.  In the
 series analytic: Use of Animal Models for Research in Human
 Nutrition / edited by A.C. Beynen and C.E. West.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Carcinogenesis; Dietary fat;
 Dietary protein; Carbohydrates; Restricted feeding; Trace
 elements; Vitamins; Literature reviews
 
 
 99                                     NAL Call. No.: QP751.L5
 Dietary fat and colon cancer: animal model studies.
 Reddy, B.S.
 Champaign, Ill. : American Oil Chemists' Society; 1992 Oct.
 Lipids v. 27 (10): p. 807-813; 1992 Oct.  Paper presented at
 the "Symposium on Lipids in Cancer" held at the AOCS Annual
 Meeting, April 1990, Baltimore, Maryland.  Includes
 references.
 
 Language:  English
 
 Descriptors: Dietary fat; Fish oils; Fatty acids; Colon;
 Neoplasms; Carcinogenesis; Animal models; Reviews
 
 
 100                                    NAL Call. No.: RA784.N8
 Dietary fat and natural killer cell function.
 Byham, L.D.
 Baltimore, Md. : Williams & Wilkins; 1991 Jan.
 Nutrition today v. 26 (1): p. 31-36. charts; 1991 Jan. 
 Literature review. Includes references.
 
 Language:  English
 
 Descriptors: Natural killer cells; Dietary fat; Immunity;
 Neoplasms; Eicosanoids; Lymphocytes; Cell membranes;
 Lipoxygenase; Animal models; Clinical trials; Literature
 reviews
 
 Abstract:  This article looks at the role of dietary fat in
 influencing the ability of natural killer cells to inhibit the
 proliferation of cancer cells. It includes: 1) an overview of
 the immune system; 2) a discussion of the lymphocytic membrane
 and; 3) a review of cyclo-oxygenase/lipoxygenase inhibition,
 and animal models and clinical trials on the role of
 eicosanoids in natural killer cell function.
 
 
 101                                    NAL Call. No.: QP751.L5
 Dietary fat and the development of pancreatic cancer.
 Roebuck, B.D.
 Champaign, Ill. : American Oil Chemists' Society; 1992 Oct.
 Lipids v. 27 (10): p. 804-806; 1992 Oct.  Paper presented at
 the "Symposium on Lipids in Cancer" held at the AOCS Annual
 Meeting, April 1990, Baltimore, Maryland.  Includes
 references.
 
 Language:  English
 
 Descriptors: Dietary fat; Fatty acids; Fish oils; Calories;
 Exercise; Pancreas; Neoplasms; Carcinogenesis; Animal models;
 Rats; Reviews
 
 
 102                                  NAL Call. No.: RA421.P684
 Dietary fat, calories, and fiber in colon cancer.
 Reddy, B.S.
 Orlando, Fla. : Academic Press; 1993 Sep.
 Preventive medicine v. 22 (5): p. 738-749; 1993 Sep.  Paper
 presented at the Fourth International Conference on Prevention
 of Human Cancer: Nutrition and Chemoprevention Controversies,
 June 3-6, 1992, Tucson, Arizona.  Includes references.
 
 Language:  English
 
 Descriptors: Carcinoma; Colon; Dietary fat; Fiber; Caloric
 intake; Carcinogenesis; Nutritional intervention; Literature
 reviews
 
 Abstract:  The purpose of this presentation is (a) to provide
 an overview of the data thus far obtained in human
 epidemiological studies and laboratory animal models on the
 relationship between dietary fat, calories, and fiber and
 colon carcinogenesis and (b) to discuss whether the effect of
 dietary fat on colon carcinogenesis is due to the specific
 action of fat or to an associated caloric effect. Although the
 primary discussion of this presentation will be on laboratory
 animal model studies, reference will be made to human studies
 where appropriate. Future research will produce additional
 evidence for the etiologic role of types of dietary fat and
 fiber and total calories in cancer of the colon discussed in
 this presentation.
 
 
 103                                  NAL Call. No.: RC620.A1J6
 Dietary fat, calories, and the risk of breast cancer in
 postmenopausal women: a prospective population-based study.
 Barrett-Connor, E.; Friedlander, N.J.
 Wilmington, NC : American College of Nutrition; 1993 Aug.
 Journal of the American College of Nutrition v. 12 (4): p.
 390-399; 1993 Aug. Includes references.
 
 Language:  English
 
 Descriptors: Dietary fat; Energy intake; Mammary gland
 neoplasms; Nutrient intake; Menopause; Literature reviews;
 Risk; Women
 
 Abstract:  We tested the hypothesis that a high-fat diet
 increases the risk of breast cancer in a population-based
 study of 590 women aged 40-79 years who were without known
 breast cancer when they provided a quantitative 24-hour diet
 recall. Fifteen postmenopausal women were diagnosed with
 incident breast cancer during the next 15 years (approximately
 7600 person-years of follow-up). These women had significantly
 higher age-adjusted intake of afl fats (monounsaturated,
 polyunsaturated, and saturated), and oleic, linoleic, and
 linolenic acids, with a stepwise increase in risk across
 tertiles of intake. Fat intake was associated with total
 calories, protein, and carbohydrates, and women with incident
 breast cancer consumed more calories, protein, and
 carbohydrates than did other subjects. When each nutrient
 variable (calories, fats, protein, and carbohydrates) was
 adjusted for age, body mass index, age at menopause, parity,
 and alcohol consumption, the strongest risks for incident
 breast cancer were associated with total calories (relative
 risk per standard deviation = 2.72, 95% confidence interval =
 1.51-4.89, p = 0.002) and total fats (relative risk per
 standard deviation = 2.01, 95% confidence interval =
 1.19-3.41, p = 0.0 1). Fat composition of the diet, expressed
 either as percent of energy or as fat intake adjusted for
 calories by regression analysis, was not significantly
 associated with risk of breast cancer. These results support
 the hypothesis that total calorie consumption, as well as
 dietary fat consumption, is a risk factor for breast cancer in
 postmenopausal women, and parallel observations in animal
 models.
 
 
 104                                    NAL Call. No.: QP751.L5
 Dietary fat, fatty acids and prostate cancer.
 Rose, D.P.; Connolly, J.M.
 Champaign, Ill. : American Oil Chemists' Society; 1992 Oct.
 Lipids v. 27 (10): p. 798-803; 1992 Oct.  Paper presented at
 the "Symposium on Lipids in Cancer" held at the AOCS Annual
 Meeting, April 1990, Baltimore, Maryland.  Includes
 references.
 
 Language:  English
 
 Descriptors: Dietary fat; Fatty acids; Prostate; Neoplasms;
 Obesity; Hormones; Growth factors; Risk; Animal models;
 Reviews
 
 
 105                                 NAL Call. No.: QP141.A1N83
 Dietary fibre in the prevention of colorectal cancer: lessons
 from studies in animal models.
 Young, G.P.
 South Perth, WA: The Society; 1990.
 Proceedings of the Nutrition Society of Australia v. 15: p.
 112-119; 1990. Meeting held November 26-28, 1990, Adelaide,
 South Australia.  Includes references.
 
 Language:  English
 
 Descriptors: Fiber; Neoplasms; Colon
 
 
 106                                    NAL Call. No.: QH301.F3
 Dietary myristic, palmitic, and linoleic acids modulate
 cholesterolemia in gerbils.
 Pronczuk, A. \u Brandeis University, Waltham, MA; Khosla, P.;
 Hayes, K.C. Bethesda, Md. : The Federation of American
 Societies for Experimental Biology; 1994 Nov.
 The FASEB journal : official publication of the Federation of
 American Societies for Experimental Biology v. 8 (14): p.
 1191-1200; 1994 Nov. Includes references.
 
 Language:  English
 
 Descriptors: Meriones unguiculatus; Cholesterol; Blood plasma;
 Blood composition; Myristic acid; Linoleic acid; Fatty acids;
 Palmitic acid; Intake; Cholesterol metabolism;
 Hypercholesterolemia; Regression analysis; Animal models
 
 
 107                                   NAL Call. No.: 447.8 AM3
 Dietary obesity and weight cycling in rats: a model of stress-
 induced hypertension?.
 Contreras, R.J.; King, S.; Rives, L.; Williams, A.; Wattleton,
 T. Bethesda, Md. : American Physiological Society; 1991 Oct.
 American journal of physiology v. 261 (4,pt.2): p. R848-R857;
 1991 Oct. Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Hypertension; Blood pressure; Heart
 rate; Stress; Diet; Body weight; Cycling; Angiotensin; Animal
 models; Rats
 
 Abstract:  The present study was designed to reproduce the
 mild hypertension seen in dietary obese weight-cycled rats [P.
 Ernsberger and D. 0. Nelson. Am. J. Physiol. 254 (Regulatory
 Integrative Comp. Physiol 23): R47-R55, 1988] and determine
 whether this mild hypertension was associated with changes in
 sodium excretion and pressor responsiveness to angiotensin II
 (ANG II). Male Sprague-Dawley rats were fed pelleted chow
 (Pellet group) or chow plus sweetened condensed milk (Milk
 group) or were exposed to four cycles of a 4-day fast
 alternated with 2 wk of refeeding of pelleted chow and
 sweetened condensed milk (Cycled group). Blood pressure and
 heart rate were measured by tail cuff at the onset and last
 day of each fast and after 3 days of refeeding. During
 fasting, urine sodium excretion was measured. Mean arterial
 pressure and heart rate responses to intravenous
 administration of ANG II (40, 80, and 120 ng/kg), metoprolol
 (1 mg/kg), and methyl scopolamine (2 mg/kg) were obtained from
 the femoral artery in awake unrestrained rats. Weight cycling
 did not lead to mild hypertension or increased bradycardic
 response to sympathetic blockade with metoprolol. ANG II-
 elicited pressor responses were similar for Pellet, Milk, and
 Cycled groups. Sodium excretion did not change with fasting.
 Mild hypertension developed when obese weight-cycled rats were
 housed together in groups and not when housed individually.
 Our preliminary data are consistent with the notion that
 stress associated with group housing may be a factor in the
 mild hypertension of obese weight-cycled rats.
 
 
 108                              NAL Call. No.: RC692.D54 1990
 Dietary proteins, cholesterol, metabolism and atherosclerosis.
 Sugano, Michihiro,_1933-; Beynen, Anton C.,
 Basel ; New York : Karger,; 1990.
 163 p. : ill. ; 25 cm. (Monographs on atherosclerosis ; vol.
 16).  Includes index.  Includes bibliographical references.
 
 Language:  English
 
 Descriptors: Atherosclerosis; Blood cholesterol;
 Hypercholesteremia; Food; Blood proteins
 
 Abstract:  Analyzes the effects of dietary animal, vegetable
 and fish proteins on serum cholesterol levels in animal models
 and humans. Explores the possible mechanisms which have been
 advanced to date and reports the results of original research
 inquiries.
 
 
 109                                   NAL Call. No.: SF95.A1C6
 Dietary-induced obesity in experimental animals.
 Kanarek, R.B.; Orthen-Gambill, N.
 Basel : Karger; 1988.
 Comparative animal nutrition v. 6: p. 83-110; 1988.  In the
 series analytic: Use of Animal Models for Research in Human
 Nutrition / edited by A.C. Beynen and C.E. West.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Rats; Obesity; Dietary fat;
 Dietary carbohydrate; Feed conversion efficiency; Feed intake;
 Adipose tissue; Fat metabolism; Nutritive ratio; Exercise;
 Carbohydrate metabolism disorders; Specific dynamic action;
 Literature reviews
 
 
 110                                 NAL Call. No.: QP141.A1N88
 Dimethylbenzanthracene-induced mammary tumorigenesis in
 ethanol-fed rats. Rogers, A.E.; Conner, B.H.
 Elmsford, N.Y. : Pergamon Press; 1990 Aug.
 Nutrition research v. 10 (8): p. 915-928; 1990 Aug.  Includes
 references.
 
 Language:  English
 
 Descriptors: Ethanol; Mammary gland neoplasms; Carcinogens;
 Rats
 
 Abstract:  Epidemiological evidence indicates that ingestion
 of alcoholic beverages is a risk factor or is associated with
 a risk factor for breast cancer. A small increase in relative
 risk (1.1-1.2) compared to non-drinkers, has been reported for
 drinkers of small amounts of alcohol, approximately 3-4 drinks
 per week; a larger increase in relative risk (1.4-1.7) with a
 significant dose relationship occurs at intakes of 2-3 drinks
 per day. Two drinks per day would supply approximately 7-10%
 of a woman's caloric intake. This evidence, coupled with the
 general association of breast cancer risk with higher
 economic, nutritional and education status, supports the view
 that relevant animal models for study of the relationship
 between alcohol and breast cancer should employ moderate
 alcohol and good nutrient intake. Two carcinogenesis
 experiments were performed in ethanol-fed, female, Sprague-
 Dawley rats. In the first, groups of 50 rats were fed control
 diet ad libitum (CON) or were fed the diet with 20% of
 calories supplied as ethanol (ETOH) or were pair-fed control
 diet in amounts determined by the intake of ETOH rats (PF).
 They were given 7,12-dimethylbenzanthracene (DMBA), 20 mg/kg,
 by gavage at 55 days of age and monitored for tumor
 development. There was no detectable effect of ethanol on
 mammary tumor latency, incidence, number, weight or histology.
 In the second experiment, rats divided into the same groups
 were given 25% of calories as ethanol, with occasional
 increases to 35%, and the dose of DMBA was increased to 30
 mg/kg. Again, there was no detectable effect of ethanol on
 mammary tumorigenesis. Thus, no effect of ethanol on mammary
 gland tumorigenesis by DMBA was observed in rats treated by 2
 different protocols.
 
 
 111                                   NAL Call. No.: 41.8 AM3A
 Dimethylnitrosamine-induced hepatotoxicosis in dogs as a model
 of progressive canine hepatic disease.
 Boothe, D.M.; Jenkins, W.L.; Green, R.A.; Corrier, D.E.;
 Cullen, J.M.; Boothe, H.W.; Weise, D.
 Schaumburg, Ill. : American Veterinary Medical Association;
 1992 Mar. American journal of veterinary research v. 53 (3):
 p. 411-420; 1992 Mar. Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Hepatitis; Disease models; Animal models;
 N-nitrosodimethylamine
 
 Abstract:  A model of toxin-induced progressive hepatitis is
 described in Beagles. The toxin, dimethylnitrosamine, was
 administered orally to 18 Beagles; 6 dogs comprised a control
 group. Clinical signs and laboratory test results were
 monitored as disease progressed and were used to determine the
 end point of disease. Following euthanasia, histologic lesions
 were scored and used to derive a total severity score for each
 dog. Severity scores were then used to allot the 18 dogs to 3
 groups of hepatic disease, defined as mild, moderate, or
 severe. Changes in clinical laboratory test results, including
 tests of hepatic function, and clinical signs indicative of
 liver disease were described chronologically for all dogs.
 Group means of clinical laboratory test results and
 quantifiable clinical signs (eg, weight loss and ascitic fluid
 accumulation) were compared. This model offers several
 advantages, compared with other experimental models of canine
 hepatic disease. These include hepatospecificity, similarity
 to natural disease (eg, the development of multiple
 extrahepatic portosystemic shunts), and the ability to titrate
 the disease to a desired end point. The major disadvantages of
 this model were the toxic nature of the drug to human beings
 and the variation in individual animal response to the toxin,
 which precludes preassignment of animals into groups.
 
 
 112                                   NAL Call. No.: 447.8 Am3
 Direct plasma radioimmunoassay for rat amylin-(1-37):
 concentrations with acquired and genetic obesity.
 Pieber, T.R.; Roitelman, J.; Lee, Y.; Luskey, K.L.; Stein,
 D.T. Bethesda, Md. : American Physiological Society, 1898-;
 1994 Jul. American journal of physiology v. 267 (1,pt.1): p.
 E156-E164; 1994 Jul. Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Polypeptides; Insulin; Measurement;
 Blood plasma; Radioimmunoassay; Aging; Pathogenesis; Animal
 models; Rats
 
 Abstract:  Amylin (islet-associated polypeptide) is a 37-amino
 acid peptide that is cosecreted with insulin from the
 pancreatic beta-cell. Accurate measurement of its plasma
 levels is important for delineating the physiological range
 over which amylin acts. We describe a reproducible, highly
 specific, and sensitive radioimmunoassay for direct
 measurement of plasma amylin-(1-37). We measured changes in
 portal and systemic plasma amylin and insulin in three groups
 of anesthetized rats: lean young adult and old adult Wistar
 rats with acquired obesity, and Wistar fatty [WDF/TaFa
 (fa/fa)] rats, a model of genetic obesity and insulin
 resistance derived from the Wistar strain. Changes in response
 to fasting, feeding, and intravenous stimulation with glucose
 plus arginine were assessed. We find that the amylin-to-
 insulin ratio is constant in fasted or fed young and old rats
 because of proportionate increases in both entities with
 aging. In genetically obese Wistar rats, amylin and insulin
 levels are three- to tenfold higher than in lean young or
 obese old normal controls. Islet stimulation by feeding or
 intravenous glucose plus arginine resulted in a decreased
 amylin-to-insulin molar ratio in all groups. When normalized
 for the degree of islet stimulation, amylin-to-insulin ratios
 were significantly elevated in genetically obese vs. normal
 rats, both in the portal and systemic circulation. These
 results demonstrate that aging-related weight gain in normal
 rats is associated with moderate and proportional increases in
 amylin and insulin, whereas genetic obesity is characterized
 by elevated amylin and an increased amylin-to-insulin ratio.
 Implications for the pathogenesis of insulin resistance and
 obesity are discussed.
 
 
 113                                     NAL Call. No.: QD1.A45
 Discovery and development of novel prototype antibiotics for
 opportunistic infections related to acquired immunodeficiency
 syndrome. Clark, A.M.; Hufford, C.D.
 Washington, D.C. : American Chemical Society, 1974-; 1993. ACS
 symposium series (534): p. 228-241; 1993.  In the series
 analytic: Human medicinal agents from plants / edited by A.D.
 Kinghorn and M.F. Balandrin. Includes references.
 
 Language:  English
 
 Descriptors: Antibiotics; Plant extracts; Antifungal
 properties; Antimicrobial properties; Opportunistic
 infections; Screening; Acquired immune deficiency syndrome;
 Research
 
 Abstract:  The major AIDS-related opportunistic fungal and
 bacterial infections are candidiasis. cryptococcosis and
 mycobacteriosis. The need for new, more effective and less
 toxic antibiotics for the treatment of these infections is
 obvious in light of the significant toxicities and failure
 rates of the currently available agents. In the past, the
 discovery of new antibiotics has relied primarily on the
 isolation of such agents from natural sources. The major
 advantage of this approach is the likelihood of identifying
 new prototype drugs with different chemical structures, and
 hence, possible new mechanisms and less likelihood of similar
 toxicities and cross-resistance. Although in the past
 microorganisms have been the primary source of new
 antibiotics, higher plants are now recognized as important
 sources of new antimicrobial agents. Recent efforts to
 discover new prototype antibiotics with potential utility
 specifically for the treatment of opportunistic disseminated
 mycoses and mycobacteriosis are discussed. Initial in vitro
 evaluation of higher plant extracts for antifungal and
 antimycobacterial activity is followed by fractionation and
 purification of active extracts using a bioassay-directed
 scheme. Pure compounds with significant in vitro activity are
 evaluated for in vivo efficacy in established animal models of
 disseminated mycosis and mycobacteriosis in order to determine
 their potential clinical utility.
 
 
 114                                      NAL Call. No.: 49 J82
 Divergent selection for immune responsiveness in chickens:
 estimation of realized heritability with an animal model.
 Pinard, M.H.; Arendonk, J.A.M. van; Nieuwland, M.G.B.; Zijpp,
 A.J. van der Champaign, Ill. : American Society of Animal
 Science; 1992 Oct. Journal of animal science v. 70 (10): p.
 2986-2993; 1992 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Fowls; Line differences; Antibody formation;
 Animal models; Heritability; Selection responses; Genetic
 trend; Selection differential; Breeding value; Phenotypes
 
 Abstract:  With the aim of improving general disease
 resistance, chickens were divergently selected for their
 antibody titers 5 d after immunization with sheep red blood
 cells for nine generations. Selected and control lines
 differed significantly for primary and secondary responses
 after three generations. Heritability of the antibody titer
 was estimated by REML fitting an animal model using a
 derivative-free algorithm. The heritability estimate using
 data on all lines simultaneously was .31. Realized
 heritability of the antibody titer in the selected lines was
 estimated by using either the phenotypic cumulative response
 as the deviation from the control line or the mean breeding
 values obtained with an animal model. Values from the two
 methods were consistent, giving a realized heritability of .21
 and .25 in the high and low lines, respectively. The genetic
 trend was not linear and the response to selection tended to
 accelerate over generations.
 
 
 115                                   NAL Call. No.: SF601.A47
 The effect of a single oral dose of tri-o-cresyl phosphate on
 neurotoxic esterase and acetylcholinesterase activities in the
 central nervous system, erythrocytes and plasma.
 Barrett, D.S.; Oehme, F.W.
 Manhattan, Kan. : Kansas State University; 1994 Feb.
 Veterinary and human toxicology v. 36 (1): p. 1-4; 1994 Feb. 
 Includes references.
 
 Language:  English
 
 Descriptors: Organophosphorus compounds; Toxicity; Oral
 administration; Esterases; Acetylcholinesterase; Enzyme
 activity; Inhibition; Erythrocytes; Leukocytes; Blood plasma;
 Pigs; Animal models; Toxicology; Nervous system diseases
 
 
 116                                    NAL Call. No.: QP501.C6
 Effect of adenine metabolites on survival of Drosophila
 melanogaster of low xanthine dehydrogenase activity.
 Ho, Y.K.; Guthrie, M.J.; Clifford, A.J.; Ho, C.C.
 Oxford : Pergamon Press; 1992 Oct.
 Comparative biochemistry and physiology : B : Comparative
 biochemistry v. 103 (2): p. 413-417; 1992 Oct.  Includes
 references.
 
 Language:  English
 
 Descriptors: Drosophila melanogaster; Adenine; Metabolism;
 Metabolites; Toxicity; Survival; Xanthine dehydrogenase;
 Enzyme activity; Metabolic disorders; Animal models
 
 Abstract:  Low xanthine dehydrogenase (LXD) mutant Drosophila
 melanogaster were fed 0.2% adenine for 7 generations, no
 adenine for the next 2 generations (relaxed) and 0.2% adenine
 again for the next 3 generations (rechallenged) to obtain
 adenine-resistant lines of Drosophila (LXD-adenine). Flies
 grown without adenine served as LXD-controls. Purines ranked
 as follows; adenine > adenosine > AMP > inosine > IMP in
 decreasing order of toxicity to LXD-adenine flies. Addition of
 ribose to 9N position, or phosphate or carboxy to 6C position
 of the purine ring alleviated the toxicity. More LXD-adenine
 offspring survived than did LXD-control offspring rechallenged
 with adenine.
 
 
 117                                   NAL Call. No.: QP534.B56
 Effect of age and sex on copper-induced toxicity in the
 macular mutant mouse--an animal model for Menkes' kinky-hair
 disease.
 Shiraishi, N.; Taguchi, T.; Kinebuchi, H.
 Totowa, N.J. : Humana Press; 1993 Nov.
 Biological trace element research v. 39 (2/3): p. 129-137;
 1993 Nov.  Includes references.
 
 Language:  English
 
 Descriptors: Copper; Subcutaneous injection; Toxicity; Age;
 Sex; Disease models; Mice
 
 
 118                                   NAL Call. No.: 381 J8282
 Effect of dietary oils on lipid peroxidation and on
 antioxidant parameters of rat plasma and lipoprotein
 fractions.
 Scaccini, C.; Nardini, M.; D'Aquino, M.; Gentili, V.; Di
 Felice, M.; Tomassi, G.
 Bethesda, Md. : Lipid Research, Inc; 1992 May.
 Journal of lipid research v. 33 (5): p. 627-633; 1992 May. 
 Includes references.
 
 Language:  English
 
 Descriptors: Dietary fat; Soybean oil; Olive oil; Triolein;
 Unsaturated fatty acids; Antioxidants; Lipid peroxidation; Low
 density lipoprotein; Very low density lipoprotein; Blood
 lipids; Blood plasma; Rats
 
 Abstract:  In order to investigate the influence of fatty acid
 pattern and antioxidants other than vitamin E on lipid
 peroxidation and antioxidant levels of plasma very low density
 and low density lipoproteins (VLDL + LDL), the effects of
 three diets (equalized for vitamin E) containing soybean oil,
 olive oil, or an oleate-rich mixture of triglycerides
 (triolein) were studied in rats. A significantly lower
 concentration of thiobarbituric acid-reactive substances (TBA-
 RS) in plasma and lipoproteins was found after the olive oil
 diet (soybean oil, 3.7 +/- 0.4 nmol/ml; triolein, 2.1 +/- 0.5
 nmol/ml; olive oil, 1.5 +/- 0.3 nmol/ml, in plasma) (soybean
 oil, 0.99 +/- 0.16 nmol/ml; triolein, 0.96 +/- 0.13 nmol/ml;
 olive oil, 0.38 +/- 0.12 nmol/ml, in the VLDL + LDL fraction).
 Furthermore, the results from in vitro copper-induced lipid
 peroxidation, expressed in terms of conjugated dienes, lipid
 hydroperoxides, and TBA-RS content, showed that VLDL + LDL
 particles from olive oil-fed rats were remarkably resistant to
 oxidative modification. The results suggest that the fatty
 acid unsaturation of dietary oils is not the only determining
 factor of the antioxidant capacity of lipoproteins in this
 animal model. The maximal protection observed after the olive
 oil diet may be explained by the presence of other
 unidentified antioxidants in addition to vitamin E, derived
 from oil intake. Therefore, the optimal balance between the
 content of unsaturated fatty acids and natural antioxidants in
 dietary oils appears to be of major importance.
 
 
 119                              NAL Call. No.: RC628.N48 1987
 The effect of different dietary carbohydrates on insulin and
 glucagon receptors in two models of genetic obesity: LA/N-
 corpulent rat and SHR/N-corpulent rat.
 Bhathena, S.J.; Kennedy, B.W.; Michaelis, O.E. IV; Jones, J.;
 Carswell, N.; Marsh, P.A.; Hansen, C.T.; Voyles, N.R.; Recant,
 L.
 Bethesda, Md. : National Institutes of Health; 1988.
 New models of genetically obese rats for studies in diabetes,
 heart disease, and complications of obesity : NIH workshop,
 June 18-19, 1987, summaries of workshop papers and current
 bibliography. p. 25-30; 1988.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Obesity; Dietary carbohydrate;
 Glucagon; Insulin; Rats
 
 
 120                                 NAL Call. No.: QP141.A1N88
 The effect of ovarian status, form of vitamin D3 steroid and
 calcium supplementation on bone metabolism in the rat and the
 quail. Osborne, M.T.; Soares, J.H. Jr
 Elmsford, N.Y. : Pergamon Press; 1990 Aug.
 Nutrition research v. 10 (8): p. 887-901; 1990 Aug.  Includes
 references.
 
 Language:  English
 
 Descriptors: Cholecalciferol; Vitamin d; Metabolites;
 Osteoporosis; Bone density; Calcium; Mineral supplements;
 Ovariectomy; Rats; Quails
 
 Abstract:  Degenerative bone conditions such as osteoporosis
 affect the elderly population by causing skeletal fractures.
 The incidence of osteoporosis is far greater in postmenopausal
 women and therefore, loss of ovarian function, leading to
 estrogen deficiency, plays an important role in the
 development of this disease. Abnormal vitamin D metabolism and
 insufficient dietary calcium may also contribute to the
 development of osteoporosis. Three experiments were conducted
 to investigate the effects of estrogen supplementation and
 dietary vitamin D3 steroids or calcium supplementation on
 skeletal metabolism. Eight week old ovariectomized (Ovx) or
 sham operated Sprague-Dawley rats or aged anovulatory Coturnix
 quail hens were used as animal models. Feeding a diet
 containing 1,25(OH)2D3 (5 microgram/kg) with 0.2% calcium was
 as effective in maintaining bone mineral concentrations as 20
 microgram/kg vitamin D3 and 1.0% calcium. However, both bone
 calcium and zinc concentrations were decreased in Ovx rats and
 anovulatory quail fed 1,25(OH)2D3 and low calcium. Estrogen
 supplementation to Ovx rats and anovulatory quail fed
 1,25(OH)2D3 and 0.2% Ca increased mineral concentrations, thus
 suggesting enhanced skeletal integrity. Therefore, these
 studies suggest improved skeletal calcification in control and
 estrogen supplemented female rats and quail fed 1,25(OH)2D3
 and 0.2% calcium versus vitamin D3 with 1.0% calcium.
 
 
 121                                  NAL Call. No.: 389.8 J824
 Effect of phytate removal on zinc absorption from soy formula.
 Lonnerdal, B.; Bell, J.G.; Hendrickx, A.G.; Burns, R.A.; Keen,
 C.L. Baltimore, Md. : American Society for Clinical Nutrition;
 1988 Nov. American journal of clinical nutrition v. 48 (5): p.
 1301-1306. charts; 1988 Nov.  Includes 28 references.
 
 Language:  English
 
 Descriptors: Zinc; Infant formulas; Soy milk; Phytate;
 Intestinal absorption; Neonates; Rhesus monkeys; Rats
 
 Abstract:  Low zinc bioavailability from soy formula may be
 the result of the formula's phytate content. We assessed the
 effect of phytate removal from soy formula on Zn absorption
 using infant rhesus monkeys and suckling rat pups as animal
 models. Zn absorption in monkeys, as determined by whole-body
 counting, was 65% from human milk, 54% from monkey milk, 60%
 from whey-predominant formula, 46% from casein-predominant
 formula, and only 27% from conventional soy formula (0.621
 mmol phytate/L). In contrast, Zn absorption from dephytinized
 soy formula (0.067 mmol phytate/L) was 45%. In suckling rats,
 Zn absorption from conventional soy formula was only 16% vs
 47% from dephytinized soy formula. Phytate concentration in a
 variety of experimental soy formulas was inversely correlated
 to Zn absorption. These results suggest that the low
 bioavailability of Zn from soy formula is a function of its
 phytate concentration and can be overcome by the removal of
 phytate.
 
 
 122                                    NAL Call. No.: 381 B522
 The effect of pravastatin on serum cholesterol levels in
 hypercholesterolemic diabetic rabbits.
 Arbeeny, C.M.; Bergquist, K.E.
 Amsterdam : Elsevier Science Publishers; 1991 Apr03.
 Biochimica et biophysica acta : International journal of
 biochemistry and biophysics v. 1096 (3): p. 238-244; 1991
 Apr03.  Includes references.
 
 Language:  English
 
 Descriptors: Diabetes mellitus; Hypercholesterolemia; Drug
 therapy; Blood serum; Cholesterol; Rabbits
 
 Abstract:  Diabetes mellitus is associated with hyperlipidemia
 and increased risk of atherosclerosis. A diabetic animal model
 has been developed to study the effect of treatment with
 pravastatin, a potent HMG CoA reductase inhibitor, on plasma
 lipoprotein levels. Hypercholesterolemia was induced in
 alloxan diabetic and control rabbits by feeding a diet
 containing 25% casein and 10% hydrogenated coconut oil for 8
 weeks. Feeding the casein-coconut oil diet to the diabetic
 group resulted in a 5-fold increase in serum cholesterol
 levels, which was not statistically different from the
 nondiabetic group fed this diet. However, in the diabetic
 group, there was more cholesterol in the VLDL fraction and
 less in LDL as compared to the nondiabetic group. Serum
 triacylglycerol levels in the diabetic rabbits were variable
 and ranged from 58-943 mg/dl. The diabetic and nondiabetic
 animals were then treated with pravastatin at a dose of 10
 mg/kg per day for 21 days. In the nondiabetic group,
 pravastatin treatment significantly lowered serum and LDL
 cholesterol concentrations by 28.5% (52.3 mg/dl, P < 0.05) and
 36.2% (40.7 mg/dl, P < 0.05) respectively, relative to the
 placebo group. Serum and VLDL triacylglycerol levels in the
 nondiabetic group were also significantly decreased following
 pravastatin treatment. In the diabetic group, serum and LDL
 cholesterol levels were decreased by 37.0% (69.1 mg/dl, P <
 0.05) and 52.7% (32.1 mg/dl, P < 0.01), respectively, relative
 to the diabetics given the placebo. Pravastatin treatment did
 not adversely affect serum glucose levels. Thus, pravastatin
 treatment was effective in controlling the
 hypercholesterolemia present in these diabetic animals.
 
 
 123                                    NAL Call. No.: 41.8 J82
 The effect of recent vaccination on the dose-response to
 experimental Dermatophilus congolensis infection in rabbits.
 How, S.J.; Lloyd, D.H.
 London : Academic Press; 1990 Feb.
 Journal of comparative pathology v. 102 (2): p. 157-163; 1990
 Feb.  Includes references.
 
 Language:  English
 
 Descriptors: Rabbits; Dermatophilus congolensis; Vaccination;
 Live vaccines; Dosage effects; Elisa; Cross immunity; Cross
 immunization; Animal models
 
 
 124                                  NAL Call. No.: RC262.C5N8
 Effect of the amount of dietary fat on the development of
 mammary tumors in BALB/c-MTV mice.
 Zevenbergen, J.L.; Verschuren, P.M.; Zaalberg, J.; Stratum, P.
 van; Vles, R.O. Hillsdale, N.J. : Lawrence Erlbaum Associates,
 Inc; 1992. Nutrition and cancer v. 17 (1): p. 9-18; 1992. 
 Includes references.
 
 Language:  English
 
 Descriptors: Dietary fat; Mammary gland neoplasms; Incidence;
 Mice
 
 Abstract:  The relationship between dietary fat consumption
 and the incidence of breast cancer, if any, needs to be
 quantified so that dietary guidelines can be issued for the
 prevention of breast cancer. Frequently, only two widely
 different dietary fat levels, often differing in essential
 fatty acid content, have been compared in animal models.
 Moreover, the latent period in common animal models for breast
 cancer is very short and does not reflect the relatively long
 latent periods in human breast cancer. We describe a study
 with BALB/c-MTV mice, a strain with a high average tumor
 incidence and a latent period of over 60 weeks on average. The
 mice were fed diets with fat levels ranging from 10% to 40% of
 energy, in which fat was isocalorically substituted for
 carbohydrates. The level of linoleic acid in these diets was
 kept constant al 6.5% of energy. Both the mean tumor incidence
 and latent periods of the groups fed diets with 10-16% of
 energy as fat were not significantly different from each
 other. There were also no differences between these parameters
 in the groups fed 22-40% of energy as fat. However, the mean
 incidence and latent period of the groups fed 22% or more of
 energy as fat was significantly higher than that of the groups
 fed less fat. We conclude that above about 22 % of energy, fat
 does not influence the incidence and latent period of mammary
 tumors in BALB/c-MTV mice.
 
 
 125                                   NAL Call. No.: 41.8 AM3A
 Effectiveness of arprinocid in the reduction of
 cryptosporidial activity in immunosuppressed rats.
 Rehg, J.E.; Hancock, M.L.
 Schaumburg, Ill. : American Veterinary Medical Association;
 1990 Oct. American journal of veterinary research v. 51 (10):
 p. 1668-1670; 1990 Oct. Includes references.
 
 Language:  English
 
 Descriptors: Cryptosporidium; Rats; Immunosuppression;
 Arprinocid; Drug effects; Disease prevention
 
 Abstract:  Immunosuppressed rats inoculated with
 Cryptosporidium oocysts isolated from calves' feces were
 treated with arprinocid, 50 mg/kg of body weight/d. As
 determined from differences in the mean number of
 cryptosporidial developmental stages per villus in treated vs
 control rats, arprinocid had a substantial effect on
 cryptosporidial activity, which was parasitistatic instead of
 parasiticidal. Drug-ranging experiments indicated that
 arprinocid was effective at 50 and 25 mg/kg/d, but not at 12.5
 mg/kg/d. These results suggest that further testing of
 arprinocid in different animal models, or in phase-I clinical
 trials, is warranted.
 
 
 126                                   NAL Call. No.: 410.9 P94
 Effects of dieatary vitamin E on clinical course and plasma
 glutamic oxaloacetic transaminase and glutamic pyruvic
 transaminase activities in hereditary hepatitis of LEC rats.
 Yamazaki, K.; Ohyama, H.; Kurata, K.; Wakabayashi, T.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1993 Feb. Laboratory animal science v. 43 (1): p.
 61-67; 1993 Feb.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Hepatitis; Vitamin e; Animal models
 
 Abstract:  Long-Evans Cinnamon (LEC) rats are autosomal
 recessive mutants that develop hepatitis and hepatocellular
 carcinoma. Because copper accumulates in the livers of these
 rats, and some of their clinical and pathological features are
 similar to those of patients with Wilson's disease, LEC rats
 are proposed as an animal model of Wilson's disease. It has
 been thought that unbound copper generates free radicals,
 which act as hemolytic and hepatocytotoxic agents. To examine
 the effects of vitamin E as an antioxidant on hereditary
 hepatitis in LEC rats, we fed 3-week-old rats for 25 weeks
 either vitamin E-deficient, control, or vitamin E-supplemented
 diets which contained < 0.1 mg of total tocopherols, 2 mg of
 d,l-alpha-tocopheryl acetate (2 I.U.), and 58.5 mg of d,l-
 alpha-tocopheryl nicotinate (50 I.U.), respectively, per 100
 mg of feed. In males, body weight loss was first observed in
 the vitamin E-deficient group, and mean ages at which jaundice
 occurred were in the order: deficient younger than control
 younger than supplemented groups. The ages when plasma
 glutamic oxaloacetic transaminase and glutamic pyruvic
 transaminase activities began to increase sharply and peaked
 followed the same order. Thus, it is likely that free radicals
 are involved in jaundice and hepatitis in LEC male rats, and
 they are a model for studying the relationship of copper, free
 radicals, and hepatitis. Conversely, in females, no apparent
 differences in clinical and biochemical changes were observed
 among the three groups. Causes for the discrepancy between the
 sexes remain to be clarified.
 
 
 127                                 NAL Call. No.: QP141.A1N88
 Effects of dietary fish oil on survival and renal fatty acid
 composition in murine polycystic kidney disease.
 Aukema, H.M.; Yamaguchi, T.; Takahashi, H.; Philbrick, D.J.;
 Holub, B.J. Tarrytown, N.Y. : Pergamon Press; 1992 Nov.
 Nutrition research v. 12 (11): p. 1383-1392; 1992 Nov. 
 Includes references.
 
 Language:  English
 
 Descriptors: Diet; Fish oils; Kidney diseases; Kidneys; Fatty
 acids; Composition; Mice
 
 Abstract:  It has been demonstrated that replacing dietary n-6
 with n-3 polyunsaturated fatty acids is beneficial in some
 animal models of renal disease, but not in others. We fed
 semi-purified diets containing either sunflowerseed oil
 (containing linoleic acid, 18:2n-6) or fish oil (containing
 eicosapentaenoic acid, 20:5n-3, plus docosahexaenoic acid,
 22:6n-3) to a mouse model of polycystic kidney disease
 (DBA/2FG-pcy). Renal phospholipid and triglyceride fatty acid
 compositions were markedly altered by dietary treatment:
 20:5n-3 and 22:6n-3 levels were elevated in the kidneys from
 mice fed fish oil at the expense of 18:2n-6 and arachidonic
 acid, 20:4n-6. Despite these lipid alterations, however,
 survival and proteinuria were not improved by long term fish
 oil consumption in mice with polycystic kidney disease.
 
 
 128                                  NAL Call. No.: RC628.A1O2
 Effects of exercise and stress on body fat distribution in
 male cynomolgous monkeys.
 Jayo, J.M.; Shively, C.A.; Kaplan, J.R.; Manuck, S.B.
 Avenel, NJ : The Macmillan Press Ltd; 1993 Oct.
 International journal of obesity and related metabolic
 disorders : journal of the International Association for the
 Study of Obesity v. 17 (10): p. 597-604; 1993 Oct.  Includes
 references.
 
 Language:  English
 
 Descriptors: Body fat; Distribution; Exercise; Mental stress;
 Nutrient intake; Computed tomography; Males; Monkeys
 
 Abstract:  The effects of exercise and stress on regional and
 whole body adiposity were examined in an established animal
 model of diet-induced coronary artery atherosclerosis, the
 cynomolgus monkey (Macaca fascicularis). A total of 79 adult
 male monkeys were assigned to four experimental groups after
 baseline stabilization and training: (i) exercise, stress, (n
 = 20); (ii) exercise, no stress (n = 20); (iii) sedentary,
 stress (n = 20); and (iv) sedentary, no stress (n = 19). The
 monkeys consumed an ad libitum diet containing 188 mg
 cholesterol per day with 43% of calories as saturated fat.
 Anthropometric measurements of regional and whole body
 adiposity were collected throughout the study. A subset (n =
 40) of animals representing all four groups underwent
 computerized tomography (CT) scans at the end of the study to
 determine amounts of total abdominal, intra-abdominal and
 subcutaneous abdominal adipose tissue. Results indicate that,
 in general, stress interacted with exercise to affect
 anthropometric measurements of regional adiposity. In
 contrast, stress had independent and significant effects on
 the amount and distribution of abdominal fat as measured using
 CT. Stressed monkeys in both the exercise and sedentary groups
 had more intra-abdominal fat (and thus greater intra-abdominal-
  :subcutaneous abdominal fat ratios) than their non-stressed
 counterparts. There were no significant interactions between
 exercise and stress or exercise effects on abdominal fat
 distribution as measured by CT. These results support the
 belief that an arousal syndrome caused by chronic stress, and
 resulting in increased activity along the hypothalamo-adrenal
 axis, may play a role in the preferential deposition of fat in
 the abdomen. Finally, anthropometric measurements did not
 predict the proportion of intra-abdominal versus subcutaneous
 fat in abdominal depots, suggesting that anthropometric
 measurements and CT assess different characteristics of fat
 distribution.
 
 
 129                                  NAL Call. No.: RC620.A1J6
 Effects of gestation, lactation, and maternal calcium intake
 on mechanical strength of equine bone.
 Glade, M.J.
 Wilmington, NC : American College of Nutrition; 1993 Aug.
 Journal of the American College of Nutrition v. 12 (4): p.
 372-377; 1993 Aug. Includes references.
 
 Language:  English
 
 Descriptors: Calcium; Nutrient intake; Lactation; Pregnancy;
 Bone strength; Postpartum period; Maternal nutrition; Horses
 
 Abstract:  Skeletal homeostasis during late gestation,
 lactation, and the post-lactational recovery period is poorly
 understood. In an experiment using an animal model (the
 horse), metacarpal breaking strengths (MBS) estimated via
 transmission ultrasonics were examined during the last 12
 weeks of gestation and for 40 weeks after parturition. MBS
 increased during the last 6-10 weeks of gestation in mares fed
 amounts of calcium (Ca) recommended by the National Research
 Council; maximum MBS coincided with the week of parturition.
 In contrast, MBS in mares fed 20% less Ca remained relatively
 constant during the last 12 weeks of gestation. In contrast to
 increases during late gestation, MBS decreased steadily in all
 mares during the first 12 weeks of lactation. MBS increased
 after approximately 12 weeks of lactation, but more slowly
 than they had declined. MBS of the bones of mares fed
 recommended amounts of Ca were fully restored at 24 weeks
 post-parturition, but those of Ca-deficient mares had not
 fully recovered even 20 weeks after milk production had ceased
 (40 weeks after parturition). Mid-cannon mediolateral
 diameters of foals born to mares fed Ca-deficient diets were
 thinner and mechanically weaker at birth (both p < 0.01).
 These differences in limb bone size and strength persisted
 during the first 40 weeks of life.
 
 
 130                                   NAL Call. No.: 448.8 M56
 Effects of high fat-feeding to rats on the interrelationship
 of body weight, plasma insulin, and fatty acyl-coenzyme A
 esters in liver and skeletal muscle. Chen, M.T.; Kaufman,
 L.N.; Spennetta, T.; Shrago, E.
 Philadelphia, Pa. : W.B. Saunders Co; 1992 May.
 Metabolism: clinical and experimental v. 41 (5): p. 564-569;
 1992 May. Includes references.
 
 Language:  English
 
 Descriptors: Dietary fat; Saturated fats; Dietary
 carbohydrate; Body weight; Blood plasma; Insulin; Glucose;
 Energy intake; Acetyl coenzyme a; Liver; Skeletal muscle;
 Hyperinsulinemia; Correlation; Lipid metabolism; Carbohydrate
 metabolism; Animal models; Rats
 
 
 131                                    NAL Call. No.: 500 N484
 Effects of marine fish oil on blood pressure and vascular
 reactivity in the hereditary hypertriglyceridemic rat.
 Edelsteinova, S.; Kyselovic, J.; Klimes, I.; Sebokova, E.;
 Kovacsova, B.; Kristek, F.; Mitkova, A.; Vrana, A.; Svec, P.
 New York : New York Academy of Sciences, 1877-; 1993.
 Annals of the New York Academy of Sciences v. 683: p. 353-356;
 1993.  In the series analytic: Dietary lipids and insulin
 action / edited by I. Klimes, B.V. Howard, L.H. Storlien, and
 E. Sebokova. Proceeding of the Second International Smolenice
 Insulin Symposium, September 12-16, 1992, Smolenice Castle,
 Slovak Republic.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Blood pressure; Fish oils; Food
 supplements; Human nutrition research; Hereditary diseases;
 Hypertriglyceridemia; Rats
 
 
 132                                  NAL Call. No.: RC628.A1O2
 Effects of maternal obesity on fasting metabolism in newborn
 rats. Heng, J.; Kliegman, R.M.
 Basingstoke, Hampshire : The Macmillan Press Ltd; 1990 Jun.
 International journal of obesity v. 14 (6): p. 505-513; 1990
 Jun.  Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Maternal nutrition; Fasting; Metabolism;
 Hypoglycemia; Weight gain; Pregnancy; Eating patterns;
 Neonates; Rats
 
 Abstract:  Maternal obesity is a risk factor for subsequent
 fasting hypoglycemia in human infants after birth. To
 investigate further this problem, we employed an animal model
 of obesity to study neonatal extrauterine metabolic
 adaptations in pups of obese and lean rats. Female Sprague-
 Dawley rats were fed a 'cafeteria diet' to induce obesity
 prior to and during pregnancy. Prior to mating, the cafeteria
 fed rats were significantly heavier (449 v. 345 g, P < 0.001)
 than the controls. Furthermore, weight gain during pregnancy
 and weight at term were also significantly greater in the
 obese rats even though they consumed less food during
 pregnancy. Pup weights and the number of pups per litter were
 similar between the two groups. Pups born to obese mothers
 demonstrated hypoglycemia after being fasted for 150 and 180
 min when compared with control pups. Hepatic glycogen stores
 were increased in the fetus of pups born to obese mothers.
 Glycogen content in pups born to obese mothers declined
 minimally after birth and remained greater than hepatic
 glycogen values in control pups throughout the study. In
 addition to increased fetal storage of glycogen, fetal hepatic
 triglyceride content was augmented in pups of obese rats.
 These triglyceride stores declined and were mobilized during
 fasting after birth. In contrast, hepatic triglyceride content
 increased after birth among control rats. These results
 suggest that maternal obesity results in augmented fetal
 hepatic tissue stores of both glycogen and triglycerides.
 Hypoglycemia among pups of excessively obese mothers may be
 due to attenuated mobilization of hepatic glycogen. Alternate
 fuel utilization as evident by the mobilization (rather than
 storage) of hepatic triglycerides may contribute to energy
 metabolism during periods of hypoglycemia.
 
 
 133                                  NAL Call. No.: RC620.A1N8
 The effects of replacing coconut oil with corn oil on human
 serum lipid profiles and platelet derived factors active in
 atherogenesis. Mendis, S.; Wissler, R.W.; Bridenstine, R.T.;
 Podbielski, F.J. Stoneham, Mass. : Butterworth; 1989 Oct.
 Nutrition reports international v. 40 (4): p. 773-782. charts;
 1989 Oct. Includes 33 references.
 
 Language:  English
 
 Descriptors: Sri lanka; Maize oil; Coconut oil; Diet; Blood
 lipids; Cholesterol; Triglycerides; High density lipoprotein;
 Low density lipoprotein; Young adults; Men
 
 Abstract:  Young, healthy individuals living in Sri Lanka
 often consume a diet containing coconut oil as their main
 source of fat. Blood lipid values and selected platelet
 related factors have been measured in a group of 16 free
 living young adults, ages 16 to 21, before and 8 weeks after
 they had been shifted from their usual diet to a similar one
 in which the coconut oil was replaced by whole milk powder and
 corn oil. The results indicate that their blood cholesterol,
 cholesteryl ester, and several other related circulating blood
 lipid values, as well as the platelet factor 4 values, were
 elevated prior to the diet change. Many of these factors,
 associated as risk factors for atherogenesis, were
 substantially reduced at the end of the diet change. The only
 plasma components which were altered substantially were the
 triglycerides and the HDL cholesterol. These results suggest
 that the special atherogenic effects of coconut oil that have
 been demonstrated in so many animal models may be similarly
 active in humans.
 
 
 134                                   NAL Call. No.: 410.9 P94
 Effects of sex hormones on fulminant hepatitis in LEC rats: a
 model of Wilson's disease.
 Kasai, N.; Miyoshi, I.; Osanai, T.; Yamashita, T.; Kamimura,
 E.; Yoshida, M.C. Cordova, Tenn. : American Association for
 Laboratory Animal Science; 1992 Aug. Laboratory animal science
 v. 42 (4): p. 363-368; 1992 Aug.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Disease models; Sex hormones; Hepatitis
 
 Abstract:  LEC rats, which have hereditary hepatitis and have
 recently been proposed as an animal model for Wilson's
 disease, were examined to determine the effects of sex
 hormones on fulminant hepatitis. After the rats had undergone
 ovariectomies or orchidectomies (castration) and were compared
 with intact rats, the age at the onset of fulminant hepatitis
 was not substantially altered but the survival rates decreased
 from 50% to 12.5% for females and 75% to 14.3% for males,
 indicating that sex hormones did not influence the occurrence
 of fulminant hepatitis but influenced mortality due to
 fulminant hepatitis. When testosterone was administered to the
 ovariectomized or orchidectomized rats, the survival rate
 increased to over 90% in both sexes. In contrast, estradiol
 did not affect the survival rate of either sex but affected
 the onset of fulminant hepatitis. That is, with the
 administration of estradiol, the age at which serum GPT
 activity reached its maximum was delayed 4 weeks in
 ovariectomized rats and 6 weeks in orchidectomized rats as
 compared with intact rats. A similar but somewhat weaker
 tendency appeared in rats given progesterone. The results of
 our study indicate that sex hormones have no effect on the
 rate of occurrence of hepatitis but affect the progression of
 hepatitis. In particular, testosterone increased the survival
 rate of rats with fulminant hepatitis, and exogenous estradiol
 delayed the onset of hepatitis for several weeks.
 
 
 135                                   NAL Call. No.: 44.8 J822
 Efficacy of tumor necrosis factor-alpha and antibiotics in
 therapy of experimental murine staphylococcal mastitis.
 Sanchez, M.S.; Ford, C.W.; Yancey, R.J. Jr
 Champaign, Ill. : American Dairy Science Association; 1994
 May. Journal of dairy science v. 77 (5): p. 1259-1266; 1994
 May.  Includes references.
 
 Language:  English
 
 Descriptors: Tumor necrosis factor; Staphylococcus aureus;
 Mastitis; Animal models; Mice; Neutrophils; Lymphocyte
 transformation; Experimental infections; Bacterial count; Drug
 combinations; Ciprofloxacin; Cloxacillin; Antibiotics; Drug
 effects; Lactation; Dry period
 
 Abstract:  The mouse model was used to determine the efficacy
 of the cytokine, tumor necrosis factor-alpha and antibiotic in
 treatment of experimentally induced staphylococcal mastitis.
 Recombinant human tumor necrosis factor-alpha alone
 administered to the mammary glands of lactating mice recruited
 significantly more polymorphonuclear neutrophils into the
 gland by 4 h posttreatment than did the untreated control. One
 hundred times less recombinant mouse tumor necrosis factor-
 alpha than human tumor necrosis factor-alpha was required to
 enhance the killing of Staphylococcus aureus within the gland.
 Human tumor necrosis factor-alpha effectively enhanced the
 killing of the bacteria when it was administered 4 to 0 h
 prior to infection, but not 4 h after infection. When mice
 were first pretreated with tumor necrosis factor-alpha,
 infected, and then treated with antibiotics (ciprofloxacin and
 pirlimycin, but not cloxacillin), the combination of
 antibiotic and cytokine significantly reduced the number of
 bacteria within the gland compared with that for mice treated
 with antibiotic alone, cytokine alone, or placebo. Recombinant
 tumor necrosis factor-alpha may be an effective adjunct to
 antimicrobial therapy in treatment of staphylococcal mastitis
 in the bovine.
 
 
 136                                   NAL Call. No.: 41.8 AM3A
 Electrocadiographic and echocardiographic features of
 trypanosomiasis in dogs inoculated with North American
 Trypanosoma cruzi isolates. Barr, S.C.; Holmes, R.A.; Klei,
 T.R.
 Schaumburg, Ill. : American Veterinary Medical Association;
 1992 Apr. American journal of veterinary research v. 53 (4):
 p. 521-527; 1992 Apr. Includes references.
 
 Language:  English
 
 Descriptors: Louisiana; Dogs; Trypanosoma cruzi;
 Trypanosomiasis; Cardiomyopathy; Disease models;
 Electrocardiograms; Recordings; Disease course; Animal models
 
 Abstract:  Purebred Beagles were inoculated with Trypanosoma
 cruzi isolates from a North American opossum or armadillo (Tc-
 W), and dog (Tc-D). Although Tc-D established infection in
 dogs, the dogs did not develop cardiac abnormalities. Dogs
 inoculated with Tc-W developed acute myocarditis associated
 with increases in P-R interval, atrioventricular block,
 depression of R wave amplitude and shifts in mean electrical
 axis. Echocardiograms were normal during this stage. Three Tc-
 W-inoculated dogs died during the acute stage. Following the
 acute stage, 5 of 8 Tc-W-inoculated dogs entered an
 indeterminate stage in which ECG changes were minor and
 echocardiograms were normal. Progression to the chronic stage
 in 5 of the 8 Tc-W-inoculated dogs was indicated by
 development of ventricular-based arrhythmias, mainly
 ventricular premature contractions, between postinoculation
 days 60 and 170. In some dogs, ventricular premature
 contractions were multifocal. Electrocardiographic
 abnormalities progressively degenerated to various forms of
 ventricular tachycardia. Worsening ECG coincided with loss of
 left ventricular function as measured by echocardiography.
 Mean percent ejection fraction and percentage of fractional
 shortening decreased to 63% and 52% of control values,
 respectively. The left ventricular free wall (LVFW) thickness
 decreased and % septal: % LVFW thickening ratio increased,
 indicating a relative preservation of septal wall motion and
 LVFW hypokinesis.
 
 
 137                                   NAL Call. No.: 442.8 Ex7
 Energy metabolism, replicative ability, intracellular calcium
 concentration, and ionic channels of horse articular
 chondrocytes.
 Vittur, F.; Grandolfo, M.; Fragonas, E.; Godeas, C.; Paoletti,
 S.; Pollesello, P.; Kvam, B.J.; Ruzzier, F.; Starc, T.;
 Mozrzymas, J.W.
 Orlando, Fla. : Academic Press; 1994 Jan.
 Experimental cell research v. 210 (1): p. 130-136; 1994 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Horses; Cartilage; Chondrocytes; Energy
 metabolism; Glycolysis; Replication; Calcium; Potassium;
 Phosphorus; Ion transport; Disease models; Arthritis
 
 Abstract:  Some aspects of the physiology of chondrocytes from
 horse articular cartilage were studied, since this animal
 model can be helpful in understanding arthritic processes. The
 replicative ability of articular chondrocytes, measured by the
 incorporation of [3H]thymidine, and their capacity of
 proteoglycan production, evaluated from the incorporation of
 [35S]sulfate, are very low. In addition, these cells do not
 differentiate in vitro as shown by the constant specific
 activity of alkaline phosphatase measured at different times
 in culture. Two types of potassium channels were identified by
 patch clamp experiments in the cell-attached configuration,
 one characterized by a conductance of 40 pS and the other of
 100 pS. No active K+ channels were found at V(pip) = 0. It was
 shown by Fura-2 experiments that the low replicative ability
 is paralleled by a modest variation of the intracellular
 calcium concentration after a mitogenic stimulus. 31P NMR
 experiments, both on slices of whole articular cartilage and
 on isolated cells, demonstrate that chondrocytes derive their
 energy mainly from the glycolytic pathway.
 
 
 138                     NAL Call. No.: 41.2 H198 1988 [no.108]
 Entwicklung eines Modelles zur Untersuchung psychosozialer und
 genetischer Einflusse auf den Verlauf einer chronisch
 respiratorischen Erkrankung (Murine Respiratorische
 Mykoplasmose) bei der Ratte  [Development of an animal model
 to estimate social and genetic influences on the course of
 chronic respiratory disease (Murine Respiratory
 Mycoplasmosis)].
 Iglauer, Franz
 Hannover : [s.n.],; 1988.
 116 p. : ill. ; 21 cm. (Inaugural-Dissertation / Tierarztliche
 Hochschule Hannover ; 1988, [no. 108]).  English summary. 
 Includes bibliographical references.
 
 Language:  German
 
 
 139                                    NAL Call. No.: QR360.J6
 Equine H7N7 influenza A viruses are highly pathogenic in mice
 without adaptation: potential use as an animal model.
 Kawaoka, Y.
 Washington, D.C. : American Society for Microbiology; 1991
 Jul. Journal of virology v. 65 (7): p. 3891-3894; 1991 Jul. 
 Includes references.
 
 Language:  English
 
 Descriptors: Equine influenzavirus; Pathogenicity; Virulence;
 Fatal infections; Experimental infections; Nervous system
 diseases; Mice; Animal models
 
 Abstract:  Equine H7N7 influenza A viruses, representing a
 broad range of isolates, were lethal in mice without
 adaptation. After repeated passages, A/Equine/London/1416/73
 acquired neurotropism upon intranasal infection. Thus, mice
 infected with equine influenza A viruses provide a model
 system for the study of highly virulent mammalian influenza
 viruses.
 
 
 140                                   NAL Call. No.: SF951.J65
 Equine infectious anemia as an AIDS animal model.
 Tashijan, R.J.; Crusberg, T.C.
 Lake Elsinore, Calif. : William E. Jones, DVM; 1989 Mar.
 Journal of equine veterinary science v. 9 (2): p. 105-110;
 1989 Mar. Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Horses; Equine infectious anemia; Equine
 infectious anemia virus; Disease models
 
 
 141                                  NAL Call. No.: 389.1 W892
 Essentiality of omega 3 fatty acids: evidence from the primate
 model and implications for human nutrition.
 Connor, W.E.; Neuringer, M.; Reisbick, S.
 Basel : S. Karger; 1991.
 World review of nutrition and dietetics v. 66: p. 118-132;
 1991.  In the series analytic: Health effects of omega-3
 polyunsaturated fatty acids in seafoods / edited by A.
 Simopoulos, R. Kifer, R. Martin and S. Barlow. Includes
 references.
 
 Language:  English
 
 Descriptors: Docosenoic acids; Fish oils; Essential fatty
 acids; Animal models; Macaca mulatta; Fat deficiencies;
 Experimental diets; Safflower oil; Blood plasma; Tissues;
 Fatty acids; Phospholipids; Vision disorders; Polydipsia
 
 Abstract:  This study shows that dietary omega-3 fatty acid
 deficiency leads to severe and progressive depletion of
 omega-3 fatty acids from the plasma and from all tissues
 analyzed including red blood cells, liver, skin, fat, cerebral
 cortex and retina in primates. It supports the conclusion that
 there should be adequate amounts of both omega-3 and omega-6
 fatty acids in the diet throughout life and that their ratio
 is of great importance.
 
 
 142                                   NAL Call. No.: 410.9 P94
 Evaluation of a nude mouse tumor model using beta-
 galactosidase-expressing melanoma cells.
 Dooley, T.P.; Stamp-Cole, M.; Ouding, R.J.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1993 Feb. Laboratory animal science v. 43 (1): p.
 48-57; 1993 Feb.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Animal models; Melanoma
 
 Abstract:  We developed and evaluated an in vivo athymic nude
 mouse model for tumor growth, angiogenesis, metastasis, and
 antineoplastic drug development. Melanoma cell lines
 expressing beta-galactosidase encoded by the Escherichia coli
 lac Z gene have been created by infecting an immortal murine
 melanocyte cell line with a recombinant retrovirus expressing
 the v-Ha-ras oncogene and lac Z to generate the MRB (melanoma,
 ras, beta-galactosidase) cell lines. The amelanotic, phorbol
 ester-independent, transformed melanoma cell lines developed
 tumors rapidly when injected subcutaneously into nude mice, as
 well as experimental lung metastases when injected i.v. into
 the tail vein. beta-galactosidase-expressing subcutaneous
 tumors and lung metastases stained blue with X-gal. The
 melanomas produced in nude mice have been characterized by
 using various histochemical and immunohistochemical staining
 methods to detect melanoma- and endothelial-cell-specific
 markers to determine the extent of neovascularization in MRB
 nude mouse tumors. Optimal staining of endothelial cells
 involved in tumor angiogenesis was observed by using ADPase
 activity and antiangiotensin-converting enzyme antibody
 staining. Attempts at indirect quantification of metastatic
 tumor cell number within the lung by either beta-galactosidase
 enzymatic activity or ELISA immunoreactivity were
 unsuccessful. However, the MRB cell lines should be useful in
 screening for and studying the mechanisms of action of
 antineoplastic, antimetastatic, and angiostatic drugs in vivo
 in athymic nude mice.
 
 
 143                                   NAL Call. No.: QL55.A1L3
 Evaluation of inbred germ-free Fischer 344 albino rats as an
 experimental model for oral candidiasis.
 Van Wyk, C.W.; Basson, N.J.; Gibson, B.M.
 London : Royal Society of Medicine Services; 1989 Jul.
 Laboratory animals v. 23 (3): p. 248-255. ill; 1989 Jul. 
 Includes references.
 
 Language:  English
 
 Descriptors: Rats; Candidosis; Candida albicans; Tongue
 lesions; Tongue; Opportunistic infections; Germfree state;
 Inbred strains; Induced resistance; Animal models; Disease
 models
 
 Abstract:  Inbred germ-free Fischer 344 albino rats were
 evaluated as models for experimental candidiasis in order to
 investigate bacterial interaction with Candida albicans.
 Female rats were exposed to C. albicans in their drinking
 water and killed at intervals from 2 to 22 days after initial
 contact with the contaminant. C. albicans was cultured from
 their mouths from day 2 but from day 12 the number of colonies
 decreased. From day 2 to 9 all rats showed oral histological
 signs of candidal infestation, but after 9 days the number
 declined to 3 out of 9 at 22 days. The dorsal surface of the
 tongue was the best histological indicator of candidal
 infestation. All the rats had tongue lesions from day 4 to 9,
 and from day 6 there was also a concomitant localized loss of
 filiform papillae. The number of rats with all forms of tongue
 involvement also decreased after 9 days with only 3 out of 9
 affected at 22 days. It is concluded that Fischer 344 inbred
 germ-free rats can be used on a limited scale as a model for
 candidiasis and bacterial interaction with C. albicans, the
 dorsal surface of the tongue would be the best site for
 studying candidal experimental lesions and it is probable that
 better results can be achieved with complete standardization
 of contamination and preparation procedures.
 
 
 144                                    NAL Call. No.: TD172.A7
 Evaluation of the polychlorobiphenyl Aroclor 1254 in an animal
 model of atherosclerosis.
 Carter, J.W.; Koo, S.I.
 New York, N.Y. : Springer-Verlag; 1988 May.
 Archives of environmental contamination and toxicology v. 17
 (3): p. 307-312; 1988 May.  Includes references.
 
 Language:  English
 
 Descriptors: Experimental atherosclerosis; Animal experiments;
 Polychlorinated biphenyls; Arochlor; Diets; Cholesterol;
 Pigeons
 
 
 145                                   NAL Call. No.: RB127.P34
 Experimental approach to reflex sympathetic dystrophy and
 related syndromes. Janig, W.
 Amsterdam : Elsevier Science Publishers; 1991 Sep.
 Pain : the journal of the International Association for the
 Study of Pain v. 46 (3): p. 241-245; 1991 Sep.  Includes
 references.
 
 Language:  English
 
 Descriptors: Rats; Animal models; Disease models; Nervous
 system diseases
 
 
 146                                   NAL Call. No.: 41.8 R312
 Experimental infectaion of the mouse mammary gland with
 Campylobacter coli. Diker, K.S.; Haziroglu, R.; Diker, F.S.
 London : British Veterinary Association; 1992 Jan.
 Research in veterinary science v. 52 (1): p. 123-125; 1992
 Jan.  Includes references.
 
 Language:  English
 
 Descriptors: Campylobacter; Bovine mastitis; Disease models;
 Animal models; Mice; Mammary glands; Experimental infection;
 Strain differences
 
 Abstract:  Campylobacter cob strains of bovine and avian
 origin were inoculated into the mammary gland of mice. A
 bovine strain isolated from a case of mastitis produced gross
 and histological changes in most of the glands; one bovine and
 one avian faecal isolate did not. Histologically, lesions were
 characterised by neutrophil infiltration in the alveolar
 spaces and necrosis and oedema in the interalveolar tissue. On
 bacteriological examination, the bovine mastitis strain could
 be isolated from most of the glands, but neither of the faecal
 strains. The mouse, therefore, appears to provide a convenient
 model for studying campylobacter mastitis.
 
 
 147                                     NAL Call. No.: QR1.I57
 Experimental infection of severe combined immunodeficient
 beige mice with Mycobacterium paratuberculosis of bovine
 origin.
 Mutwiri, G.K.; Butler, D.G.; Rosendal, S.; Yager, J.
 Washington, D.C. : American Society for Microbiology; 1992
 Oct. Infection and immunity v. 60 (10): p. 4074-4079; 1992
 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Cattle; Mice; Disease models; Mycobacterium
 paratuberculosis; Enteritis; Experimental infection; Cachexia;
 Pathogenesis; Immunological deficiency; Histology
 
 Abstract:  Severe combined immunodeficient beige mice were
 inoculated orally and intraperitoneally with a bovine strain
 of Mycobacterium paratuberculosis to explore their potential
 as laboratory animal models in the study of paratuberculosis
 (Johne's disease). Control animals were similarly inoculated
 with heat-killed M. paratuberculosis. In the mice inoculated
 intraperitoneally, focal lesions and acid-fast bacilli were
 first detected in the livers (4 weeks postinfection) and later
 in the spleens and intestines of the test but not the control
 animals. No bacteria were seen in the hearts, kidneys, or
 lungs. At 12 weeks postinfection, all test mice had
 significant losses in body weight compared with those in
 controls (P < 0.05), a characteristic sign of bovine
 paratuberculosis. Tumor necrosis factor alpha was not detected
 in the serum. Histologic lesions were seen in the intestines,
 livers, and spleens of the animals in the orally inoculated
 test group after 26 weeks of infection. Our results suggest
 that the severe combined immunodeficient beige mouse may be a
 useful model for the investigation of paratuberculosis and
 cachexia and the evaluation of antimycobacterial drugs.
 
 
 148                                   NAL Call. No.: 41.8 AM3A
 An experimental model for subclinical edema disease
 (Escherichia coli enterotoxemia) manifest as vascular necrosis
 in pigs.
 Kausche, F.M.; Dean, E.A.; Arp, L.H.; Samuel, J.E.; Moon, H.W.
 Schaumburg, Ill. : American Veterinary Medical Association;
 1992 Mar. American journal of veterinary research v. 53 (3):
 p. 281-287; 1992 Mar. Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Edema; Latent infections; Disease models;
 Escherichia coli; Enterotoxemia; Animal models; Oral
 administration
 
 Abstract:  An experimental model for subclinical edema disease
 was developed in weanling pigs. In multiple experiments, 3-
 week-old pigs were weaned, then inoculated intragastrically
 with 10(10) colony-forming units of an SLT-IIv-positive strain
 of Escherichia coli originally isolated from a pig with edema
 disease (principals). Control pigs were inoculated with a
 nonpathogenic E coli strain. Of 39 principals, 8 developed
 clinical edema disease within 14 days after inoculation.
 However, 20 of 21 principals that did not develop clinical
 signs of edema disease, but were submitted for necropsy
 examination at 14 days after inoculation, had characteristic
 vascular lesions of edema disease. Vascular lesions, found
 principally in ileum and brain, consisted of segmental
 necrosis of myocytes in the tunica media of small arteries and
 arterioles. None of the pigs inoculated with a nonpathogenic
 strain of E coli developed edema disease or vascular lesions.
 None of the principals necropsied at 2 days after inoculation
 had vascular lesions. Development of vascular lesions by 14
 days after inoculation was used as the end point for detecting
 subclinical edema disease in the model.
 
 
 149                                    NAL Call. No.: 41.8 J82
 Experimental proliferative glomerulonephritis in the cat.
 Bishop, S.A.; Stokes, C.R.; Lucke, V.M.
 London : Academic Press; 1992 Jan.
 Journal of comparative pathology v. 106 (1): p. 49-60; 1992
 Jan.  Includes references.
 
 Language:  English
 
 Descriptors: Cats; Glomerulonephritis; Disease models; Serum
 albumin; Intravenous injection; Symptoms; Animal models
 
 
 150                                    NAL Call. No.: RB125.E9
 Experimental surgery and physiology induced animal models of
 human disease. Swindle, M. Michael; Adams, Robert J.
 Baltimore : Williams & Wilkins,; 1988.
 x, 350 p. : ill. ; 27 cm.  Includes bibliographies and index.
 
 Language:  English
 
 Descriptors: Diseases; Animal models; Surgery, Experimental
 
 
 151                                   NAL Call. No.: RB127.P34
 The expression of a deafferentation syndrome in the Sprague-
 Dawley rat: effects of frontoparietal cortical lesions.
 Ovelmen-Levitt, J.; Young, J.N.; Rossitch, E. Jr; Nashold,
 B.S. Jr Amsterdam : Elsevier Science Publishers; 1991 Nov.
 Pain : the journal of the International Association for the
 Study of Pain v. 47 (2): p. 203-209; 1991 Nov.  Includes
 references.
 
 Language:  English
 
 Descriptors: Rats; Animal models; Lesions; Cerebral cortex;
 Nervous system diseases
 
 
 152                                   NAL Call. No.: SF601.J65
 Factors associated with failure of passive transfer of
 colostral antibodies in Standardbred foals.
 Clabough, D.L.; Levine, J.F.; Grant, G.L.; Conboy, H.S.
 Hagerstown, Md. : American College of Veterinary Medicine;
 1991 Nov. Journal of veterinary internal medicine v. 5 (6): p.
 335-340; 1991 Nov. Includes references.
 
 Language:  English
 
 Descriptors: Foals; Maternal antibodies; Maternal immunity;
 Colostrum; Mares; Blood serum; Igg; Medical treatment; Animal
 models; Age
 
 
 153                                    NAL Call. No.: 41.8 Ad9
 Fasting hyperbilirubinemia in Bolivian squirrel monkeys with a
 Gilbert's-like syndrome.
 Cornelius, C.E. \u University of California, Davis, CA
 San Diego, Calif. : Academic Press; 1993.
 Advances in veterinary science and comparative medicine v. 37:
 p. 127-147; 1993.  In the series analytic: Animal models in
 liver research / edited by Charles E. Cornelius.  Includes
 references.
 
 Language:  English
 
 Descriptors: Hyperbilirubinemia; Fasting; Saimiri boliviensis;
 Animal models; Skin diseases; Nutrition; Bilirubin;
 Transferases
 
 
 154                                   NAL Call. No.: 410.9 P94
 Fasting hyperbilirubinemia in normal squirrel monkeys.
 Cornelius, C.E.; Freedland, R.A.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Feb. Laboratory animal science v. 42 (1): p.
 35-37; 1992 Feb.  Includes references.
 
 Language:  English
 
 Descriptors: Saimiri sciureus; Hyperbilirubinemia; Fasting;
 Animal models; Bilirubin
 
 Abstract:  The plasma of Bolivian squirrel monkeys, unlike
 that of Brazilian squirrel monkeys, is markedly yellow due to
 unconjugated hyperbilirubinemia after an overnight fast. The
 fasting hyperbilirubinemia in Bolivian squirrel monkeys is
 likely due to two mechanisms. First, a twofold increase in the
 bilirubin turnover/production rate occurs during a 24-hour
 fast. A second mechanism is the decreased hepatic conjugation
 potential for bilirubin due to the presence of a higher
 bilirubin UDP-glucuronosyltransferase (UDPGA)Km and a lower
 Vm; this results in higher steady-state plasma and hepatic
 bilirubin levels during a fast when hepatic UDP-glucuronic
 acid levels are low. The Bolivian squirrel monkey provides an
 excellent animal model for human Gilbert's syndrome type I in
 which to study rate-limiting mechanisms in the movement of
 bilirubin from plasma to bile.
 
 
 155                                      NAL Call. No.: QP1.P4
 Feeding conditions and estrous cycle of female rats under the
 activity-stress procedure from aspects of anorexia nervosa.
 Watanabe, K.; Hara, C.; Ogawa, N.
 Tarrytown, N.Y. : Pergamon Press; 1992 Apr.
 Physiology & behavior v. 51 (4): p. 827-832; 1992 Apr. 
 Includes references.
 
 Language:  English
 
 Descriptors: Anorexia nervosa; Food restriction; Feeding
 behavior; Activity; Stress; Food intake; Body weight; Estrous
 cycle; Mortality; Gastric ulcer; Histopathology; Animal
 models; Female animals; Rats
 
 Abstract:  The present study investigated the application of
 female rats with activity stress as an animal model for
 anorexia nervosa. Young female rats were singly housed in
 activity-wheel cages with food-restricted schedule (2, 3, or 4
 h of food availability per day) for 3 weeks. Estrous cycle,
 body, weight, food intake, and wheel revolution were recorded
 daily. Gastric pathology was also observed using the
 endoscopic technique. Rats that were subjected to either a 3-
 or 4-h feeding schedule exhibited the cessation of estrous
 cycle, loss of body weight, and suppression of food intake.
 These animals also showed a remarkable increase in running
 activity. However, they had no gastric lesions throughout the
 experimental period. On the contrary, the 2-h feeding schedule
 elicited severe gastric lesions and high mortality. The
 results suggest that behavioral and physiological changes of
 the young female rats with 3 or 4 h feeding share some
 symptoms of anorexia nervosa, although their anorexia is not
 self starvation.
 
 
 156                                     NAL Call. No.: QR46.J6
 Feeding trials of Listeria monocytogenes with a nonhuman
 primate model. Farber, J.M.; Daley, E.; Coates, F.;
 Beausoleil, N.; Fournier, J. Washington, D.C. : American
 Society for Microbiology; 1991 Nov. Journal of clinical
 microbiology v. 29 (11): p. 2606-2608; 1991 Nov.  Includes
 references.
 
 Language:  English
 
 Descriptors: Listeria monocytogenes; Foodborne diseases;
 Inoculum; Inoculum density; Infection; Symptoms; Disease
 models; Macaca fascicularis
 
 Abstract:  One of the major unanswered questions regarding the
 presence of Listeria monocytogenes in foods is how many cells
 must be ingested in order to cause illness. To answer this
 question, studies were undertaken by using Macaca fascicularis
 (cynomolgus monkey) as an animal model. Healthy nonhuman
 primates were dosed with various concentrations of L.
 monocytogenes suspended in sterile whole milk. Final
 concentrations of 10(5), 10(7), and 10(9) total cells of the
 organism were used; a control was also included. Blood
 samples, as well as fecal and nasal specimens, were taken at
 various time intervals. Only animals that received 10(9) cells
 of L. monocytogenes became noticeably ill, with symptoms of
 septicemia, irritability, loss of appetite, and occasional
 diarrhea. Monkeys that received 10(7) and 10(9) cells shed L.
 monocytogenes in the feces for approximately 21 days. In
 monkeys that received the dose of 10(9) cells, severe
 lymphopenia and neutrophilia occurred within 48 h. In a
 separate trial, monkeys received Maalox to reduce the gastric
 acidity of the stomach. However, no substantial differences
 were observed between Maalox-treated and control monkeys.
 
 
 157                                    NAL Call. No.: 41.8 P27
 Feline mucopolysaccharidosis VII due to beta-glucuronidase
 deficiency. Gitzelmann, R.; Bosshard, N.U.; Superti-Furga, A.;
 Spycher, M.A.; Briner, J.; Wiesmann, U.; Lutz, H.; Litschi, B.
 Lawrence, Kan. : American College of Veterinary Pathologists;
 1994 Jul. Veterinary pathology v. 31 (4): p. 435-443; 1994
 Jul.  Includes references.
 
 Language:  English
 
 Descriptors: Cats; Beta-glucuronidase; Enzyme deficiencies;
 Mucopolysaccharidosis; Symptoms; Enzyme activity; Animal
 models; Case reports
 
 
 158                                   NAL Call. No.: TX345.B74
 Food allergy--role of mucosal immune regulation and oral
 tolerance: facts, fiction, and hypotheses.
 Strobel, S.
 San Diego : Academic Press, c1990-; 1993.
 Bristol-Myers Squibb/Mead Johnson nutrition symposia :
 [proceedings] v. 11: p. 335-364; 1993.  Includes references.
 
 Language:  English
 
 Descriptors: Food allergies; Immune response; Regulation;
 Intestinal mucosa; Oral administration; Human milk; Neonates;
 Autoimmunity; Antigens; Antibodies; T lymphocytes; Literature
 reviews
 
 Abstract:  Physiological and immunological requirements for
 the acquisition of tolerance to dietary antigens (oral
 tolerance), based on experimental animal models and studies
 performed in human infants are discussed in this chapter.
 Tolerance in this context is defined as antigen-specific
 suppression of humoral antibody responses (IgM, IgG, IgE) and
 cell-mediated immunity after prior oral antigen exposure.
 
 
 159                                  NAL Call. No.: 391.8 T662
 Formate metabolism in young swine.
 Makar, A.B.; Tephly, T.R.; Sahin, G.; Osweiler, G.
 Orlando, Fla. : Academic Press; 1990 Sep01.
 Toxicology and applied pharmacology v. 105 (2): p. 315-320;
 1990 Sep01. Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Formic acid; Formates (salts); Methanol;
 Metabolism; Folic acid; Toxicity
 
 Abstract:  Formate generated from methanol metabolism in vivo
 is the chemical entity responsible for the development of the
 methanol toxicity syndrome in the monkey. Compared to rats,
 monkeys are in a state of folate deficiency. This leads to a
 decreased ability to dispose of formate generated leading to
 its accumulation and the subsequent development of the classic
 symptoms of methanol toxicity. Rats possess a more efficient
 folate system; therefore, they metabolize formate very readily
 and do not exhibit methanol toxicity symptoms. In this report,
 the hepatic folate content and the ability to handle a formate
 "load" were evaluated in another animal species, the pig. The
 results obtained indicate that the pig, compared to all other
 species studied, has extremely low levels of folates and very
 low levels of a key enzyme in the folate pathway, namely 10-
 formyl H4folate dehydrogenase. Also the pig's ability to
 dispose of formate was extremely limited and slower than that
 observed in rats or monkeys. These results suggest that the
 pig may be a suitable animal model for studying formate
 metabolism and possibly methanol toxicity.
 
 
 160                                   NAL Call. No.: QP501.B64
 Fulvic acid supplementation and selenium deficiency disturb
 the structural integrity of mouse skeletal tissue.
 Yang, C.; Niu, C.; Bodo, M.; Gabriel, E.; Notbohm, H.; Wolf,
 E.; Muller, P.K. London : The Biochemical Society; 1993 Feb01.
 The Biochemical journal v. 289 (pt.3): p. 829-835; 1993 Feb01. 
 Includes references.
 
 Language:  English
 
 Descriptors: Fulvic acids; Supplements; Selenium; Mineral
 deficiencies; Bone diseases; Collagen; Heat stability;
 Proline; Lysine; Bone strength
 
 Abstract:  High concentrations of fulvic acid and selenium
 deficiency are the main causative factors of Kashin-Beck
 disease, an endemic, chronic and degenerative osteoarticular
 disorder found in China. In the search for an animal model of
 this disease, mice were exposed to these pathogenetic
 conditions for two generations and the collagen types from
 skin, bone and cartilage were analysed. The growth of the
 treated mice was slightly retarded, and the rate of
 reproduction was lower in animals maintained on a fulvic acid-
 supplemented and/or selenium-deficient diet. Irregular bone
 formation was seen by radiography and morphometry. Biochemical
 analysis indicated that lysine residues in collagen I from
 bone and in collagen II from cartilage were overmodified. The
 values of Hyl/(Hyl + Lys) in bone collagen alpha 1(I) chains
 from treated mice were about 0.434-0.484, i.e. substantially
 higher than that of the control (0.277). The values of this
 parameter for collagen II were 0.482 for control and
 0.546-0.566 for treated mice. The melting temperature of
 collagen I from bones of treated mice was 1 degrees C lower
 than that of control collagen, indicating decreased thermal
 stability. The breakage point of the tibiae of treated mice
 occurred at a lower preload force than for controls,
 suggesting that the overmodified and thermally less stable
 collagen molecules are causally related to a lower mechanical
 strength of bones.
 
 
 161                                 NAL Call. No.: QP141.A1N88
 Gastrointestinal food allergy in childhood: current problems.
 Walker-Smith, J.A.
 Elmsford, N.Y. : Pergamon Press; 1992 Jan.
 Nutrition research v. 12 (1): p. 123-135; 1992 Jan. 
 Literature review. Includes references.
 
 Language:  English
 
 Descriptors: Food allergies; Gastroenteritis; Digestive tract;
 Infections; Animal models; Antigens; Intestinal absorption;
 Diagnosis; Children; Literature reviews
 
 Abstract:  Two of the principal issues concerning
 gastrointestinal food allergy in infancy and early childhood
 are discussed. These are: The role of gastroenteritis, either
 in the initiation or unmasking of clinical manifestations of
 gastrointestinal food allergy. Secondly, the diagnostic
 criteria of gastrointestinal food allergy in childhood. The
 absolute first criterion for diagnosis must be a response to
 food elimination. The diagnostic approach is clearly defined
 for quick onset and slow onset cases. There are also a group
 of children who have mixed quick and slow onset symptoms.
 
 
 162                                  NAL Call. No.: HV5285.A43
 Genetic animal models.
 Crabble, J.C.; Phillips, T.J.
 Washington, D.C. : U.S. Department of Health and Human
 Services; 1990. Alcohol health and research world - National
 Institute on Alcohol Abuse and Alcoholism v. 14 (3): p.
 179-180; 1990.
 
 Language:  English
 
 Descriptors: U.S.A.; Animal experiments; Animal models;
 Genetic models; Alcoholism; Genetic regulation; Laboratory
 animals
 
 
 163                                   NAL Call. No.: 44.8 J822
 Genetic evaluation of somatic cell scores for United States
 dairy cattle. Schutz, M.M.
 Champaign, Ill. : American Dairy Science Association; 1994
 Jul. Journal of dairy science v. 77 (7): p. 2113-2129; 1994
 Jul.  Includes references.
 
 Language:  English
 
 Descriptors: U.S.A.; Cabt; Dairy cows; Somatic cell count;
 Bovine mastitis; Genetic gain; Milk yield; Selection criteria;
 Selection index; Genetic resistance; Breeding value;
 Heritability; Animal models; Genetic correlation; Breed
 differences; Literature reviews
 
 Abstract:  Increases in milk yield from genetic selection may
 be accompanied by correlated increases in genetic
 susceptibility to clinical mastitis and somatic cells. Unlike
 clinical mastitis, somatic cell scores can be easily
 determined and recorded and are related to milk loss from
 subclinical mastitis. Selection against high somatic cell
 scores should decrease incidence of clinical mastitis and
 provide direct economic benefits through higher milk quality
 premiums. Genetic evaluation for lactation means of linear
 somatic cell scores has been implemented by USDA and parallels
 that for yield traits. Because additive genetics accounts for
 only about 10% of differences in somatic cell scores among
 cows, more information is needed for the same degree of
 confidence in genetic estimates as for yield. Only 80% of DHIA
 cows currently have somatic cell records. Thus, reliabilities
 of somatic cell evaluations are smaller than those for yield
 traits. Most progress in selection for lower somatic cell
 scores will come through sires of cows considered as bull
 dams. Somatic cell evaluations may best be reported through an
 economic index with a small amount of emphasis on somatic cell
 score relative to yield traits. Greater emphasis on somatic
 cell scores would decrease genetic gain in yield traits, which
 are economically more important.
 
 
 164                                   NAL Call. No.: QP534.B56
 Genetic influences on tissue deposition of aluminum in mice.
 Fosmire, G.J.; Focht, S.J.; McClearn, G.E.
 Totowa, N.J. : Humana Press; 1993 May.
 Biological trace element research v. 37 (2/3): p. 115-121;
 1993 May.  Includes references.
 
 Language:  English
 
 Descriptors: Diet; Aluminum; Toxicity; Mineral metabolism;
 Tissues; Composition; Strain differences; Animal models;
 Disease models; Alzheimer's disease; Mice
 
 
 165                                   NAL Call. No.: 410.9 P94
 Genetic lipid storage disease with lysosomal acid lipase
 deficiency in rats. Yoshida, H.; Kuriyama, M.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1990 Sep. Laboratory animal science v. 40 (5): p.
 486-489; 1990 Sep.  Includes references.
 
 Language:  English
 
 Descriptors: Human diseases; Disease models; Rats;
 Triacylglycerol lipase; Lysosomes; Symptoms; Pathology
 
 Abstract:  We describe a new animal model of a genetic lipid
 storage disease analogous to human Wolman's disease. Affected
 Donryu rats, who inherited the disease in an autosomal
 recessive mode, manifested marked hepatosplenomegaly, lymph
 node enlargement, and thickened, dilated intestine.
 Morphologically, many characteristic foam cells were observed
 in livers and spleens. No adrenal calcification could be found
 in affected rats. Biochemical studies on spleen and liver
 tissues showed massive accumulation of esterified cholesterol
 and triglycerides, and deficiency of acid lipase for [14Cl-
 cholesteryl oleate. This animal model could contribute greatly
 to the clarification of the physiological and pathological
 roles of lysosomal acid lipase in the metabolism of
 lipoproteins and cholesterol, and of the pathogenesis of
 atherosclerosis.
 
 
 166                                    NAL Call. No.: QR360.J6
 Genetically engineered foot-and-mouth disease viruses with
 poly(C) tracts of two nucleotides are virulent in mice.
 Reider, E.; Bunch, T.; Brown, F.; Mason, P.W.
 Washington, D.C. : American Society for Microbiology; 1993
 Sep. Journal of virology v. 67(9): p. 5139-5145; 1993 Sep. 
 Includes references.
 
 Language:  English
 
 Descriptors: Aphthovirus; Genetic engineering; Rna; Cytosine;
 Infectivity; Cell lines; Hamsters; Transfection; Deletions;
 Recombination; Cell culture; Virulence; Mice
 
 Abstract:  To determine the role of the poly(C) tract found at
 the 5' end of the genome of foot-and-mouth disease virus,
 synthetic RNAs (in vitro transcripts) with poly(C) tracts of
 different lengths have been produced and evaluated. RNAs with
 poly(C) tracts of 35, 25, 16, 6, or 2 residues displayed
 similar specific infectivities in baby hamster kidney (BHK)
 cells. Viruses recovered from cells transfected with in vitro
 transcripts containing 6 to 35 Cs had properties similar to
 those of the wild-type virus in cell culture, and poly(C)
 tracts present in the synthetic RNA-derived viruses ranged
 from 75 to 140 bases in length. Viruses recovered from
 transcripts containing only two Cs showed very different
 properties. Specifically, viruses grew to much lower levels in
 cell culture and maintained a poly(C) tract of only two
 residues. The pool of viruses harvested from cells transfected
 with the synthetic C, RNA also contained a small amount of a
 virus with a 42-base deletion in the region of the poly(C)
 tract, which appeared to have arisen by recombination. Taken
 together, these data suggest that recombination provides the
 mechanism of poly(C) elongation and that viruses with poly(C)
 tracts over 75 bases in length have a selective advantage in
 cell culture. Interestingly, all of the in vitro transcript-
 derived viruses [including viruses with poly(C) tracts of only
 two residues] were equally virulent in mice, indicating that
 poly(C) tract length has no effect on virulence in this animal
 model.
 
 
 167                                   NAL Call. No.: 410.9 P94
 The gerbil, hamster, and guinea pig as rodent models for
 hyperlipidemia. Sullivan, M.P.; Cerda, J.J.; Robbins, F.L.;
 Burgin, C.W.; Beatty, R.J. Cordova, Tenn. : American
 Association for Laboratory Animal Science; 1993 Dec.
 Laboratory animal science v. 43 (6): p. 575-578; 1993 Dec. 
 Includes references.
 
 Language:  English
 
 Descriptors: Hyperlipemia; Disease models; Animal models;
 Diets; Atherogenic diet; Gerbils; Hamsters; Guinea pigs;
 Cholesterol; Triacylglycerols
 
 Abstract:  The purpose of this study was to compare the
 effects of a hyperlipidemic diet on three different rodent
 models to evaluate them on how their responses simulate human
 serum lipid diseases. Forty hamsters, 40 gerbils, and 20
 guinea pigs were given either a chow diet or a modified high-
 fat, high-cholesterol diet (HF/HC) for 7 days. Food was
 withheld from half of the animals on each diet for 12 hours
 prior to collecting the blood for analysis of total
 cholesterol and triglyceride concentration. In all species,
 HF/HC feeding resulted in at least a 370% increase in total
 cholesterol concentration. Withholding food significantly
 decreased total cholesterol concentration in hamsters and
 gerbils fed HF/HC but had no effect on animals fed chow diet.
 Triglyceride concentrations were increased by the HF/HC in the
 hamster and the gerbil. As with total cholesterol,
 triglyceride concentration was decreased after food was
 withheld in these two animal groups. We suggest that the
 guinea pig is the most appropriate model for studying
 hypercholesterolemia because of its moderate plasma
 cholesterol response and normal triglyceride response to a
 HF/HC. We also suggest that the hamster is a good model for
 studying hypertriglyceridemia since increased serum
 triglyceride concentrations can be easily maintained on a
 HF/HC.
 
 
 168                                    NAL Call. No.: 41.8 J82
 Glycogen accumulation in the renal tubular cells of
 spontaneously occurring diabetic WBN/kob rats.
 Tsuchitani, M.; Kuroda, J.; Nagatani, M.; Miura, K.; Katoh,
 T.; Saegusa, T.; Narama, I.; Itakura, C.
 London : Academic Press; 1990 Feb.
 Journal of comparative pathology v. 102 (2): p. 179-190. ill;
 1990 Feb. Includes references.
 
 Language:  English
 
 Descriptors: Diabetes; Rats; Kidneys; Glycogen;
 Histopathology; Animal models; Disease models
 
 
 169                                 NAL Call. No.: QP141.A1A63
 Growth factors in milk as mediators of infant development.
 Donovan, S.M. \u University of Illinois, Urbana, IL; Odle, J.
 Palo Alto, Calif. : Annual Reviews Inc., c1981-; 1994 Jul.
 Annual review of nutrition v. 14: p. 147-167; 1994 Jul. 
 Includes references.
 
 Language:  English
 
 Descriptors: Human milk; Neonatal development; Epidermal
 growth factor; Insulin; Insulin-like growth factor; Relaxin;
 Peptides; Literature reviews
 
 Abstract:  This review discusses findings on growth factors in
 milk and their potential roles in the neonate. The focus is on
 human milk, the human infant, and animal models used in
 research. The role of growth factors both in normal growth and
 development as well as their potential therapeutic role during
 recovery from intestinal injury is addressed.
 
 
 170                                    NAL Call. No.: 41.8 Ad9
 Gunn rat: a model for inherited deficiency of bilirubin
 glucuronidation. Chowdhury, J.R. \u Albert Einstein College of
 Medicine, Bronx, NY; Kondapalli, R.; Chowdhury, N.R.
 San Diego, Calif. : Academic Press; 1993.
 Advances in veterinary science and comparative medicine v. 37:
 p. 149-173; 1993.  In the series analytic: Animal models in
 liver research / edited by Charles E. Cornelius.  Includes
 references.
 
 Language:  English
 
 Descriptors: Liver diseases; Bilirubin; Animal models; Rats;
 Transferases; Bile pigments; Toxicity; Treatment
 
 
 171                                  NAL Call. No.: QR360.A1J6
 A hamster model of equine herpesvirus type 1 (EHV-1)
 infection; passive protection by monoclonal antibodies to
 EHV-1 glycoproteins 13, 14 and 17/18. Stokes, A.; Allen, G.P.;
 Pullen, L.A.; Murray, P.K.
 Reading : Society for General Microbiology; 1989 May.
 The Journal of general virology v. 70 (pt.5): p. 1173-1183;
 1989 May. Includes references.
 
 Language:  English
 
 Descriptors: Hamsters; Herpetoviridae; Glycoproteins;
 Monoclonal antibodies; Models
 
 
 172                              NAL Call. No.: RL79.H36  1994
 Handbook of mouse mutations with skin and hair abnormalities
 animal models and biomedical tools..  Mouse mutations with
 skin and hair abnormalities Sundberg, John P.
 Boca Raton : CRC Press,; 1994.
 544 p. : ill. ; 27 cm. (CRC series in dermatology).  Includes
 bibliographical references and index.
 
 Language:  English
 
 Descriptors: Skin; Hair; Mice as laboratory animals; Mice
 
 
 173                                  NAL Call. No.: S451.P4P45
 The hangover that lasts a lifetime.
 Ciresi, R.
 University Park, Pa. : Pennsylvania State University; 1991.
 PennState agriculture. p. 15-17; 1991.
 
 Language:  English
 
 Descriptors: Fetal alcohol syndrome; Fetus; Animal models;
 Chicks
 
 
 174                                    NAL Call. No.: 41.8 J82
 Hepatic pathology of the colon carcinogen, azoxymethane, in
 Hanford-Moore miniature pigs.
 Wargovich, M.J.; Satterfield, W.; Price, R.E.; Stephens, L.C.;
 Coghlan, L. London : Academic Press; 1991 Oct.
 Journal of comparative pathology v. 105 (3): p. 271-278; 1991
 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Miniature pigs; Animal models; Disease models;
 Colon; Azoxymethane; Carcinogens; Neoplasms; Toxicity; Liver;
 Histopathology
 
 
 175                                   NAL Call. No.: 389.8 Z33
 Hepatic selenium concentration in pigs with microangiopathy
 (mulberry heart disease)--an animal model for the study of
 oxidative damage. Korpela, H.
 Bern : Hogrefe & Huber Publishers; 1990.
 International journal for vitamin and nutrition research v. 60
 (2): p. 156-159; 1990.  Includes references.
 
 Language:  English
 
 Descriptors: Diet; Mineral deficiencies; Selenium; Heart
 diseases; Pigs
 
 Abstract:  The significance of selenium deficiency was
 investigated in pigs that died suddenly of microangiopathy
 (MAP, mulberry heart disease). Hepatic selenium concentration
 (mean +/- SD) in pigs with MAP (1.04 +/- 0.47 microgram/g dry
 weight) was lower than in healthy pigs (1.23 +/- 0.53
 microgram/g). The lowest hepatic selenium values were found in
 pigs with MAP and in 22.2% of MAP pigs hepatic selenium
 concentration was below 0.5 microgram/g which reflects
 selenium deficiency. Thus, pigs with a low selenium status are
 at risk of MAR The low selenium status together with vitamin E
 deficiency increases oxidative stress and thus contributes to
 the development of oxidative damage.
 
 
 176                                    NAL Call. No.: 41.8 P27
 Hepatic storage of glycosaminoglycans in feline and canine
 models of mucopolysaccharidoses I, VI, and VII.
 Haskins, M.E.; Otis, E.J.; Hayden, J.E.; Jezyk, P.F.; Stramm,
 L. Lawrence, Kan. : American College of Veterinary
 Pathologists; 1992 Mar. Veterinary pathology v. 29 (2): p.
 112-119; 1992 Mar.  Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Cats; Animal models; Disease models;
 Mucopolysaccharidosis; Glycosaminoglycans; Liver; Hereditary
 diseases; Vacuoles
 
 
 177                                   NAL Call. No.: 410.9 P94
 Hereditary hydroenphrosis in C57BL/KsJ mice.
 Weide, L.G.; Lacy, P.E.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1991 Oct. Laboratory animal science v. 41 (5): p.
 415-418; 1991 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Nephrosis; Hereditary diseases; Incidence;
 Age differences; Kidneys
 
 Abstract:  We sought to determine if the incidence of renal
 hydronephrosis in male C57BL/KsJ mice increased with age and
 if grossly normal kidneys would develop hydronephrosis over
 time. Spontaneous hydronephrosis was found incidentally in 32%
 of 234 male C57BL/KsJ mice killed as pancreas donors for islet
 transplantation experiments. The incidence of hydronephrosis
 increased with age; the incidence was 15% in 6- to 8-week-old
 mice, 52% in 8- to 10-week-old mice and 63% in 11- to 15-week-
 old mice (P < 0.001). Additional mice received islet isografts
 beneath the renal capsule. Only mice with grossly normal
 kidneys received islet grafts. These same kidneys were then
 re-examined when the graft recipients were killed at the end
 of the experiment and the incidence of hydronephrosis was
 determined. The conversion of normal kidneys to hydronephrotic
 kidneys increased with the time since islet transplantation.
 Kidneys re-examined less than 4 weeks since transplantation
 had only 5.8% new hydronephrosis, while those re-examined
 later than 4 weeks after transplantation had a new
 hydronephrosis incidence rate of 40% (P < 0.001). Our findings
 suggest that hydronephrosis is hereditary but not congenital,
 that it develops rapidly, and that it can complicate
 experiments using this strain. This may also represent a
 useful new animal model of progressive hydronephrosis.
 
 
 178                                 NAL Call. No.: QP141.A1P46
 Heterogeneity in sympathoadrenal activity in obesity: a
 function of type of obesity, nutrient effects, and regional
 responses.
 Young, J.B.
 Baton Rouge : Louisiana State University Press; 1992.
 Pennington Center nutrition series v. 2: p. 121-131; 1992. 
 Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Nutrition physiology; Sympathetic
 nervous system; Energy metabolism; Epinephrine;
 Norepinephrine; Animal models; Literature reviews
 
 Abstract:  Alterations in sympathetic nervous system activity,
 especially in brown fat, contribute to the regulation of
 energy expenditure in mammals. Adrenergic regulation of energy
 metabolism is believed to be abnormal in obesity, a phenomenon
 widely attributed to diminished sympathetic nervous system
 activity in brown fat. While reduced sympathetic nervous
 system activity in brown fat has been noted in many obese
 animals, it is not present in all. Furthermore, in one model
 of obesity, dogs or rodents fed lard-enriched diets,
 sympathetic nervous system activity is increased (elevated
 plasma norepinephrine levels and tissue norepinephrine
 turnover). Another abnormality noted with increasing frequency
 in both human and animal obesity is diminished adrenal
 epinephrine secretion, a process that is also influenced by
 nutrient intake. Although epinephrine is a potential regulator
 of energy metabolism in normal physiology, its role is
 incompletely understood. Moreover skeletal muscle, not brown
 fat, may be the principal site for thermic effects of
 epinephrine. Thus, while depressed sympathetic nervous system
 activity in brown fat may be sufficient, it is not a necessary
 explanation for obesity; adrenal medullary suppression may
 also contribute to the development of this condition.
 
 
 179                                  NAL Call. No.: RC620.A1J6
 Histidinemia: a biochemical variant or a disease?.
 Virmani, K.; Widhalm, K.
 Wilmington, NC : American College of Nutrition; 1993 Apr.
 Journal of the American College of Nutrition v. 12 (2): p.
 115-124; 1993 Apr. Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Histidinemia; Amino acids; Metabolism; Genetic
 factors; Diet treatment; Diagnosis; Literature reviews;
 Maternal effects; Animal models
 
 Abstract:  Histidinemia, first described by Ghadimi in 1961,
 is caused by a defect in histidase. The defect results in
 elevated urinary excretion of histidine and its transamination
 products, and in high blood histidine. Blood histidine levels
 in histidinemic patients range from 290 to 1420 micromolar
 (normal 70-120 micromolar). The clinical picture of
 histidinemia varies from complete normality to severe
 retardation, with many patients being asymptomatic. No
 correlation has been found between clinical and biochemical
 data. Most reported cases have been identified in newborn
 screening programs. Frequency of histidinemia ranges from 1 in
 8000 (Japan) to 1 in 37,000 (Sweden). Histidinemia is
 inherited as an autosomal recessive trait. Maternal
 histidinemia is believed to be benign. Studies in animal
 models have shown similar metabolic changes in animals and
 humans, but clinical changes differ. Histidinemia may be
 treated with a low-histidine diet, which reduces elevated
 histidine levels, although in most cases no improvement of
 clinical symptoms has been observed.
 
 
 180                                    NAL Call. No.: 41.8 J82
 Histopathological and morphometrical comparison of
 granulomatous lesions in BALB/c and C3H/HeJ mice inoculated
 with Mycobacterium paratuberculosis. Tanaka, S.; Sato, M.;
 Taniguchi, T.; Yokomizo, Y.
 London : Academic Press; 1994 May.
 Journal of comparative pathology v. 110 (4): p. 381-388; 1994
 May.  Includes references.
 
 Language:  English
 
 Descriptors: Mycobacterium paratuberculosis; Histopathology;
 Susceptibility; Mice; Strain differences; Animal models;
 Genes; Disease course; Granuloma; Liver; Spleen
 
 
 181                                   NAL Call. No.: QL55.A1L3
 Housing, breeding and selecting chickens of the Obese strain
 (OS) with spontaneous autoimmune thyroiditis.
 Dietrich, H.M.
 London : Royal Society of Medicine Services; 1989 Oct.
 Laboratory animals v. 23 (4): p. 345-352. ill; 1989 Oct. 
 Includes references.
 
 Language:  English
 
 Descriptors: Fowls; Thyroid diseases; Autoimmune diseases;
 Hereditary diseases; Disease models; Chicken housing; Animal
 breeding; Selection methods
 
 Abstract:  A management programme is described for a small
 colony of Obese strain (OS) chickens afflicted with
 spontaneous hereditary thyroiditis. Animals of this White
 Leghorn fine are used as an animal model for Hashimoto's
 thyroiditis of man to study possible mechanisms of
 autoimmunity in general and organ-specific autoimmune diseases
 in particular. Due to the severe mononuclear cell infiltration
 of the thyroid glands, OS chickens show symptoms of
 hypothyroidism, including small body size, subcutaneous and
 abdominal fat deposits, long silky feathers, small combs and
 wattles, cold sensitivity, low fertility and poor
 hatchability. Successful breeding of this line, especially in
 a small population, can therefore be done only if rigid
 precautions are taken in aspects of animal care. The selection
 of breeding stock, the principal requirements for adequate
 housing and food, the artificial insemination procedure, and
 recommendations for collecting and incubating chicken eggs are
 reported in detail. Precautions necessary during the
 incubation of fertilized eggs, and fertility and hatchability
 are reported. During the hatching period several specific
 features must be considered. The important role of staff
 involved in a small chicken breeding unit is emphasized.
 
 
 182                                  NAL Call. No.: RC620.A1J6
 The human intestinal response to enteral nutrients: a review.
 Jackson, W.D.; Grand, R.J.
 New York, N.Y. : John Wiley & Sons; 1991 Oct.
 Journal of the American College of Nutrition v. 10 (5): p.
 500-509; 1991 Oct. Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Malnutrition; Gastrointestinal diseases;
 Literature reviews; Enteral feeding; Starvation; Parenteral
 feeding; Digestive tract mucosa; Nutrient requirements;
 Nutritional assessment
 
 Abstract:  This review identifies the factors which influence
 mucosal integrity during enteral nutrition. These include
 biliary and pancreatic secretions, trophic influences of
 endocrine and gastrointestinal polypeptides, intestinal blood
 flow, and innervation. Fiber, bacterial fermentation products,
 purines, and glutamine are potential essential nutrients which
 may not be provided by parenteral nutrition. However, contrary
 to experience in animal models, the specific advantages of
 intraluminal delivery of nutrients for the maintenance of
 mucosal integrity and structure remain unproven in the human.
 Current evidence in the human suggests that changes in small
 bowel structure and function when enteral nutrients are
 excluded are minor and rapidly reversible as long as general
 nutritional status is maintained.
 
 
 183                                    NAL Call. No.: 500 N21P
 Hyperinsulinemia induces a reversible impairment in insulin
 receptor function leading to diabetes in the sand rat model on
 non-insulin-dependent diabetes mellitus.
 Kanety, H.; Moshe, S.; Shafrir, E.; Lunenfeld, B.; Karasik, A.
 Washington, D.C. : National Academy of Sciences,; 1994 Mar01.
 Proceedings of the National Academy of Sciences of the United
 States of America v. 91 (5): p. 1853-1857; 1994 Mar01. 
 Includes references.
 
 Language:  English
 
 Descriptors: Psammomys obesus; Diabetes mellitus; Experimental
 diabetes; Hyperinsulinemia; Insulin; Hormone receptors; Liver;
 Muscles; Protein kinase; Animal models; Overfeeding
 
 Abstract:  The insulin receptor was evaluated at different
 disease stages in the sand rat (Psammomys obesus), a model for
 nutrition-induced diabetes. Nondiabetic sand rats showed
 markedly low receptor number in liver compared with albino
 rats. Their receptor had an intact tyrosine kinase activity
 but a higher Km, for ATP in the phosphorylation reaction of
 exogenous substrates. The initial effects of overeating (i.e.,
 development of hyperinsulinemia without hyperglycemia) were
 associated in the sand rat with a dramatic decrease in in
 vitro and in vivo insulin-induced receptor tyrosine kinase
 activity in both liver and muscle. In muscle, this coincided
 with a decrease in receptor number and an increase in basal
 tyrosine kinase activity. Similar changes were observed upon
 development of hyperinsulinemia with hyperglycemia. Upon
 recovery from the diabetic state by diet restriction, the
 impaired receptor kinase activation was corrected. Complete
 restoration occurred only in animals that fully recovered from
 the diabetic state and became normoinsulinemic. These
 observations indicate that loss and gain of receptor tyrosine
 kinase activity were dependent on insulin levels. Thus,
 overeating may lead to the development of hyperinsulinemia
 through ineffective extraction of excess insulin by the scarce
 liver receptors. Hyperinsulinemia, in turn, causes a
 reversible reduction in receptor kinase activity, leading to
 insulin resistance. This sequence of events may be relevant to
 diet-related changes in human non-insulin-dependent diabetes
 mellitus.
 
 
 184                                    NAL Call. No.: 500 N21P
 Hyperuricemia and urate nephropathy in urate oxidase-deficient
 mice. Wu, X.; Wakamiya, M.; Vaishnav, S.; Geske, R.;
 Montgomery, C. Jr; Jones, P.; Bradley, A.; Caskey, C.T.
 Washington, D.C. : National Academy of Sciences,; 1994 Jan18.
 Proceedings of the National Academy of Sciences of the United
 States of America v. 91 (2): p. 742-746; 1994 Jan18.  Includes
 references.
 
 Language:  English
 
 Descriptors: Mice; Oxidoreductases; Uric acid; Targeted
 mutagenesis; Homologous recombination; Structural genes;
 Embryonic stem cells; Mutants; Hyperuricemia; Nephropathy;
 Animal models; Disease models
 
 Abstract:  Urate oxidase, or uricase (EC 1.7.3.3), is a purine
 metabolic enzyme that catalyzes the conversion of uric acid to
 allantoin in most mammals except humans and certain other
 primates. The loss of urate oxidase in the human during
 primate evolution predisposes man to hyperuricemia, a
 metabolic disturbance that can lead to gouty arthritis and
 renal stones. To create a mouse model for hyperuricemia and
 gout, and to address the question of whether urate oxidase is
 essential in lower mammalian species, we have disrupted the
 urate oxidase gene in the mouse by homologous recombination in
 embryonic stem cells. Unlike the human situation, urate
 oxidase deficiency in mice causes pronounced hyperuricemia and
 urate nephropathy. More than half of the mutant mice died
 before 4 weeks of age, indicating that urate oxidase is
 essential in mice. These mutant mice may also serve as animal
 models for hyperuricemia and its related nephropathy in
 humans.
 
 
 185                                    NAL Call. No.: 500 N21P
 Identification and prevalence of genetic defect that causes
 leukocyte adhesion deficiency in Holstein cattle.
 Shuster, D.E.; Kehrli, M.E. Jr; Ackermann, M.R.; Gilbert, R.O.
 Washington, D.C. : The Academy; 1992 Oct01.
 Proceedings of the National Academy of Sciences of the United
 States of America v. 89 (19): p. 9225-9229. ill; 1992 Oct01. 
 Includes references.
 
 Language:  English
 
 Descriptors: Calves; Holstein-friesian; Animal models; Bovine
 leukosis; Genetic defects; Identification; Incidence;
 Mutations; Nucleotide sequences; Screening; Bulls; Culling
 
 Abstract:  Two point mutations were identified within the gene
 encoding bovine CD18 in a Holstein calf afflicted with
 leukocyte adhesion deficiency (LAD). One mutation causes an
 aspartic acid to glycine substitution at amino acid 128
 (D128G) in the highly conserved extracellular region of this
 adhesion glycoprotein, a region where several mutations have
 been found to cause human LAD. The other mutation is silent.
 Twenty calves with clinical symptoms of LAD were tested, and
 all were homozygous for the D128G allele. In addition, two
 calves homozygous for the D128G allele were identified during
 widespread DNA testing, and both were subsequently found to
 exhibit symptoms of LAD. The carrier frequency for the D128G
 allele among Holstein cattle in the United States is
 approximately 15% among bulls and 6% among cows. This mutation
 is also prevalent among Holstein cattle throughout the world,
 placing this disorder among the most common genetic diseases
 known in animal agriculture. All cattle with the mutant allele
 are related to one bull, who through the use of artificial
 insemination sired many calves in the 1950s and 1960s. The
 organization of the dairy industry and the diagnostic test
 described herein will enable nearly complete eradication of
 bovine LAD within 1 year. These results also demonstrate that
 bovine LAD is genetically homologous and phenotypically
 similar to human LAD, thus providing a useful animal model for
 studies of LAD and beta 2 integrin function.
 
 
 186                                   NAL Call. No.: 41.8 AM3A
 Immune response of cattle to Haemophilus somnus lipid A-
 protein conjugate vaccine and efficacy in a mouse abortion
 model.
 Inzana, T.J.; Todd, J.
 Schaumburg, Ill. : American Veterinary Medical Association;
 1992 Feb. American journal of veterinary research v. 53 (2):
 p. 175-179; 1992 Feb. Includes references.
 
 Language:  English
 
 Descriptors: Cattle; Antibody formation; Haemophilus somnus;
 Vaccines; Lipids; Abortion; Animal models; Mice
 
 Abstract:  Immunogenicity of the lipid A component of
 Haemophilus somnus lipooligosaccharide in cattle and mice was
 examined after purification, detoxification, and covalent
 conjugation to a protein carrier. After 2 inoculations, a
 substantial antibody response was induced in most cattle to
 lipid A and the protein carrier. To determine whether
 antibodies to lipid A would be protective, 5 X 10(7) colony-
 forming units of H somnus strain 649 were administered IV to
 endotoxin-responsive (C3H/HEN) mice. In one study, 8 of 13
 C3H/HEN mice aborted when inoculated. In contrast, abortion
 did not result when mice were inoculated with the same dose of
 an isolate of H somnus normally found in the prepuce or with
 the rough mutant Escherichia coli J5. In addition, endotoxin-
 nonresponsive (C3H/HeJ) mice were significantly (P = 0.03)
 more resistant to abortion by strain 649 than were C3H/HeN
 mice, but inoculated C3H/HeN mice were only slightly more
 resistant to H somnus abortion, compared with control mice.
 Although a large antibody response to lipid A was detected,
 there was no significant difference in the immunized group
 between mice that aborted and mice that delivered normally.
 Thus, lipooligosaccharide and other properties of virulent H
 somnus strains may contribute to abortion in mice.
 
 
 187                              NAL Call. No.: RC267.I53 1988
 Immune-deficient animals in experimental medicine.
 Wu, Bing-quan,_1930-; Zheng, Jie
 International Workshop on Immune-Deficient Animals 6th : 1988
 : Peking, China. Basel ; New York : Karger,; 1989.
 xiii, 361 p. : ill. ; 25 cm.  Includes bibliographical
 references and index.
 
 Language:  English
 
 Descriptors: Cancer; Animal models; Congresses; Immunological
 deficiency syndromes; Animal models; Congresses; Mice;
 Immunology; Congresses; Rats; Immunology; Congresses
 
 
 188                                   NAL Call. No.: RC606.I45
 Immunodeficient rodents a guide to their immunobiology,
 husbandry, and use. Institute of Laboratory Animal Resources
 (U.S.), Committee on Immunologically Compromised Rodents
 Washington, D.C. : National Academy Press,; 1989.
 x, 246 p. : ill. ; 24 cm.  Includes index.  Bibliography: p.
 165-211.
 
 Language:  English
 
 Descriptors: Immunological deficiency syndromes; Animal
 models; Rodents; Immunology; Rodents as laboratory animals
 
 
 189                                    NAL Call. No.: 41.8 P27
 Immunohistochemical, ultrastructural, and hormonal studies on
 the endocrine pancreas of voles (Microtus arvalis) with
 monosodium aspartate-induced diabetes.
 Sasaki, M.; Arai, T.; Usui, T.; Oki, Y.
 Lawrence, Kan. : American College of Veterinary Pathologists;
 1991 Nov. Veterinary pathology v. 28 (6): p. 497-505; 1991
 Nov.  Includes references.
 
 Language:  English
 
 Descriptors: Diabetes mellitus; Hormones; Ultrastructure;
 Immunohistochemistry; Endocrine system; Pancreas islets;
 Microtus arvalis; Histopathology; Animal models; Disease
 models
 
 
 190                                     NAL Call. No.: QR46.J6
 Immunomagnetic separation and DNA hybridization for detection
 of enterotoxigenic Escherichia coli in a piglet model.
 Lund, A.; Wasteson, Y.; Olsvik, O.
 Washington, D.C. : American Society for Microbiology; 1991
 Oct. Journal of clinical microbiology v. 29 (10): p.
 2259-2262; 1991 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Norway; Piglets; Diarrhea; Feces; Digesta;
 Escherichia coli; Enterotoxins; Bacterial antigens; Fimbriae;
 Genes; Dna hybridization; Magnetic separation; Immunodiagnosis
 
 Abstract:  Enterotoxigenic Escherichia coli (ETEC) strains
 were detected by stool blot hybridization assays using
 different oligonucleotide probes for the colonization fimbrial
 antigen F4, heat-stable enterotoxin I (ST I), and heat-labile
 enterotoxin (LT I) genes. Forty-eight fecal samples and seven
 samples of intestinal content from ETEC-challenged newborn
 piglets were processed in two ways: (i) by direct inoculation
 of bacterial suspension onto nylon membranes overlaying blood
 agar and (ii) by immunomagnetic enrichment of F4+ ETEC using
 magnetic beads coated with F4 monoclonal antibodies before
 inoculation onto nylon membranes. In samples obtained from
 nondiarrheic piglets pre- and postchallenge, E. coli genes for
 F4, ST I, and LT I could be detected only after immunomagnetic
 enrichment. No difference between the two methods in detection
 of these E. coli genes was observed when stool blots from
 diarrheic piglets were examined. By using magnetic separation,
 it was easy to decrease background bacterial flora, intestinal
 cells, and fecal debris and thus produce purer specimens. The
 method evaluated in this animal model appeared simple and
 quick and increased the sensitivity of detection of ETEC
 strains 100-fold compared with the direct stool blot
 hybridization assays. Prior bacterial isolation and
 identification were not necessary.
 
 
 191                                   NAL Call. No.: QP141.H78
 The immunopathology of zinc deficiency in humans and rodents.
 A possible role for programmed cell death.
 Fraker, P.J.; King, L.E.; Garvy, B.A.; Medina, C.A.
 New York ; London, Plenum; 1993.
 Human nutrition : a comprehensive treatise v. 8: p. 267-283;
 1993.  In the series analytic: Nutrition and immunology /
 edited by D.M. Klurfeld.  Includes references.
 
 Language:  English
 
 Descriptors: Zinc; Mineral deficiencies; Animal models;
 Immunopathology; Cells; Nutrition research; Death; Thymus
 gland; Endocrine glands; B lymphocytes; Phagocytes; Protein
 energy malnutrition; Bone marrow; Glucocorticoids; Elderly;
 Nutritional state; Nutrition physiology; Species differences;
 Rats; Adults; Literature reviews
 
 Abstract:  This chapter explores whether or not the zinc
 deficient rat appears to be a useful model for humans and
 whether there are common patterns of immune defects observed
 between the species. Studies are reviewed on the efficacy of
 zinc supplementation on the immune status of the mildly
 deficient elderly.
 
 
 192                                   NAL Call. No.: QP901.A33
 Impaired glucose-induced insulin secretion: studies in animal
 models with spontaneous NIDDM.
 Ostenson, C.G.; Khan, A.; Efendic, S.
 New York : Plenum Press, 1967-; 1993.
 Advances in experimental medicine and biology v. 334: p. 1-11;
 1993.  In the series analytic: New concepts in the
 pathogenesis of NIDDM / edited by C.G. Ostenson, S. Efendic,
 and M. Vranic. Proceedings of the "Second Toronto-Stockholm
 Symposium on Perspectives in Diabetes Research," September
 13-16, 1992, Stockholm, Sweden.  Includes references.
 
 Language:  English
 
 Descriptors: Diabetes mellitus; Insulin secretion; Glucose;
 Animal models
 
 
 193                                  NAL Call. No.: 389.8 B773
 Impaired T lymphocyte immune response in vitamin A depleted
 rats and chicks. Friedman, A.; Sklan, D.
 Cambridge : Cambridge University Press; 1989 Sep.
 The British journal of nutrition v. 62 (2): p. 439-449; 1989
 Sep.  Includes references.
 
 Language:  English
 
 Descriptors: Diet; Vitamin deficiencies; Retinol; T
 lymphocytes; Immune response; Rats; Chicks
 
 Abstract:  Vitamin A deficiency results in decreased immune
 responses; the objective of the present study was to
 investigate the involvement of T lymphocytes in the depression
 of immune responses resulting from vitamin A depletion. This
 objective was achieved by evaluating antigen-specific T
 lymphocyte proliferative responses in vitro as vitamin A
 depletion developed. The evaluation was performed in both rat
 and chick to examine the generality of immune effects due to
 vitamin A depletion. Our findings show that vitamin A
 depletion led to severe impairment of T lymphocyte activity in
 both animal models, and that this was directly related to the
 vitamin A status in both species. Immune response impairment
 was found to precede other manifestations of vitamin A
 deficiency, and was rapidly corrected by feeding retinyl
 acetate boluses. This implied a possible regulatory, rather
 than constitutive, role of vitamin A in immune responsiveness.
 
 
 194                                    NAL Call. No.: 381 J824
 In vivo correction of low density lipoprotein receptor
 deficiency in the Watanabe heritable hyperlipidemic rabbit
 with recombinant adenoviruses. Kozarsky, K.F.; McKinley, D.R.;
 Austin, L.L.; Raper, S.E.; Stratford-Perricaudet, L.D.;
 Wilson, J.M.
 Baltimore, Md. : American Society for Biochemistry and
 Molecular Biology; 1994 May06.
 The Journal of biological chemistry v. 269 (18): p.
 13695-13702; 1994 May06. Includes references.
 
 Language:  English
 
 Descriptors: Rabbits; Hyperlipemia; Hypercholesterolemia;
 Animal models; Low density lipoprotein; Receptors; Deficiency;
 Hereditary diseases; Gene therapy; Gene transfer;
 Complementary  DNA; Recombinant  DNA; Adenoviridae; Gene
 expression; Reporter genes; Beta-galactosidase; Liver cells;
 Promoters; Cholesterol metabolism
 
 Abstract:  A rabbit animal model of the human disease familial
 hypercholesterolemia (FH), which is the result of low density
 lipoprotein (LDL) receptor deficiency, was used to develop an
 in vivo approach to gene therapy based on recombinant
 adenoviruses. Recombinant, replication-defective adenoviruses
 expressing the lacZ gene under the control of different
 promoters were infused into the portal circulation of New
 Zealand White (NZW) rabbits. Expression of lacz could be
 obtained in virtually all hepatocytes within 3 days post-
 infusion, but was undetectable by 3 weeks. This was not
 associated with liver pathology.An LDL receptor expressing
 adenovirus was constructed using the most active promoter and
 was infused into the portal vein of rabbits deficient in LDL
 receptor. Analysis of liver tissues harvested 3 days after
 virus infusion demonstrated human LDL receptor protein in the
 majority of hepatocytes that exceeded the levels found in
 human liver by at least 10-fold. Transgene expression was
 stable for 7-10 days and diminished to undetectable levels
 within 3 weeks. Infusion of LDL receptor expressing virus led
 to substantial reductions in serum cholesterol that returned
 to base line within 3 weeks; this acute reduction in serum
 cholesterol was associated with accumulations of lipid in
 hepatocytes. The development of neutralizing antibodies to the
 recombinant adenovirus markedly diminished the effectiveness
 of a second dose. These studies illustrate the advantages of
 recombinant adenoviruses for the treatment of liver metabolic
 diseases and define issues, such as viral genome instability
 and blocking immune response, that need to be overcome before
 the promise of this technology can be fully realized.
 
 
 195                                  NAL Call. No.: QR360.A1J6
 In vivo detection of metabolic changes in a mouse model of
 scrapie using nuclear magnetic resonance spectroscopy.
 Bell, J.D.; Cox, I.J.; Williams, S.C.R.; Belton, P.S.;
 McConnell, I.; Hope, J. Reading : Society for General
 Microbiology; 1991 Oct.
 The Journal of general virology v. 72 (pt.10): p. 2419-2423;
 1991 Oct. Includes references.
 
 Language:  English
 
 Descriptors: Scrapie; Mice; Metabolites; Nuclear magnetic
 resonance spectroscopy; Membranes; Proteins; Animal models
 
 Abstract:  In vivo proton nuclear magnetic resonance (NMR)
 spectroscopy studies of scrapie in a mouse model have shown
 the appearance of an abnormal peak in the brain early in the
 incubation period. This abnormal peak was detected weeks
 before the detection of a protease-resistant form of a
 membrane protein and vacuolar histopathology in vitro, and
 several months before clinical signs, and the signal increased
 in intensity as the disease progressed. In the chronic stage
 of the disease, a reduction in N-acetyl aspartate levels was
 observed using in vivo and in vitro proton NMR spectroscopy.
 
 
 196                                   NAL Call. No.: QL55.A1L3
 Influence of chronic oestrogen treatment on severity of
 hydronephrosis in inbred DDD mice.
 Mannen, H.; Tsuji, S.; Goto, N.
 London : Royal Society of Medicine Services; 1993 Apr.
 Laboratory animals v. 27 (2): p. 124-130; 1993 Apr.  Includes
 references.
 
 Language:  English
 
 Descriptors: Mice; Estrogens; Urination disorders; Animal
 models
 
 Abstract:  It has been reported that mice treated chronically
 with oestrogen (oestradiol propionate) increase their bladder
 urine volume. Since inbred DDD mice, particularly male DDD
 mice, lack a protective mechanism against vesicoureteral
 reflux (VUR), chronic oestrogen treatment may increase the
 pressure in the renal pelvis and lead to severe
 hydronephrosis. The present studies were carried out to
 confirm this hypothesis. Results of a least-squares analysis
 of variance showed that the severity of hydronephrosis was
 more severe after treatment with high doses of oestrogen (1.0
 and 5.0 mg/kg/week) in entire and castrated male DDD mice.
 Hydroureter was also observed in the same groups. Intra-
 vesicular pressure was 7 to 12 cmH2O higher in mice of these
 groups than in control DDD mice. High doses of oestrogen had
 no effect on the kidneys of C57BL/6 mice which showed normal
 protection against VUR, though it increased bladder urine
 volume. These findings support the hypothesis that
 hydronephrosis in DDD mice is caused by an incomplete
 protective mechanism against VUR.
 
 
 197                                   NAL Call. No.: 410.9 P94
 Influenza virus infections and immunity: a review of human and
 animal models. Renegar, K.B.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Jun. Laboratory animal science v. 42 (3): p.
 222-232; 1992 Jun.  Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Influenzavirus; Influenza; Animal models; Immune
 response; Man; Domestic animals; Experimental infection;
 Vaccination; Literature reviews
 
 Abstract:  Studies of the pathogenesis of influenza infection
 have involved the extensive use of animal models. The
 development of the current concepts of immunity to influenza
 and of the contribution the secretory immune system makes
 toward the protection of mucosal surfaces against influenza
 infection would have been impossible without this use of
 animals. The pathology, and clinical signs of influenza
 infection in both natural and experimental hosts, the
 advantages and disadvantages of the most common experimental
 influenza infection models, and the contribution of animal
 models to the understanding of local and systemic immunity to
 influenza infection are discussed.
 
 
 198                                   NAL Call. No.: RA1190.F8
 Inhibition of hen brain acetylcholinesterase and neurotoxic
 esterase by chloropyrifos in vivo and kinetics of inhibition
 by chlorpyrifos oxon in vitro: application to assessment of
 neuropathic risk.
 Richardson, R.J.; Moore, T.B.; Kayyali, U.S.; Fowke, J.H.;
 Randall, J.C. Orlando, Fla. : Academic Press; 1993 Apr.
 Fundamental and applied toxicology : official journal of the
 Society of Toxicology v. 20 (3): p. 273-279; 1993 Apr. 
 Includes references.
 
 Language:  English
 
 Descriptors: Chlorpyrifos; Metabolites; Toxicity; Nervous
 system diseases; Dosage effects; Enzyme activity;
 Acetylcholinesterase; Esterases; Inhibition; Kinetics; Brain;
 In vitro; Hens; Lethal dose
 
 Abstract:  Chlorpyrifos (CPS, O,O-diethyl 3,5, 6-trichloro-2-
 pyridyl phosphorothionate; Dursban) is a widely used broad-
 spectrum organophosphorus (OP) insecticide. Because some OP
 compounds can cause a sensory-motor distal axonopathy called
 OP compound-induced delayed neurotoxicity (OPIDN), CPS has
 been evaluated for this paralytic effect. Early studies of the
 neurotoxicity of CPS in young and adult hens reported
 reversible leg weakness but failed to detect OPIDN. More
 recently, a human case of mild OPIDN was reported to result
 from ingestion of a massive dose (about 300 mg/kg) in a
 suicide attempt. Subsequent experiments in adult hens (the
 currently accepted animal model of choice for studies of
 OPIDN) showed that doses of CPS in excess of the LD50 in
 atropine-treated animals inhibited brain neurotoxic esterase
 (NTE) and produced mild to moderate ataxia. Considering the
 extensive use of CPS and its demonstrated potential for
 causing OPIDN at supralethal doses, additional data are needed
 to enable quantitative estimates to be made of the neuropathic
 risk of this compound. Previous work has shown that the
 ability of OP insecticides to cause acute cholinergic toxicity
 versus OPIDN can be predicted from their relative tendency to
 inhibit the intended target, acetylcholines (AChE), versus the
 putative neuropathic target, NTE, in brain tissue. The present
 study was designed to clarify the magnitude of neuropathic
 risk associated with CPS exposures by measuring hen brain AChE
 and NTE inhibition following dosing in vivo and determining
 the bimolecular rate constant of inhibition (ki) for each
 enzyme by the active metabolite, CPS oxon (CPO), in vitro. CPS
 administered to atropine-treated adult hens at 0, 75, 150, and
 300 mg/kg po in corn oil produced mean values for brain AChE
 inhibition 4 days after dosing of 0, 58, 75, and 86%.
 respectively, and mean values for brain NTE inhibition of 0,
 21. 40, and 77%, respectively. Only the high dose (six times
 the unprotected LD50 in hens) pro
 
 
 199                                     NAL Call. No.: QR1.I57
 Inoculation of barrier-born pigs with Helicobacter pylori: a
 useful animal model for gastritis type B.
 Engstrand, L.; Gustavsson, S.; Jorgensen, A.; Schwan, A.;
 Scheynius, A. Washington, D.C. : American Society for
 Microbiology; 1990 Jun. Infection and immunity v. 58 (6): p.
 1763-1768. ill; 1990 Jun.  Includes references.
 
 Language:  English
 
 Descriptors: Bacteria; Pigs; Models; Gastritis; Inoculation
 
 
 200                                    NAL Call. No.: 500 N21P
 Insulin-induced activation of glycerol-3-phosphate
 acyltransferase by a chiro-inositol-containing insulin
 mediator is defective in adipocytes of insulin-resistant, type
 II diabetic, Goto-Kakizaki rats.
 Farese, R.V.; Standaert, M.L.; Yamada, K.; Huang, L.C.; Zhang,
 C.; Cooper, D.R.; Wang, Z.; Yang, Y.; Suzuki, S.; Toyota, T.;
 Larner, J. Washington, D.C. : National Academy of Sciences,;
 1994 Nov08. Proceedings of the National Academy of Sciences of
 the United States of America v. 91 (23): p. 11040-11044; 1994
 Nov08.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Diabetes mellitus; Glycerol-3-phosphate
 acyltransferase; Enzyme activity; Insulin; Regulation;
 Adipocytes; Hormonal control; Inositol phosphates; Animal
 models; Phosphatidylinositols; Experimental diabetes
 
 Abstract:  Type II diabetic Goto-Kakizaki (GK) rats were
 insulin-resistant in euglycemic-hyperinsulinemic clamp
 studies. We therefore examined insulin signaling systems in
 control Wistar and diabetic GK rats. Glycerol-3-phosphate
 acyltransferase (G3PAT), which is activated by headgroup
 mediators released from glycosyl-phosphatidylinositol (GPI).
 was activated by insulin in intact and cell-free adipocyte
 preparations of control, but not diabetic, rats. A specific
 chiro-inositol-containing inositol phosphoglycan (IPG)
 mediator, prepared from beef liver, bypassed this defect and
 comparably activated G3PAT in cell-free adipocyte preparations
 of both diabetic GK and control rats. A myo-inositol-
 containing IPG mediator did not activate G3PAT. Relative to
 control adipocytes, labeling of GPI by [3H]glucosamine was
 diminished by 50% and insulin failed to stimulate GPI
 hydrolysis in GK adipocytes. In contrast to GPI-dependent
 G3PAT activation, insulin-stimulated hexose transport was
 intact in adipocytes and soleus and gastrocnemius muscles of
 the GK rat, as was insulin-induced activation of mitogen-
 activated protein kinase and protein kinase C. We conclude
 that (i) chiro-inositol-containing IPG mediator activates
 G3PAT during insulin action, (ii) diabetic GK rats have a
 defect in synthesizing or releasing functional chiro-inositol-
 containing IPG, and (iii) defective IPG-regulated
 intracellular glucose metabolism contributes importantly to
 insulin resistance in diabetic GK rats.
 
 
 201                                  NAL Call. No.: QR360.A1J6
 Interactions between equine herpesvirus type 1 and equine
 herpesvirus type 4: T cell responses in a murine infection
 model.
 Azmi, M.; Field, H.J.
 Reading : Society for General Microbiology; 1993 Nov.
 The Journal of general virology v. 74 (pt.11): p. 2339-2345;
 1993 Nov. Includes references.
 
 Language:  English
 
 Descriptors: Equine herpesvirus; Immune response; T
 lymphocytes; Animal models; Mice
 
 Abstract:  Interactions involving the immune responses to
 equine herpesvirus types 1 and 4 (EHV-1 and EHV-4) were
 studied in a murine infection model. When mice were inoculated
 intranasally with EHV-1, virus replication occurred in the
 respiratory tract and clinical signs were produced. In
 contrast, mice that were similarly inoculated with EHV-4
 produced no evidence of virus replication and showed no
 clinical signs. When mice that had been inoculated with live
 EHV-4 were challenged 1 month later with EHV-1 they were
 partially protected. Although clinical signs were apparent on
 reinfection, virus replication in the respiratory tract was
 reduced in these mice compared with control mice that had not
 been previously immunized. Mice primed with heat-inactivated
 EHV-4, however, were not so protected. Live EHV-4-primed mice
 developed very low levels of antibody to EHV-1 and the humoral
 response could not account for this protection. However, the
 infected mice did give a strong delayed-type hypersensitivity
 reaction in a skin test using either EHV-1 or EHV-4 antigen.
 Spleen cells from EHV-4-primed donors provided a source of
 immune cells, including T cells which were used for transfer
 to recipient mice which were then challenged with EHV-1. The
 cells were protective; there was a reduction of virus
 replication on challenge with EHV-1 which correlated with the
 number of cells transferred. Modulation of the protective
 effect of primed cell populations was tested after depletion
 in vivo by means of complement-mediated lysis. The depletion
 of CD4-bearing cells produced the least effect on the
 protection afforded by cell transfer. In contrast, depletion
 of CD8-bearing cells markedly reduced the protection in
 recipients. EHV-1 and EHV-4 are widespread in horses and
 cross-infections are common. These results gained from a
 murine model indicate that important interactions occur at the
 level of T cell immunity. between the two virus types which
 warrant further investigation in the natural host.
 
 
 202                                   NAL Call. No.: 447.8 AM3
 Intraluminal and intracellular phases of fat adsorption are
 impaired in essential fatty acid deficiency.
 Levy, E.; Garofalo, C.; Thibault, L.; Dionne, S.; Daoust, L.;
 Lepage, G.; Roy, C.C.
 Bethesda, Md. : American Physiological Society; 1992 Feb.
 American journal of physiology v. 262 (2,pt.1): p. G319-G326;
 1992 Feb. Includes references.
 
 Language:  English
 
 Descriptors: Essential fatty acids; Fat deficiencies;
 Triacylglycerols; Lipoproteins; Nutrient transport; Fat
 absorption; Intestinal absorption
 
 Abstract:  The structure and function of enterocyte membranes
 are particularly sensitive to the degree of fatty acid
 saturation. The objective of the present study was to assess
 intestinal fat transport in essential fatty acid (EFA)-
 deficient animal models. Both the digestive and absorptive
 phases leading to the formation and the secretion of
 triglyceride (TG)-rich lipoproteins were investigated. After
 an intraduodenal fat infusion, the percentage increase of
 plasma TG over fasting values was examined over a period of 4
 h in two groups of control and EFA-deficient rats. Lower
 values at 1 and 2 h (P < 0.05) were observed in EFA deficient
 rats, suggesting fat malabsorption. Likewise, postprandial
 chylomicronemia was diminished. In a separate group of rats,
 EFA deficiency was associated with reduced TG and chylomicron-
 TG transport into lymph. Although pancreatic lipase activity
 did not change (47.1 vs. 46.2 micromoles free fatty acids.mg
 protein-1.h-1), bile flow was decreased over the 8-h period of
 collection. Concomitantly, a significant decline (nmol.min-1.g
 liver-1, P < 0.05) was discernible in the biliary secretory
 rate of bile salts (14.09 +/- 2.13 vs. 35.09 +/- 3.73),
 phospholipids (7.01 +/- 0.61 vs. 11.79 +/- 1.65) and
 cholesterol (0.19 +/-0.01 vs. 0.83 +/- 0.06). In vitro
 studies, utilizing everted sacs incubated with mixed micelles,
 revealed that EFA-deficient jejunal segments of rats
 incorporated and esterified less [14C]oleic acid (21 and 32%,
 respectively). Moreover, the synthesis and secretion of TG-
 rich lipoproteins were found markedly reduced in mouse jejunal
 explant cultures. We conclude that EFA deficiency modifies
 both the intraluminal and intracellular phases of fat
 absorption.
 
 
 203                                   NAL Call. No.: 389.8 J82
 Iron and folate utilization in reproducing swine and their
 progeny. O'Connor, D.L.; Picciano, M.F.; Roos, M.A.; Easter,
 R.A.
 Bethesda, Md. : American Institute of Nutrition; 1989 Dec. The
 Journal of nutrition v. 119 (12): p. 1984-1991; 1989 Dec. 
 Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Pregnancy; Lactation; Diet; Iron; Folic
 acid; Metabolism
 
 Abstract:  The purpose of this investigation was to assess the
 usefulness of maternal and neonatal swine as animal models for
 studying iron (Fe) and folate nutrition during reproduction
 and growth. Sows (n = 18) were fed a purified diet containing
 0.6 mg folate/kg diet and either 25 (Fe-) or 125 (Fe+) mg
 iron/kg diet throughout gestation and lactation. Litters were
 culled to eight on d 2 of lactation and four piglets/litter
 were given an intramuscular injection of iron dextran (100
 mg/kg body wt). Plasma and red blood cell folate
 concentrations among all sows decreased (>50%) after
 conception (P < 0.001). Plasma folate concentration of Fe-
 sows was 47% and 69% of Fe+ sows on d 7 and 21 of lactation,
 respectively (P < 0.05). All sows secreted milk that contained
 low levels of folate (12-36 nmol/l) and was devoid of long-
 chain folylpolyglutamates While mean milk folate concentration
 significantly decreased after d 1 of lactation among Fe- sows,
 no such decrease was observed in milk from Fe+ sows (P <
 0.05). Liver folate concentration was significantly reduced in
 piglets nursed by Fe- sows and given intramuscular iron
 dextran. It is concluded that there is an increased dietary
 requirement for folate and iron during reproduction in swine,
 and that current recommended amounts of folate (0.6 mg/kg
 diet) and iron (80 mg/kg diet) may be underestimates of
 requirements for reproduction. Further, results show that iron
 nutrition may alter folate utilization in maternal and
 neonatal swine.
 
 
 204                                 NAL Call. No.: QP141.A1P72
 Is vitamin E supplementation a useful agent in AIDS therapy?.
 Wang, Y.; Watson, R.R.
 Tarrytown, N.Y. : Pergamon Press; 1993 Oct.
 Progress in food & nutrition science v. 17 (4): p. 351-375;
 1993 Oct. Includes references.
 
 Language:  English
 
 Descriptors: Vitamin e; Acquired immune deficiency syndrome;
 Vitamin supplements; Immune response; Oxidation; Stress;
 Cytokines; Human immunodeficiency virus; Nervous system
 diseases; Antioxidants; Neutrophils; Nutritional state;
 Literature reviews
 
 Abstract:  Acquired immune deficiency syndrome (AIDS) is a
 clinical disorder caused by a retrovirus infection,
 representing the end point in a progressive sequence of
 immunosuppressive changes. The literature is briefly
 summarized as to immunological, nutritional and other
 pathological modifications caused by AIDS, and properties of
 immunoenhancing, anti-oxidant and undernutrition-restoration
 of vitamin E supplementation. All these abnormalities in AIDS
 are similar to those that are stimulated or restored by intake
 of high doses of vitamin E. The drawbacks of pharmacological
 therapy like zidovudine (AZT), e.g. deleterious toxic side
 effects, inability to improve the immune dysfunctions and
 undernutrition initiated by the retrovirus infection, and
 finding of AZT-resistant HIV strains, necessitate new
 strategies for the clinical trials of novel therapies to treat
 AIDS with the existing medical therapies. Low toxicity
 nutritional agents with immunoenhancing and antioxidant
 activities like vitamin E may help to normalize retrovirus-
 induced immune dysfunctions, undernutrition and other
 pathological symptoms, thereby retarding the progression of
 the disease to AIDS. To address this vitamin E therapeutic
 role in HIV-positive individuals. This paper presents a review
 of vitamin E-related therapeutic roles in animals and humans,
 thereby showing why vitamin E supplementation could be used as
 a useful therapeutic agent in human AIDS therapy. Since there
 is a paucity of information available regarding the
 nutritional therapy in AIDS individuals, our purpose is to
 provide evidence from animal models or humans of the potential
 therapeutic role of vitamin E supplementation in the treatment
 of AIDS individuals.
 
 
 205                                    NAL Call. No.: 385 J822
 Isolation and localization of the 120 kDa protein in the liver
 of genetically obese Zucker rats.
 Maeda, H.; Kasahara, K.
 Tokyo : Japanese Biochemical Society; 1994 Jan.
 The Journal of biochemistry v. 115 (1): p. 37-40; 1994 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Rats; Obesity; Liver; Animal proteins; Cytosol;
 Lipogenesis; Lipid metabolism; Animal models
 
 Abstract:  The genetically obese Zucker rat is a well-
 characterized model of early-onset human obesity. The 120 kDa
 protein was recently found in the liver cytosol of obese
 Zucker rats at levels higher than that in lean Zucker rats. We
 isolated this protein using precipitation with ammonium
 sulfate, DEAE-Sephacel chromatography, and preparative
 polyacrylamide gel electrophoresis; the product showed a
 single band on SDS-polyacrylamide gel electrophoresis.
 Immunoblotting analysis revealed that the 120 kDa protein was
 predominantly localized in the liver cytosol of obese Zucker
 rats. The amount of this protein in lean Zucker rats was less
 than one-fifth of that found in obese Zucker rats. Further,
 there were only trace amounts of this protein in the lung
 tissues, and no detectable amount in other tissues, such as
 kidney, epididymal adipose tissue, brain, spleen, skeletal
 muscle, or serum, in either strain of rat. These data suggest
 that the 120 kDa protein contributes to the abnormal lipid
 metabolism in obese Zucker rats.
 
 
 206                                   NAL Call. No.: 410.9 P94
 Isotype-specific rabbit antibodies against chinchilla
 immunoglobulins G, M, and A.
 Konietzko, S.; Koskela, M.; Erdmann, G.; Giebink, G.S.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Jun. Laboratory animal science v. 42 (3): p.
 302-306; 1992 Jun.  Includes references.
 
 Language:  English
 
 Descriptors: Chinchillas; Isolation; Igg; Igm; Iga; Blood
 serum; Milk; Isotypes; Rabbits; Antibodies; Immune serum
 
 Abstract:  Chinchillas have become a preferred animal model
 for studying otitis media, and are also useful in studying
 insulin release, gastrin physiology, intestinal infection, and
 hepatocellular pathophysiology. Immunopathologic studies in
 the model, however, have been limited by absence of specific
 antibody reagents against chinchilla immunoglobulins. We
 describe a method for preparing isotype-specific rabbit
 antibodies against the heavy-chain components of chinchilla
 immunoglobulins G, M, and A. Chromatographic techniques were
 used to isolate chinchilla immunoglobulins from serum and
 breast milk; heavy-chain fractions were isolated and used as
 antigens to produce isotype-specific antibodies in New Zealand
 White rabbits. Enzyme-linked immunosorbent assay of these
 antisera disclosed anti-light chain cross-reactivity, which
 was removed by affinity chromatography. The isolation and
 affinity purification techniques were highly reproducible. The
 availability of these reagents should greatly enhance the
 utility of the chinchilla in modeling human disease.
 
 
 207                                  NAL Call. No.: QL55.A1I43
 Jcr:LA-corpulent rat: a strain with spontaneous vascular and
 myocardial disease.
 Russell, J.C.; Koeslag, D.G.
 Washington, D.C. : Institute of Laboratory Animal Resources,
 National Research Council; 1990.
 I.L.A.R. news v. 32 (3): p. 27-32; 1990.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Animal models; Vascular diseases; Heart
 diseases
 
 
 208                              NAL Call. No.: RC628.N48 1987
 The LA/N-corpulent rat as a model of atherosclerosis.
 Russell, J.C.; Heisler, O.R.; Amy, R.M.
 Bethesda, Md. : National Institutes of Health; 1988.
 New models of genetically obese rats for studies in diabetes,
 heart disease, and complications of obesity : NIH workshop,
 June 18-19, 1987, summaries of workshop papers and current
 bibliography. p. 163-165; 1988.
 
 Language:  English
 
 Descriptors: Atherosclerosis; Animal models; Rats
 
 
 209                                  NAL Call. No.: QL55.A1L33
 Large animal models of human disease.
 Lewis, S.M.; Carraway, J.H.
 New York, N.Y. : Nature Publishing Company; 1992 Jan.
 Lab animal v. 21 (1): p. 22-29; 1992 Jan.  Includes
 references.
 
 Language:  English
 
 Descriptors: Animal models; Human diseases
 
 
 210                                    NAL Call. No.: QH442.B5
 Lipoproteins and heart disease.
 Breslow, J.
 New York, N.Y. : Nature Publishing,; 1994 Apr.
 Bio/technology v. 12 (4): p. 365-370; 1994 Apr.
 
 Language:  English
 
 Descriptors: Mice; Transgenic animals; Apolipoproteins;
 Structural genes; Molecular genetics; Experimental
 atherosclerosis; Animal models; Very low density lipoprotein
 
 
 211                                 NAL Call. No.: 442.8 B5236
 Liver and muscle-fat type glucose transporter gene expression
 in obese and diabetic rats.
 Yamamoto, T.; Fukumoto, H.; Koh, G.; Yano, H.; Yasuda, K.;
 Masuda, K.; Ikeda, H.; Imura, H.; Seino, Y.
 Duluth, Minn. : Academic Press; 1991 Mar29.
 Biochemical and biophysical research communications v. 175
 (3): p. 995-1002. ill; 1991 Mar29.  Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Diabetes mellitus; Carbohydrate
 metabolism; Glucose; Insulin; Resistance; Genes; Gene
 expression; Messenger  RNA; Liver; Skeletal muscle; Rats
 
 Abstract:  In order to investigate the regulation of glucose
 transporter gene expression in the altered metabolic
 conditions of obesity and diabetes, we have measured mRNA
 levels encoding GLUT2 in the liver and GLUT4 in the
 gastrocnemius muscle from various insulin resistant animal
 models, including Zucker fatty, Wistar fatty, and
 streptozocin(STZ)-treated diabetic rats. Northern blot
 analysis revealed that GLUT2 mRNA levels were significantly
 (P<0.001) elevated in 14 wk Zucker fatty and Wistar fatty rats
 relative to lean littermates but were similar in these two
 groups at 5 wk of age. Furthermore, there was significant
 increase (P<0.01) in GLUT2 mRNA levels in STZ diabetic rats at
 3 wk after treatment. GLUT4 mRNA levels were not significantly
 different between control and insulin resistant rats in all
 animal models. These results indicate that neither
 hyperinsulinemia nor hyperglycemia affects GLUT4 mRNA levels
 in the muscle. However, GLUT2 mRNA levels in the liver were
 elevated in obesity and diabetes, although this regulatory
 event occurred independently from circulating insulin or
 glucose concentrations.
 
 
 212                                 NAL Call. No.: RC660.A1D53
 Low-protein diets in renal disease.
 Zeller, K.R.
 Alexandria, Va. : American Diabetes Association; 1991 Sep.
 Diabetes care v. 14 (9): p. 856-866; 1991 Sep.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Kidney diseases; Morbidity; Mortality; Protein
 intake; Animal models; Protein secretion; Renal function;
 Renal failure; Literature reviews; Man
 
 Abstract:  End-stage renal disease is a major cause of
 morbidity and mortality in the U.S. population and a
 significant contributor to national health-care expenditures.
 In recent years, a growing body of literature has accumulated
 from studies in animals and humans to suggest that dietary
 protein restriction can significantly retard the progression
 of chronic renal insufficiency. This article reviews the
 relevant literature and outlines the questions that remain for
 future investigation.
 
 
 213                                   NAL Call. No.: 410.9 P94
 Lymphoblastic lymphoma in a colony of N:NIH (S)-bg-nu-xid
 mice. Waggie, K.S.; Wu-Owens, J.; Hollifield, V.; Hansen, C.T.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Aug. Laboratory animal science v. 42 (4): p.
 375-377; 1992 Aug.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Lymphoma
 
 Abstract:  During a 1-year period, 28 animals from a breeding
 colony of N:NIH(S)-bg-nu-xid mice were discovered to have
 rapidly enlarging subcutaneous swellings in the ventral,
 cervical, and axillary regions. Five of the mice also had hind
 limb paresis. Twenty-two of the mice were heterozygous nude
 females, five were homozygous nude males, and one was a
 homozygous nude female. All of the above mice were homo- or
 hemizygous for the beige and X-linked immunodeficiency
 mutations. The average age of the mice was 8.3 months.
 Generalized enlargement of the peripheral and internal lymph
 nodes was present at the time of necropsy examination. Other
 lesions commonly noted at necropsy included splenomegaly (15
 mice), pale and thickened ventral lumbar spinal musculature
 (11 mice), and opaque, thickened meninges of the brain (10
 mice). Histologic examination consistently disclosed
 infiltrates of neoplastic lymphoblasts in multiple tissues
 including lymph nodes, spleen, bone marrow, and meninges of
 the brain and spinal cord. The cells were positive for IgG on
 immunofluorescent staining, suggesting that the tumors were of
 B cell origin. The neoplasms observed in these mice have
 several similarities to tumors found in immunodeficient
 humans, suggesting that these mice may serve as useful animal
 models of lymphoma.
 
 
 214                             NAL Call. No.: RC628.T697 1992
 Marked caloric restriction and organ response in normal-weight
 and obese experimental animals.
 Young, E.A.
 New York : Guilford Press; 1992.
 Treatment of the seriously obese patient / edited by Thomas A.
 Wadden, Theodore B. VanItallie ; foreward by Per Bjorntorp. p.
 107-135; 1992. Includes references.
 
 Language:  English
 
 Descriptors: Calorie-restricted diets; Metabolic studies;
 Nutrition physiology; Animal models
 
 
 215                                  NAL Call. No.: 389.9 N953
 The mechanisms and treatment of weight loss in cancer.
 Fearon, K.C.H.
 Cambridge : Cambridge University Press; 1992 Aug.
 Proceedings of the Nutrition Society v. 51 (2): p. 251-265;
 1992 Aug.  The Sir David Cuthbertson Medal lecture 1991
 presented at the University of Leeds, November 1991.  Includes
 references.
 
 Language:  English
 
 Descriptors: Carcinoma; Cachexia; Anorexia; Protein
 metabolism; Cytokines; Diet treatment; Energy metabolism; Drug
 therapy; Literature reviews
 
 Abstract:  In this lecture, the author examines the metabolic
 disturbance, specifically weight loss, in patients with
 cancer. It covers: changes in body composition; the role of
 anorexia; animal models of cancer cachexia; the role of
 cytokines; protein metabolism; tumor energy metabolism; and
 dietary and pharmacological manipulation of tumor growth.
 
 
 216                                   NAL Call. No.: TX551.N87
 Mechanisms of food intolerances: development and use of
 experimental animal models.
 Miller, K.; Nicklin, S.
 London : Taylor & Francis; 1988.
 Nutritional and toxicological aspects of food processing :
 proceedings of an interntional symposium held at the Istituto
 Superiore di Sanita, Rome, Italy, 14-16 April 1987 / edited by
 R. Walker and E. Quattrucci. p. 351-364; 1988. Includes
 references.
 
 Language:  English
 
 Descriptors: Food intolerance; Animal experiments
 
 
 217                                   NAL Call. No.: 448.8 M56
 Membrane fluidity and sodium transport by renal membranes from
 dogs with spontaneous idiopathic Fanconi syndrome.
 Hsu, B.Y.L.; McNamara, P.D.; Mahoney, S.G.; Fenstermacher,
 E.A.; Rea, C.T.; Bovee, K.C.; Segal, S.
 Orlando, Fla. : W.B. Saunders Co; 1992 Mar.
 Metabolism: clinical and experimental v. 41 (3): p. 253-259;
 1992 Mar. Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Fanconi syndrome; Kidneys; Membranes;
 Sodium; Nutrient uptake; Nutrient transport; Animal models
 
 
 218                                   NAL Call. No.: 448.8 M56
 Metabolic abnormalities of the hyperglycemic obese Zucker rat.
 McCaleb, M.L.; Sredy, J.
 Philadelphia, Pa. : W.B. Saunders Co; 1992 May.
 Metabolism: clinical and experimental v. 41 (5): p. 522-525;
 1992 May. Includes references.
 
 Language:  English
 
 Descriptors: Diabetes mellitus; Hyperglycemia; Obesity;
 Metabolism; Physiopathology; Animal models; Rats
 
 
 219                                    NAL Call. No.: 41.8 Ad9
 Metabolic fatty liver of ruminants.
 Bruss, M.L. \u University of California, Davis, CA
 San Diego, Calif. : Academic Press; 1993.
 Advances in veterinary science and comparative medicine v. 37:
 p. 417-449; 1993.  In the series analytic: Animal models in
 liver research / edited by Charles E. Cornelius.  Includes
 references.
 
 Language:  English
 
 Descriptors: Cows; Sheep; Fatty liver; Liver;
 Triacylglycerols; Lipid metabolism; Long chain fatty acids;
 Animal models; Literature reviews
 
 
 220                                   NAL Call. No.: QL55.A1L3
 A method for hyperthermic treatment of mouse skin.
 Gragtmans, N.J.; Jevcak, J.J.; Mitchel, R.E.J.; Morrison,
 D.P.; McCann, R.A.; Murphy, J.W.
 London : Royal Society of Medicine Services; 1992 Apr.
 Laboratory animals v. 26 (2): p. 122-126; 1992 Apr.  Includes
 references.
 
 Language:  English
 
 Descriptors: Mice; Skin; Animal models; Disease models;
 Hyperthermia; Carcinogenesis; Promoters; Carcinogens
 
 Abstract:  The Sencar mouse skin system is a recognized model
 for tumour initiation, promotion and progression. The current
 interest in the effect of hyperthermia on this multi-stage
 tumorigenesis model prompted the need for a technique to
 accurately heat a section of dorsal skin of a large number of
 mice for 30 min per heat treatment. In the technique
 described, experimental groups of 25 female Sencar mice were
 treated at 7-8 weeks of age under general methoxyflurane
 anaesthesia. Treatment consisted of the application of
 initiating and/or promoting agents with or without
 hyperthermia. For hyperthermic skin treatments, each group of
 mice was placed onto a platform in a water bath so that the
 dorsal skin of the mice was in contact with 44 degrees C
 temperature controlled water.
 
 
 221                                    NAL Call. No.: QP43.M47
 Methods in animal physiology.
 Deyl, Zdenek; Zicha, Joseph
 Boca Raton, Fla. : CRC Press,; 1989.
 438 p. : ill. ; 26 cm.  Includes bibliographies and index.
 
 Language:  English
 
 Descriptors: Physiology, Experimental; Methodology; Pathology,
 Experimental; Methodology; Diseases; Animal models
 
 
 222                                 NAL Call. No.: QP141.A1J54
 Methyl deficiency, DNA methylation, and cancer: studies on the
 reversibility of the effects of a lipotrope-deficient diet.
 Christman, J.K.; Chen, M.L.; Sheikhnejad, G.; Dizik, M.;
 Abileah, S.; Wainfan, E.
 Newton, Mass. : Butterworth-Heinemann; 1993 Dec.
 The Journal of nutritional biochemistry v. 4 (12): p. 672-680;
 1993 Dec. Includes references.
 
 Language:  English
 
 Descriptors: Lipotropic factors; Deficiency; Carcinoma; Diet;
 Dna methylation; Carcinogenesis; Gene expression; Animal
 models; Rats
 
 Abstract:  Methylation of C residues in CpG sites in the
 regulatory, regions of a wide variety of genes has been linked
 to silencing of their expression. During normal mammalian
 development, loss of methylation at specific sites accompanies
 tissue-specific activation of genes. Overall decreases in the
 level of DNA methylation and alterations in the pattern of
 methylation of specific genes are also closely linked to tumor
 development in humans and other mammals. Dietary methyl
 deficiency sufficient to cause hepatocarcinogenesis in male
 rats induces profound and rapid changes in the morphology and
 metabolic activity of liver cells. As we have previously
 reported, these changes include a decrease in the overall
 level of DNA methylation and alternations in the patterns of
 methylation and levels of transcripts of specific growth-
 related genes. These alterations persist as long as the rats
 are maintained on a methyl-deficient diet. The starting
 hypothesis for the studies summarized here is that methyl
 deficiency induced changes in liver cells that persist, even
 when dietary sources of methyl groups are restored, are more
 likely to be critical for establishment of neoplasia than
 those that are reversible. We find that loss of methylation at
 specific sites in liver DNA persists for at least 9 weeks
 after restoration of methionine, choline, folate, and vitamin
 B12 to the diet of rats previously deprived of these nutrients
 for 4 weeks. Other molecular changes are reversed in less than
 3 weeks. This suggests that exposure of rats to alternating
 periods of dietary methyl deficiency and sufficiency may
 provide an experimental model for determining whether
 persistent alterations in methylation of growth regulatory
 genes allow affected hepatocytes to escape constraints on cell
 division because they respond to growth stimuli differently
 than cells in which the genes are normally methylated.
 
 
 223                                    NAL Call. No.: 500 N484
 The microepidemiology of wasting syndrome, a common link to
 diarrheal disease, cancer, rabies, animal models of AIDS, and
 HIV-AIDS (HAIDS): the feline leukemia virus and rabies virus
 models.
 Tshikuka, J.G.; Torres-Anjel, M.J.; Blenden, D.C.; Elliott,
 S.C. New York, N.Y. : The Academy; 1992.
 Annals of the New York Academy of Sciences v. 653: p. 274-296.
 ill; 1992.  In the series analytic: Tropical veterinary
 medicine: current issues and perspectives / edited by J.C.
 Williams, K.M. Kocan, and E.P.J. Gibbs. Literature review. 
 Includes references.
 
 Language:  English
 
 Descriptors: Acquired immune deficiency syndrome;
 Epidemiology; Human immunodeficiency virus; Disease models;
 Feline oncovirus; Rabies virus; Literature reviews
 
 
 224                                   NAL Call. No.: 442.9 SO1
 Minimum requirements of n-3 and n-6 essential fatty acids for
 the function of the central nervous system and for the
 prevention of chronic disease. Okuyama, H.
 Baltimore, Md. : Williams & Wilkins; 1992 Jun.
 Proceedings of the Society for Experimental Biology and
 Medicine v. 200 (2): p. 174-176; 1992 Jun.  Proceedings of a
 "Conference on Molecular and Comparative Nutrition," July
 22-24, 1991, National Institutes of Health, Bethesda,
 Maryland.  Includes references.
 
 Language:  English
 
 Descriptors: Linoleic acid; Linolenic acid; Safflower oil;
 Perilla; Plant oils; Nutrition; Animal behavior; Animal
 physiology; Central nervous system; Diseases; Disease
 prevention; Animal models; Rats; Mice
 
 Abstract:  General behavioral patterns of rats or mice fed 5
 wt% safflower oil (75% linolenate [n-6] and < 0.1% alpha-
 linolenate [n-3]) for two generations were significantly
 different from those of animals fed 5 wt% perilla oil (15% n-6
 and 55% n-3). Also, brightness-discrimination learning ability
 and retinal function were higher in the perilla group than in
 the group fed 5 wt% soybean oil (53% n-6 and 4.7% n-3) or
 safflower oil, indicating that the requirement of n-3 for the
 maximum responses of the nervous system is above 0.6 en% when
 there is 6.8 en% linoleate n-6. Perilla oil has been found to
 be beneficial for the suppression of carcinogenesis, allergic
 hyperreactivity, thrombotic tendency, apoplexy, hypertension,
 and aging in animals, as compared with soybean oil and
 safflower oil. These results are against a lipid peroxide
 theory of aging, carcinogenesis, and chronic diseases. Animal
 experiments and epidemiological studies lead to a
 recommendation that the intake of n-6 should be decreased to
 as low as 2-4 en% and that of n-3 be increased to levels
 higher than linoleate n-6 for the prevention of chronic
 diseases prevailing in the industrialized countries.
 
 
 225                                  NAL Call. No.: QD341.A2N8
 Mitochondrial genome expression in a mutant strain of D.
 subobscura, an animal model for large scale mtDNA deletion.
 Beziat, F.; Morel, F.; Volz-Lingenhol, A.; Saint Paul, N.;
 Alziari, S. Oxford : IRL Press; 1993 Feb11.
 Nucleic acids research v. 21 (3): p. 387-392; 1993 Feb11. 
 Includes references.
 
 Language:  English
 
 Descriptors: Drosophila subobscura; Mitochondrial  DNA;
 Deletions; Mitochondrial genetics; Genomes; Transcription;
 Gene expression; Messenger RNA; Genes; Transfer  RNA;
 Structural genes; Nadh dehydrogenase; Cytochrome b
 
 Abstract:  A mitochondrial mutant strain of D. subobscura has
 two mitochondrial genome populations (heteroplasmy): the first
 (20-30% of the population, 15.9 kb) is the same as could be
 found in the wild type; the second (70-80% of the population,
 11 kb) has lost by deletion several genes coding for complex I
 and III subunits, and four tRNAs. In human pathology, this
 kind of mutation has been correlated with severe diseases such
 as the Kearns-Sayre syndrome, but the mutant strain does not
 seem to be affected by the mutation. Studies reported here
 show that: a) Transcripts from genes not concerned by the
 mutation are present at the same level in both strains. b) In
 contrast, transcript concentrations from genes involved in the
 deletion are significantly decreased (30-50%) in the mutant.
 c) Deleted DNA was expressed as shown by the detection of the
 fusion transcript. d) The mtDNA/nuc.DNA ratio is 1.5 times
 higher in the mutant strain than in the wild type. The
 mutation leads to change in the transcript level equilibrium.
 The apparent innocuousness of the mutation may suggest some
 post-transcriptional compensation mechanisms. This drosophila
 strain is an interesting model to study the consequence of
 this type of mitochondrial genome deletion.
 
 
 226                                   NAL Call. No.: 410.9 P94
 A model of postprandial hyperinsulinemia in miniature swine.
 Weingard, K.W.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1989 Sep. Laboratory animal science v. 39 (5): p.
 394-399; 1989 Sep.  Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Hyperinsulinemia; Insulin; Diets; Disease
 models; Atherosclerosis
 
 Abstract:  This report describes a new animal model of
 postprandial hyperinsulinemia (PPH) in adult miniature swine
 that consume a diet simulating that of affluent Western
 societies. Two progressive levels of PPH were induced
 experimentally by injecting subcutaneously low and high doses
 of purified porcine insuline without causing acute detrimental
 clinical effects or significant biological effects on total
 serum cholesterol, sodium and potassium concentrations, mean
 arterial blood pressure, or heart rate. Physiologic
 postprandial increments in total serum triglyceride
 concentrations were inhibited by experimentally-induced PPH.
 With this model, the in vivo effects of homologous PPH can be
 studied in a dose-responsive manner. Areas of potential
 research use of this model include study of the chronic
 effects of PPH on lipoprotein metabolism, the development of
 atherosclerosis and diabetes mellitus, and the association
 with regional body fat distribution and metabolism.
 
 
 227                                   NAL Call. No.: 447.8 AM3
 Model of spontaneous obesity in aging male Wistar rats.
 Newby, F.D.; DiGirolamo, M.; Cotsonis, G.A.; Kutner, M.H.
 Bethesda, Md. : American Physiological Society; 1990 Dec.
 American journal of physiology v. 259 (6,pt.2): p. R1117-
 R1125; 1990 Dec. Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Adipose tissue; Growth; Adipocytes;
 Morphology; Body fat; Body weight; Animal models; Rats; Aging;
 Male animals
 
 Abstract:  We analyzed retrospectively data from 148 chow-fed
 male Wistar rats killed between the age of 6 wk and 2 yr while
 varying in body weight from 136 to 917 g. The purpose of this
 study was to clarify the relationship of body weight and body
 lipid content with the composition and cellularity of the
 epididymal and retroperitoneal fat depots. A positive linear
 association was found between body weight and body water or
 fat-free dry residue, whereas total body lipid exhibited a
 curvilinear relationship with body weight. The weight of the
 epididymal pads was linearly related to body weight but not to
 body lipid. In contrast, retroperitoneal pad weight was
 exponentially related to body weight and paralleled total body
 lipid. A strong linear correlation was found between total
 body lipid and weight (r = 0.959) or depot lipid content (r =
 0.967) of the retroperitoneal fat pads. In this rat model of
 aging and spontaneous obesity, significant regional
 differences exist in adipose depot composition and
 cellularity. A practical outcome of this study is a simple and
 accurate prediction of body lipid content from the gravimetric
 determination of the retroperitoneal fat depots.
 
 
 228                                  NAL Call. No.: QL55.A1I43
 Modeling in biomedical research: an assessment of current and
 potential approaches.
 Washington, D.C. : Institute of Laboratory Animal Resources,
 National Research Council; 1990.
 I.L.A.R. news v. 32 (2): p. 2-3; 1990.
 
 Language:  English
 
 Descriptors: Animal models; Disease models; Cardiovascular
 diseases; Diabetes mellitus; Animal experiments; Computer
 simulation; Medical research
 
 
 229                                    NAL Call. No.: 41.8 J82
 Morphological changes associated with furazolidone-induced
 cardiomyopathy: effects of digoxin and propranolol.
 Gwathmey, J.K.
 London : Academic Press; 1991 Jan.
 Journal of comparative pathology v. 104 (1): p. 33-45; 1991
 Jan.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Disease models; Cardiomyopathy;
 Poults; Furazolidone; Histopathology; Digoxin; Propranolol;
 Muscular hypertrophy
 
 
 230                                 NAL Call. No.: RC280.L5M67
 Mouse liver carcinogenesis mechanisms and species comparisons
 : proceedings of a symposium held in Austin, Texas, November
 30-December 3, 1988. Stevenson, Donald E.
 M.D. Anderson Cancer Center, Science-Park Research Division
 New York : A.R. Liss,; 1989.
 xix, 444 p. : ill. ; 24 cm. (Progress in clinical and
 biological research ; v. 331).  Conference hosted by the
 Science Park-Research Division of the University of Texas M.D.
 Anderson Cancer Center in Smithville, Tex.  Includes
 bibliographical references.
 
 Language:  English
 
 Descriptors: Liver; Tumors; Congresses; Cancer; Animal models;
 Congresses; Carcinogenicity testing; Congresses;
 Carcinogenesis; Congresses; Mice; Diseases; Congresses
 
 
 231                                   NAL Call. No.: 410.9 P94
 Mouse model for disseminated Trichosporon beigelii infection.
 Bannatyne, R.M.; Fong, I.W.; Cheng, P.; Capellan, J.M.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Apr. Laboratory animal science v. 42 (2): p.
 168-169; 1992 Apr.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Animal models; Trichosporon beigelii;
 Mycoses; Experimental infection
 
 
 232                                   NAL Call. No.: 410.9 P94
 Mouse models of short- and long-term foreign body in the
 urinary bladder: analogies to the bladder segment of urinary
 catheters.
 Johnson, D.E.; Lockatell, C.V.; Hall-Craggs, M.; Warren, J.W.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1991 Oct. Laboratory animal science v. 41 (5): p.
 451-455; 1991 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Animal models; Bladder; Catheters; Foreign
 bodies; Bacterial diseases; Experiments; Long term experiments
 
 Abstract:  Catheter-associated bacteriuria is the most common
 infection occurring in hospitals, where urethral catheters are
 generally in place for a few days, and in nursing homes, where
 catheters may be in place for months or years. We developed
 murine models with intrabladder urinary catheters for studying
 complications of bacteriuria in short- and long-term
 catheterization. In the short-term model, a catheter segment
 was inserted transurethrally and lay free within the bladder
 lumen. Half of the animals expelled segments during a 2-to-7-
 day period, durations similar to catheterizations in
 hospitalized patients. For studies of long-term catheter use,
 the catheter segment was secured within the bladder by a
 single suture for up to 12 months. Antibiotics administered
 for 7 days after catheter placement and housing mice in cages
 with wire screen floors reduced spontaneous bacteriuria to an
 acceptably low incidence rate of only 7%. Proteus mirabilis
 bacteriuria of high concentration provoked the same
 complications that are common in patients with long-term
 catheters: acute pyelonephritis, chronic renal inflammation,
 and struvite stone formation. These models allow inoculation
 of the bacteria of interest and are suitable for studies of
 short- and long-term foreign body-associated bacteriuria and
 its complications.
 
 
 233                                   NAL Call. No.: 410.9 P94
 The muskrat in biomedical research.
 Doyle, R.E.; Panneton, W.M.; Vogler, G.A.; Romeo, J.P.;
 Watson, B.J.; Higgins, B.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1988 Dec. Laboratory animal science v. 38 (6): p.
 667-674. ill; 1988 Dec.  Includes references.
 
 Language:  English
 
 Descriptors: Muskrats; Animal husbandry; Animal health;
 Handling; Quarantine; Medical research; Animal experiments
 
 Abstract:  Muskrats are aquatic rodents of moderate size which
 are plentiful throughout North America, but are not used
 commonly in the laboratory. Recently, we tested the
 feasibility of muskrats as experimental models and have found
 them to be acquired and cared for easily in conventional
 laboratory animal facilities. Some of their natural
 characteristics and diseases are described. The husbandry
 techniques that we used are presented and form a base for the
 preparation of future guidelines for the maintenance and use
 of feral animals in research. The results of some initial
 experiments testing the muskrat's utility for investigations
 of cardiorespiratory control mechanisms also are presented.
 Our data show that even anesthetized muskrats possess brisk
 and dramatic cardiovascular and respiratory reflexes. Our
 findings that their brains possess the cytoarchitectural and
 myeloarchitectural features comparable to other mammals,
 combined with their relative uniformity in size, has allowed
 us to locate specific neuronal loci stereotaxically. We
 suggest that the muskrat be considered as an experimental
 animal model for studies of the neural control of
 cardiorespiratory systems.
 
 
 234                                    NAL Call. No.: 41.8 P27
 Mycobacterium paratuberculosis monossociated nude mice as a
 paratuberculosis model.
 Hamilton, H.L.; Cooley, A.J.; Adams, J.L.; Czuprynski, C.J.
 Lawrence, Kan. : American College of Veterinary Pathologists;
 1991 Mar. Veterinary pathology v. 28 (2): p. 146-155; 1991
 Mar.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Mycobacterium paratuberculosis; Disease
 models; Peptides; Necrosis; Animal models
 
 
 235                                 NAL Call. No.: QP141.A1P72
 Neuroendocrine alterations in iron deficiency.
 Beard, J.L.
 Elmsford, N.Y. : Pergamon Press; 1990.
 Progress in food and nutrition science v. 14 (1): p. 45-80.
 charts; 1990. Literature review.  Includes 141 references.
 
 Language:  English
 
 Descriptors: Iron; Mineral deficiencies; Mineral metabolism;
 Neurophysiology; Neurosecretory systems; Temperature;
 Catecholamines; Animal experiments; Human nutrition research
 
 Abstract:  A model of iron metabolism has been used for
 several years and suggests that the deleterious consequences
 of iron deficiency occur only after depletion of body iron
 stores. The biochemical consequences of iron deficiency have
 been adequately reviewed by others and will be covered only
 briefly here. This review will focus on those effects of iron
 deficiency on neuroendocrine processes. Out of necessity, many
 of these observations are derived from the rat as a animal
 model and are limited in breadth and depth of investigation.
 The rat model has been reasonable for many studies of iron
 metabolism and tissue biochemistry, but serious concerns can
 and should be raised when neuroendocrine relationships are
 being investigated. Nonetheless, strong parallels have been
 observed between effects of iron deficiency anemia in humans
 and the rat model especially with regard to thyroid metabolism
 and catecholamines. The discrepancies may reflect the greater
 severity of the deficiency generated in the rat as well as the
 rate of development of the deficiency.
 
 
 236                                  NAL Call. No.: QR360.A1J6
 Neurological abnromalities associated with feline
 immunodeficiency virus infection.
 Phillips, T.R.; Prospero-Garcia, O.; Puaoi, D.L.; Lerner,
 D.L.; Fox, H.S.; Olmsted, R.A.; Bloom, F.E.; Henriksen, S.J.;
 Elder, J.H.
 Reading : Society for General Microbiology; 1994 May.
 The Journal of general virology v. 75 (pt.5): p. 979-987; 1994
 May.  Includes references.
 
 Language:  English
 
 Descriptors: Cats; Feline immunodeficiency virus; Central
 nervous system; Cerebrospinal fluid; Brain; Lesions
 
 Abstract:  Specific pathogen-free cats were infected with the
 Maryland strain of FIV (FIV-MD) for the purpose of assessing
 the effects of FIV infection on the central nervous system
 (CNS). Two separate studies were performed, involving a total
 of 13 infected cats and six age-matched, sham-inoculated
 controls. All animals infected with FIV-MD seroconverted by 8
 weeks post-infection and virus was recovered from peripheral
 blood mononuclear cells of all infected cats. All of the
 infected animals had lower absolute CD4(+) cell counts and
 decreased CD4(+)/CD8(+) ratios. Virus was recovered from the
 cerebrospinal fluid (CSF) of certain infected individuals, and
 antiviral antibody and pleocytosis were evident in the CSF of
 the majority of infected cats. Additionally, virus was
 recovered from tissue explants from the cerebellum, midbrain
 and brainstem of one sacrificed FIV(+) cat. Specific
 neurological changes included anisocoria, delayed righting
 reflex and delayed pupillary reflex, as well as delayed visual
 and auditory evoked potentials, and marked alterations in
 sleep patterns similar to those reported for human
 immunodeficiency virus (HIV)-positive individuals.
 Histological evaluation revealed the presence of perivascular
 cuffing and glial nodules in FIV-infected cats. These results
 indicate that FIV causes an acute neurological disease that
 closely resembles the early neurological effects of HIV
 infection in humans and should serve well as an animal model
 for lentivirus-induced CNS disease.
 
 
 237                                   NAL Call. No.: 410.9 P94
 A new mouse strain manifesting high proteinuria and kinney
 glomerular defect. Hyun, B.H.; Wakasugi, N.; Nose, M.; Saito,
 T.; Tomita, T. Cordova, Tenn. : American Association for
 Laboratory Animal Science; 1991 Oct. Laboratory animal science
 v. 41 (5): p. 442-446; 1991 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Mutants; Proteinuria; Glomerulopathy;
 Recessive genes; Animal models; Disease models
 
 Abstract:  A mutant strain of mice manifesting high
 proteinuria, wasting syndrome, and kidney glomerular defect
 was established from the F5 offspring of an interstrain cross
 of CBA/Nga and RFM/Nga mice. Affected mice had high levels of
 proteinuria after 40 days of age. The body weight of about
 22.6% of affected mice decreased rapidly and they died between
 3 and 5 months of age. We learned that this abnormality is
 controlled by two pairs of autosomal recessive genes; the
 mutant strain of mice is designated FGS/Nga. The mutant strain
 has been characterized by high proteinuria and renal lesions
 with focal sclerosis of glomeruli and tubular atrophy with
 interstitial nephritis in the kidney resembling the human
 disease. The FGS/Nga mouse strain is a potential animal model
 for studying kidney glomerular defect in humans.
 
 
 238                                   NAL Call. No.: 410.9 P94
 A new rat mutant with chronic conjugated hyperbilirubinemia
 and renal glomerular lesions.
 Hosokawa, S.; Tagaya, O.; Mikami, T.; Nozaki, Y.; Kawaguchi,
 A.; Yamatsu, K.; Shamoto, M.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Feb. Laboratory animal science v. 42 (1): p.
 27-34; 1992 Feb.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Mutants; Hyperbilirubinemia; Animal models;
 Hereditary diseases; Disease models; Glomerulus;
 Histopathology
 
 Abstract:  A new mutant strain of inbred Sprague Dawley rats
 with autosomal recessive hyperbilirubinuria, were studied by
 biochemical, histologic, and ultrastructural methods. The
 plasma bilirubin concentration in the homozygote was
 significantly higher than that of the heterozygote, and about
 80% of the bilirubin was conjugated. Plasma BSP and ICG
 clearance were both severely delayed in the homozygote. Plasma
 BSP elimination kinetics suggested that the pathophysiologic
 defect was not hepatic uptake or storage but rather in
 secretion into bile. Histopathology of the liver demonstrated
 brown pigment in the hepatocytes that appeared to be
 lipofuscin. The electron microscopic features of the hepatic
 pigment resembled those of the Dubin-Johnson syndrome.
 Homozygote histopathology also revealed glomerular lesions
 with mesangial expansion and proliferation in the kidneys.
 Immunohistologic studies disclosed mesangial granular
 deposition of IgG, IgA, and to a lesser degree, IgM and C3.
 These renal changes resembled those of IgA nephropathy. The
 spontaneous hyperbilirubinuric rat (EHBR) may be a useful
 animal model for studying constitutive conjugated
 hyperbilirubinemia, bilirubin metabolism, cholestasis, and
 glomerulonephropathy subsequent to hepatic dysfunction.
 
 
 239                                  NAL Call. No.: RC262.C5N8
 No effect of adult dietary fat on tumors induced prenatally by
 diethylstilbestrol.
 Walker, B.E.
 Hillsdale, N.J. : Lawrence Erlbaum Associates, Inc; 1992.
 Nutrition and cancer v. 17 (2): p. 161-169; 1992.  Includes
 references.
 
 Language:  English
 
 Descriptors: Female animals; Prenatal period;
 Diethylstilbestrol; Maturation; Dietary fat; Neoplasms
 
 Abstract:  Strain CD-1 female mice exposed prenatally to
 diethylstilbestrol (DES) or vehicle were placed on
 semipurified diets containing 2.6%, 10%, 20%, or 29% fat by
 weight at four weeks of age. These mice were used as a
 breeding colony for a few weeks and then maintained to
 terminal illness on the semipurified diets. Females exposed
 prenatally to DES developed mammary tumors, pituitary tumors,
 and glandular tumors of the reproductive tract. There was no
 significant difference in tumor frequency between low- and
 high-fat dietary groups. Fewer tumors appeared in the vehicle-
 exposed mice, as expected, and their frequency did not differ
 between the dietary groups. Pregnancy reduced tumor frequency
 in DES-exposed mice, but the incidence of pregnancy was not
 significantly different between low- and high-fat dietary
 groups. In the adult the failure of a high-fat diet to
 increase the frequency of reproductive system tumors induced
 prenatally is in marked contrast to the effectiveness of high-
 fat diets in promoting mammary tumors induced by carcinogens
 given to rats postnatally. This difference is critical in the
 interpretation of epidemiological studies. The relationship of
 dietary fat to reproductive system cancer in human populations
 was reviewed in comparison with these two animal models. The
 epidemiological literature was found to be more consistent
 with the animal model, showing high sensitivity to dietary fat
 prenatally but no significant sensitivity at the adult stage
 of life.
 
 
 240                                  NAL Call. No.: QL55.A1I43
 The NOD mouse: a model for analyzing the interplay between
 heredity and environment in development of autoimmune disease.
 Leiter, E.H.
 Washington, D.C. : Institute of Laboratory Animal Resources,
 National Research Council; 1993.
 I.L.A.R. news v. 35 (1): p. 4-14; 1993.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Animal models; Autoimmune diseases
 
 
 241                                   NAL Call. No.: QP141.H78
 Nutrition and aging in animal models.
 Masoro, E.J.
 New York, N.Y. : Plenum; 1989.
 Human nutrition : a comprehensive treatise v. 6: p. 25-41;
 1989.  Includes references.
 
 Language:  English
 
 Descriptors: Elderly nutrition; Laboratory animals; Food
 restriction; Caloric intake; Dietary proteins; Source fat;
 Nutrient intake; Minerals; Vitamins
 
 
 242                                NAL Call. No.: QP141.A1J685
 Nutritional immunology: methodological considerations.
 Fraker, P.
 Binghamton, NY : Haworth Medical Press, c1991-; 1994.
 Journal of nutritional immunology v. 2 (4): p. 87-92; 1994. 
 Paper presented at the Workshop on Nutrition, Immunity and
 Infection, October 7-9, 1992, Bethesda, Maryland.  Includes
 references.
 
 Language:  English
 
 Descriptors: Immunology; Nutritional state; Nutrition
 physiology; Immune response; Nutrient deficiencies; Animal
 models
 
 
 243                                    NAL Call. No.: 500 N484
 Nutritional influence on neonatal infections in animal models
 and man. Harris, M.C.; Douglas, S.D.
 New York, N.Y. : The Academy; 1990.
 Annals of the New York Academy of Sciences v. 587: p. 246-256;
 1990.  In the series analytic: Micronutrients and immune
 functions / edited by A. Bendich and Ranjit K. Chandra. 
 Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Infant nutrition; Infectious diseases;
 Malnutrition; Neonates; Neutrophils; Rats; Animal models;
 Disease resistance; Literature reviews
 
 
 244                                    NAL Call. No.: QH301.F3
 Obesity, diabetes, and neoplasia in yellow A(vy)/-mice:
 ectipic expression of the agouti gene.
 Yen, T.T.; Gill, A.M.; Frigeri, L.G.; Barsh, G.S.; Wolfe, G.L.
 Bethesda, Md. : The Federation of American Societies for
 Experimental Biology; 1994 May.
 The FASEB journal : official publication of the Federation of
 American Societies for Experimental Biology v. 8 (8): p.
 479-488; 1994 May.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Obesity; Diabetes; Mutations; Loci; Genes;
 Phenotypes; Metabolic disorders; Literature reviews; Animal
 models
 
 
 245                              NAL Call. No.: RC628.E97 1991
 Obesity in Europe 91 proceedings of the 3rd European Congress
 on Obesity. Ailhaud, G.
 European Congress on Obesity 3rd : 1991 : Nice, France.
 London : John Libbey,; 1992.
 xii, 464 p. : ill. ; 25 cm.  "Obesity in Europe 91 represents
 the edited proceedings of the 3rd European Congress on
 Obesity, held in Nice, France, 30 May-1 June 1991"--2nd
 prelim. page.  Includes bibliographical references and
 indexes.
 
 Language:  English
 
 Descriptors: Obesity
 
 Abstract:  Discusses the multifaceted aspects of human
 obesity; neuro-endocrine regulation of food intake; the
 genetics of obesity in animal models and humans;
 epidemiological aspects of obesity; management of obesity;
 CNS-periphery relationships; enzymatic and metabolic
 regulation of adipose tissue; control of energy expenditure;
 cellular and molecular biology in the analysis of obesity;
 psychosocial aspects of obesity; etc.
 
 
 246                                   NAL Call. No.: QP141.C65
 Obesity--role of animal models.
 McCracken, K.J.
 London : J. Libbey; 1988.
 Comparative nutrition / editors, Sir Kenneth Blaxter, Ian
 Macdonald. p. 163-184; 1988.  Literature review.  Includes
 references.
 
 Language:  English
 
 Descriptors: Obesity; Nutrition physiology; Animal experiments
 
 
 247                                  NAL Call. No.: 389.8 J824
 Omega-3 fatty acids in health and disease and in growth and
 development. Simopoulos, A.P.
 Baltimore, Md. : American Society for Clinical Nutrition; 1991
 Sep. American journal of clinical nutrition v. 54 (3): p.
 438-463. charts; 1991 Sep.  Literature review.  Includes
 references.
 
 Language:  English
 
 Descriptors: Polyenoic fatty acids; Eicosapentaenoic acid;
 Docosenoic acids; Metabolism; Nutrient sources; Diet;
 Evolution; Food composition tables; Heart diseases;
 Hypertension; Inflammation; Autoimmune diseases; Neoplasms;
 Diabetes; Nutrient deficiencies; Disease prevention; Nutrition
 physiology; Literature reviews
 
 Abstract:  Several sources of information suggest that man
 evolved on a diet with a ratio of omega 6 to omega 3 fatty
 acids of approximately 1 whereas today this ratio is
 approximately 10:1 to 20-25:1, indicating that Western diets
 are deficient in omega 3 fatty acids compared with the diet on
 which humans evolved and their genetic patterns were
 established. Omega-3 fatty acids increase bleeding time;
 decrease platelet aggregation, blood viscosity, and
 fibrinogen; and increase erythrocyte deformability, thus
 decreasing the tendency to thrombus formation. In no clinical
 trial, including coronary artery graft surgery, has there been
 any evidence of increased blood loss due to ingestion of omega
 3 fatty acids. Many studies show that the effects of omega 3
 fatty acids on serum lipids depend on the type of patient and
 whether the amount of saturated fatty acids in the diet is
 held constant. In patients with hyperlipidemia, omega 3 fatty
 acids decrease low-density-lipoprotein (LDL) cholesterol if
 the saturated fatty acid content is decreased, otherwise there
 is a slight increase, but at high doses (32 g) they lower LDL
 cholesterol; furthermore, they consistently lower serum
 triglycerides in normal subjects and in patients with
 hypertriglyceridemia whereas the effect on high-density
 lipoprotein (HDL) varies from no effect to slight increases.
 The discrepancies between animal and human studies most likely
 are due to differences between animal and human metabolism. In
 clinical trials eicosapentaenoic acid (EPA) and
 docosahexaenoic acid (DHA) in the form of fish oils along with
 antirheumatic drugs improve joint pain in patients with
 rheumatoid arthritis; have a beneficial effect in patients
 with ulcerative colitis; and in combination with drugs,
 improve the skin lesions, lower the hyperlipidemia from
 etretinates, and decrease the toxicity of cyclosporin in
 patients with psoriasis. In various animal models omega 3
 fatty acids decrease the number and size of tumors and
 increase the time
 
 
 248                             NAL Call. No.: QL737.P6C6 v.25
 Osteoarthritis in rhesus monkeys and gibbons a locomotor model
 of joint degeneration.
 DeRousseau, C. Jean
 Basel ; New York : Karger,; 1988.
 xii, 145 p. : ill. ; 25 cm. (Contributions to primatology ; v.
 25).  Includes index.  Bibliography: p. [103]-131.
 
 Language:  English
 
 Descriptors: Osteoarthritis; Animal models; Primates;
 Diseases; Medical anthropology
 
 
 249                                   NAL Call. No.: SF380.I52
 Ovine GM1 gangliosidosis.
 Murnane, R.D.; Ahern-Rindell, A.J.; Prieur, D.J.
 New York : Elsevier; 1991 Oct.
 Small ruminant research v. 6 (1/2): p. 109-115; 1991 Oct. 
 Includes references.
 
 Language:  English
 
 Descriptors: Sheep; Gangliosidosis; Lysosomes; Neurons;
 Histopathology; Diagnosis; Symptoms; Animal models
 
 
 250                                    NAL Call. No.: 500 N484
 Oxygen free radical-mediated heart injury in animal models and
 during bypass surgery in humans: effects of alpha-tocopherol.
 Ferrari, R.; Curello, S.; Boffa, G.M.; Condorelli, E.; Pasini,
 E.; Guarnieri, G.; Albertini, A.
 New York, N.Y. : The Academy; 1989.
 Annals of the New York Academy of Sciences v. 570: p. 237-253;
 1989.  In the series analytic: Vitamin E--biochemistry and
 health implications / edited by A.T. Diplock, L.J. Machlin, L.
 Packer and W.A. Pryor.  Literature review. Includes
 references.
 
 Language:  English
 
 Descriptors: Myocardial ischemia; Oxygen; Stress; Surgery;
 Vitamin e; Vitamin deficiency; Human nutrition research; Rats;
 Literature reviews
 
 
 251                                   NAL Call. No.: 410.9 P94
 Pancreatectomized swine as a model of diabetes mellitus.
 Stump, K.C.; Swindle, M.M.; Saudek, C.D.; Strandberg, J.D.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1988 Aug. Laboratory animal science v. 38 (4): p.
 439-443. ill; 1988 Aug.  Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Pancreatectomy; Disease models; Diabetes;
 Blood glucose; Insulin; Mortality
 
 Abstract:  The development of a model of diabetes mellitus
 using swine offers the potential for new investigations in the
 study of human diabetic complications. In particular, animal
 models for the study of accelerated atherosclerosis associated
 with diabetes are important and presently lacking. Swine were
 selected because they have a natural susceptibility to
 atherosclerosis and have plasma lipoprotein patterns which are
 close to those of humans. Diabetes mellitus was induced in
 nine miniature swine by total pancreatectomy. Following
 surgery, they were maintained on porcine derived insulin at
 doses predicated on blood glucose levels. Pancreatic enzymes
 were replaced by dietary supplementation. Eight of the nine
 pigs were pancreatectomized successfully and stabilized with
 insulin. After initial weight loss, the pancreatectomized pigs
 maintained growth rates comparable to controls. Hypoglycemia
 and bacterial infections were the major problems experienced.
 Post-operative survival ranged from 50 days to 455 days. Our
 study shows that swine can be pancreatectomized successfully
 and maintained as insulin dependent animals, presenting a
 realistic model for research on the complications of diabetes.
 
 
 252                                   NAL Call. No.: TX345.B74
 The pathogenesis of obesity.
 Bray, G.A.
 San Diego, Calif. : Academic Press; 1989.
 Bristol-Myers Squibb/Mead Johnson nutrition symposia v. 7: p.
 129-143. charts; 1989.  In the series analytic: Nutrition and
 the Origins of Disease / edited by C.H. Halsted and R.B.
 Rucker.  Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Nutrient balance; Energy expenditure;
 Regulation; Feedback; Neurotransmitters; Brain; Sympathetic
 nervous system; Adrenalectomy; Nutrition physiology;
 Literature reviews
 
 Abstract:  The regulation of body weight is presented as a
 controlled system for nutrient balance. Nutrient intake and
 storage; energy expenditure; a nutrient control equation; and
 animal models of obesity (hypothalamic, genetic and dietary)
 are discussed. The role of the brain (anatomy and
 neurotransmitters); feedback signals; and efferent controls as
 regulators of food intake and nutrient metabolism are also
 reviewed.
 
 
 253                               NAL Call. No.: DISS F1991140
 Pathogenetische Rolle zytotoxischer T-Lymphozyten bei der
 Masernenzephalitis im Tiermodell  [Pathogenetic relevance of
 cytotoxic T lymphocytes (CTL) in measles virus-induced
 encephalitis in two animal models]. Niewiesk, Stefan
 Hannover : [s.n.],; 1991.
 ix, 134 p. : ill. ; 21 cm.  Summary in English.  Includes
 bibliographical references (p. 107-126).
 
 Language:  German
 
 
 254                                     NAL Call. No.: QR1.I57
 Pathogenicity of porcine intestinal spirochetes in gnotobiotic
 pigs. Neef, N.A.; Lysons, R.J.; Trott, D.J.; Hampson, D.J.;
 Jones, P.W.; Morgan, J.H.
 Washington, D.C., American Society for Microbiology; 1994 Jun.
 Infection and immunity v. 62 (6): p. 2395-2403; 1994 Jun. 
 Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Spirochaetales; Pathogenicity; Phenotypes;
 Enzymes; Animal models; Colonization; Gnotobiotic animals;
 Bacteroids; Intestinal microorganisms; Yersinia
 pseudotuberculosis
 
 Abstract:  Twelve intestinal spirochete strains of porcine
 origin were characterized on the basis of their phenotypic
 properties, by multilocus enzyme electrophoresis, and by
 pathogenicity testing in gnotobiotic pigs. The spirochetes
 used included two strains of Serpulina hyodysenteriae (B204
 and P18A), two strains of Serpulina innocens (B256 and 4/71),
 one strain from the proposed new genus and species "Anguillina
 coli" (P34/6/78), and seven non-S. hyodysenteriae strains
 recently isolated from United Kingdom pigs herds with a
 history of nonspecific diarrhea and typhlocolitis. By
 multilocus enzyme electrophoresis, five of these were
 identified as S. innocens, one was identified as an
 unspecified Serpulina sp., and one was identified as "A.
 coli." S. hyodysenteriae B204 and P18A, "A. coli" P43/6/78 and
 2/7, and three (22/7, P2801/1, and 14/5) of the five S.
 innocens field isolates induced mucoid feces and typhlocolitis
 in gnotobiotic pigs. None of the other spirochetes produced
 clinical signs or large intestinal pathology in this model.
 The "A. coli" strains induced a more watery diarrhea, with
 lesions present more proximally in the large intestine, than
 did the other pathogenic spirochetes. S. innocens 22/7 was
 also tested for pathogenicity in hysterotomy-derived pigs that
 had previously been artificially colonized with a spirochete-
 free intestinal flora and shown to be susceptible to swine
 dysentery. Despite effective colonization, strain 22/7 did not
 produce any disease, nor was there any exacerbation of large
 intestinal pathology or clinical signs when pigs with an
 experimentally induced existing colitis caused by Yersinia
 pseudotuberculosis were superinfected with strain 22/7.
 Certain non-S. hyodysenteriae spirochetes are therefore
 capable of inducing disease in gnotobiotic pigs, but their
 role as primary or opportunistic pathogens in conventional
 pigs remains equivocal.
 
 
 255                                   NAL Call. No.: 410.9 P94
 Pharmacokinetics of fusidic acid in laboratory animals.
 Findon, G.; Miller, T.E.; Rowe, L.C.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1991 Oct. Laboratory animal science v. 41 (5): p.
 462-465; 1991 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Mice; Rabbits; Guinea pigs; Antibiotics;
 Pharmacokinetics; Oral administration; Subcutaneous injection;
 Intramuscular injection
 
 Abstract:  The ability to evaluate the efficacy of fusidic
 acid in animal models of infectious disease is limited by the
 absence of pharmacokinetic data for the agent in laboratory
 animals. In our study, aspects of fusidic acid
 pharmacokinetics were compared in rats (Rattus norwegicus),
 mice (Mus musculus), rabbits (Oryctolagus cuniculus), and
 guinea pigs (Cavia porcellus). Sodium fusidate was poorly
 absorbed after oral administration to rats, although limited
 absorption occurred in guinea pigs, mice, and rabbits.
 Subcutaneous injections of diethanolamine fusidate to
 laboratory rats, however, achieved a serum profile similar to
 that observed in humans. There was no evidence of drug
 accumulation in rats given repeated subcutaneous doses of
 diethanolamine fusidate during a 4-day period, but rabbits
 showed clear evidence of a cumulative effect.
 
 
 256                           NAL Call. No.: TD888.C65C68 1988
 Physiologic and cellular changes in an animal model of
 byssinosis. Hara, K.S.; Scanlon, P.D.; Schroeder, M.A.;
 Rohrbach, M.S. Memphis, TN : National Cotton Council; 1988.
 Cotton dust : proceedings of the Twelfth Cotton Dust Research
 Conference, beltwide cotton research conferences, New Orleans,
 LA, January 6-7, 1988 / proc of Endotoxin Inhalation Workshop,
 Clearwater, FL, Sept 28-30, 1987. p. 171-175; 1988.  Includes
 references.
 
 Language:  English
 
 Descriptors: Guinea pigs; Cotton; Dusts; Respiratory diseases
 
 
 257                                  NAL Call. No.: 389.1 W892
 The piglet as a model animal for studying aspects of digestion
 and absorption in milk-fed human infants.
 Moughan, P.J.; Nirtles, M.J.; Cranwell, P.D.; Smith, W.C.;
 Pedraza, M. Basel : S. Karger; 1992.
 World review of nutrition and dietetics v. 67: p. 40-113;
 1992.  In the series analytic: Nutritional triggers for health
 and disease / edited by A. P. Simopoulos.  Literature review. 
 Includes references.
 
 Language:  English
 
 Descriptors: Infants; Diet; Milk; Human milk; Digestion;
 Absorption; Animal models; Piglets; Literature reviews
 
 
 258                                    NAL Call. No.: 41.8 Am3
 Polysulfated glycosaminoglycan in the treatment of
 osteoarthritis. Todhunter, R.J.; Lust, G.
 Schaumburg, Ill. : The Association; 1994 Apr15.
 Journal of the American Veterinary Medical Association v. 204
 (8): p. 1245-1251; 1994 Apr15.  Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Horses; Glycosaminoglycans; Osteoarthritis;
 Drug therapy; Disease prevention; Drug effects; Enzymes;
 Inhibition; Animal models; Dosage; Adverse effects; Literature
 reviews
 
 
 259                                    NAL Call. No.: 41.8 Ad9
 Portosystemic hepatic encephalopathy related with congenital
 and acquired hepatopathies in the dog.
 Rothuizen, J.
 San Diego, Calif. : Academic Press; 1993.
 Advances in veterinary science and comparative medicine v. 37:
 p. 403-416; 1993.  In the series analytic: Animal models in
 liver research / edited by Charles E. Cornelius.  Includes
 references.
 
 Language:  English
 
 Descriptors: Hepatitis; Cirrhosis; Portal vein; Hypoplasia;
 Encephalopathy; Animal models; Dogs; Vascular diseases;
 Literature reviews
 
 
 260                                     NAL Call. No.: QP86.P6
 The Potential for nutritional modulation of the aging process.
 Ingram, Donald K.; Baker, George T.; Shock, Nathan Wetherill,
 Trumbull, Conn. : Food & Nutrition Press,; 1991.
 xiii, 417 p. : ill. ; 24 cm. (Publications in food science and
 nutrition). Proceedings of an international conference
 sponsored by the American Health Foundation, co-sponsored by
 National Institutes on Aging, Food and Drug Administration,
 The Gerontological Society of America, September 13-15, 1988,
 New York, NY.  Includes bibliographical references and index.
 
 Language:  English
 
 Descriptors: Aging
 
 Abstract:  Reports the proceedings of a conference on the
 fundamental effects of nutritional variables on aging
 processes. Variables range from population demography and
 epidemiology to biochemistry and molecular genetics to the
 involvement of nutritional variables in the etiology of
 specific diseases. Research on animal models of the effects of
 calorie restriction on a number of age-related phenomena
 ranging from genetic expression to learning and memory and the
 involvement of specific nutrients on age-related processes are
 presented.
 
 
 261                                    NAL Call. No.: 500 N484
 Prenatal protein malnutrition and postnatal brain function.
 Tonkiss, J.; Galler, J.; Morgane, P.J.; Bronzino, J.D.;
 Austin-Lafrance, R.J. New York, N.Y. : The Academy; 1993.
 Annals of the New York Academy of Sciences v. 678: p. 215-227;
 1993.  In the series analytic: Maternal nutrition and
 pregnancy outcome / edited by C.L. Keen, A. Bendich, and C.C.
 Willhite.  Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Human nutrition research; Prenatal period;
 Protein deficiencies; Puerperium; Animal models; Brain;
 Neurophysiology; Literature reviews
 
 
 262                                     NAL Call. No.: QR1.I57
 Production and purification of heat-stable exterotoxin b from
 a porcine Escherichia coli strain.
 Dubreuil, J.D.; Faribrother, J.M.; Lallier, R.; Lariviere, S.
 Washington, D.C. : American Society for Microbiology; 1991
 Jan. Infection and immunity v. 59 (1): p. 198-203; 1991 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Rats; Escherichia coli; Enterotoxins; Heat
 stability; Purification; Characterization; Animal models
 
 Abstract:  Production of heat-stable enterotoxin b (STb) by
 porcine Escherichia coli strains belonging to serogroup O115
 was evaluated in ligated intestinal segments of adult rats.
 The conditions for optimal production and detection of STb
 were studied by using the STb-producing strain 4247. As STb
 production was similar in complex Trypticase soy broth and
 minimal Davis medium, the latter was used for the fermentation
 of strain 4247 and the production of STb in large quantities.
 STb was then purified to apparent homogeneity by sequential
 ultrafiltration, ultracentrifugation, and preparative gel
 electrophoresis. The enterotoxin was purified more than 500-
 fold and exhibited a molecular weight of approximately 5,000
 as determined by urea-sodium dodecyl sulfate gel
 electrophoresis. Purified STb retained such chemical
 characteristics as resistance to heating (60 degrees C/30 min)
 and sensitivity to trypsin. A rabbit polyclonal antiserum was
 produced against the purified toxin. Numerous booster doses
 were required to obtain a significant enzyme-linked
 immunosorbent assay titer, suggesting that STb is a poor
 immunogen. Nevertheless, the antiserum was used successfully
 to discriminate between culture supernatants of STb-positive
 and STb-negative O115 E. coli strains, thus demonstrating the
 immunogenicity of purified STb.
 
 
 263                                  NAL Call. No.: QP501.B474
 A profile of cerebral and hepatic carnitine, ammonia, and
 energy metabolism in a model of organic aciduria:BALB/cByJ
 mouse with short-chain acyl-CoA dehydrogenase deficiency.
 Qureshi, I.A.; Ratnakumari, L.; Michalak, A.; Giguere, R.;
 Cyr, D.; Butterworth, R.F.
 Orlando, Fla. : Academic Press; 1993 Oct.
 Biochemical medicine and metabolic biology v. 50 (2): p.
 145-158; 1993 Oct. Includes references.
 
 Language:  English
 
 Descriptors: Metabolic disorders; Oxidoreductases; Enzyme
 deficiencies; Energy metabolism; Mice
 
 Abstract:  Spontaneous animal models of inborn errors of
 metabolism are valuable tools for defining the pathogenesis of
 these disorders and also the mechanism of various therapeutic
 approaches. In the present study, we have employed BALB/cByJ
 mice with an autosomal recessive deficiency of short-chain
 acyl-CoA dehydrogenase (SCAD). These animals were
 characterized by a marked urinary excretion of ethylmalonic
 and methylsuccinic acids along with butyrylglycine. Using
 adult homozygous mice we have studied the basic cerebral and
 hepatic profile of carnitine, ammonia, and energy metabolism.
 The effects of fasting and a short-term supplement of L-
 carnitine have been evaluated in comparison with control
 BALB/cJ mice. The mutant mice had low levels of acetyl-CoA and
 high levels of lactate compared to control mice. Fasting
 aggravated this condition by further decreasing acetyl- CoA
 and increasing lactate levels in the mutant mice. Free
 carnitine levels were significantly decreased in liver with
 fasting. Long-chain acylcarnitines were significantly lower in
 the brain of mutant mice. A short-term supplementation of L-
 carnitine resulted in general increases of carnitine levels in
 liver and muscle, but they still remained lower in mutant
 BALB/cByJ mice as compared to control BALB/cJ mice. L-
 carnitine treatment increased cerebral CoA-SH levels and both
 hepatic and cerebral acetyl-CoA levels in mutant mice.
 Hyperammonemia which has been described frequently in acyl-CoA
 dehydrogenase deficiencies was not observed in adult BALB/cByJ
 mice. This could be due to a rapid conjugation of butyryl-CoA
 with glycine by an increased activity of glycine N-
 acyltransferase.
 
 
 264                                     NAL Call. No.: QR1.I57
 Protection of C3H/HeN mice from challenge with Borrelia
 burgdorferi through active immunization with OspA, OspB, or
 OspC, but not with OspD or the 83-kilodalton antigen.
 Probert, W.S.; LeFebvre, R.B.
 Washington, D.C., American Society for Microbiology; 1994 May.
 Infection and immunity v. 62 (5): p. 1920-1926; 1994 May. 
 Includes references.
 
 Language:  English
 
 Descriptors: Borrelia burgdorferi; Immunization; Mice; Surface
 antigens; Disease prevention; Antibody formation;
 Antibacterial properties
 
 Abstract:  Recent advances in the development of animal models
 for Lyme borreliosis have provided means of identifying
 potential targets for the design of a subunit vaccine to
 prevent this disease. The C3R/HeN mouse model was used to
 study several Borrelia burgdorferi antigens from a single
 isolate for their ability to elicit borreliacidal and
 protective antibodies. The ospA, ospB, ospC, ospD, and 83-kDa
 genes from a California isolate, SON 188, were cloned and
 expressed in Escherichia coli as proteins fused to the C-
 terminal end of maltose-binding protein. Active immunization
 of mice with these fusion proteins elicited high titers of
 antibodies that recognized the homologous SON 188 antigens
 upon immunoblotting. Antibodies generated to the OspA and OspB
 fusion proteins, but not to the OspC, OspD, and the 83-kda
 fusion proteins, demonstrated in vitro borreliacidal activity.
 Challenge of all actively immunized mice with 10(7) SON 188
 spirochetes resulted in infection in all mice receiving the
 OspD or 83-kDa immunogens but not in any mice receiving the
 OspA, OspB, or OspC fusion proteins. These results demonstrate
 the potential of OspA, OspB, and OspC as components of a
 subunit vaccine for the prevention of Lyme borreliosis.
 
 
 265                                   NAL Call. No.: 410.9 P94
 Pulmonary responses of conscious strain 13 guinea pigs to
 pichinde viral infection.
 Guo, Z.M.; Liu, C.T.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1991 Dec. Laboratory animal science v. 41 (6): p.
 581-584; 1991 Dec.  Includes references.
 
 Language:  English
 
 Descriptors: Guinea pigs; Pichinde virus; Animal models;
 Respiration; Measurement
 
 Abstract:  A laboratory animal model for studying pulmonary
 responses to arenaviral infection was established with
 advanced technologies. Tidal volume (TV), respiratory rate
 (RR), minute volume (MV), expiratory time (TE), inspiratory
 time (TI), peak expiratory flow (PEF), and specific pulmonary
 airway resistance (RES) were measured with a double
 plethysmograph and a computer data-acquisition system in six
 conscious, strain 13 guinea pigs. Using the same animal,
 experiments were conducted before and after subcutaneous
 inoculation with 10(4) plaque-forming units of Pichinde virus.
 Pulmonary functions were determined for 1 minute every 10
 minutes for 2 hours before and at postinoculation days (PUD)
 3, 6, 8, and daily thereafter until shortly before death. The
 mean time to death was 18 +/- 0.7 days. Tidal volume, RR, MV,
 PEF, RES, and rectal temperature increased slightly on PID 3
 and reached peak values at the midpoint of disease. At 95% of
 the mean time to death (16.5 +/- 0.5 days), RR, MV, and rectal
 temperatures suddenly decreased to lower than baseline values;
 while TV, RES, and PEF values remained high. When TE decreased
 with the increase in RR, TI did not change. When RR decreased
 at the terminal stage, both TE and TI increased.
 Hyperventilation, increased specific pulmonary airway
 resistance, terminal hypoventilation, and respiratory arrest
 were noted in strain 13 guinea pigs infected with Pichinde
 virus.
 
 
 266                                   NAL Call. No.: RA1190.F8
 Quantitative analysis of neuronal damage induced by tri-ortho-
 cresyl phosphate in Wistar rats.
 Inui, K.; Mitsumori, K.; Harada, T.; Maita, K.
 Orlando, Fla. : Academic Press; 1993 Jan.
 Fundamental and applied toxicology : official journal of the
 Society of Toxicology v. 20 (1): p. 111-119; 1993 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Organophosphorus compounds; Toxicity;
 Neurotoxins; Nervous system diseases; Neurons; Histopathology;
 Ultrastructure; Animal models; Toxicology; Rats
 
 Abstract:  A quantitative analysis of neuronal damage was
 performed on the fasciculus gracilis (FG) of the cervical
 spinal cord in male Wistar rats that received orally a single
 dose of tri-ortho-cresyl phosphate (TOCP) at 1500 mg/kg. FG
 tissues were sampled at 1, 2, and 3 weeks after treatment and
 examined histopathologically. Wallerian degeneration of
 myelinated nerve fibers was observed in FG at 2 weeks.
 Morphological changes were most evident at 3 weeks after
 treatment and the number of fibers was reduced.
 Ultrastructurally, axonal swelling due to the accumulation of
 cytoplasmic contents was observed near the node of Ranvier in
 the affected animals, indicating paranodal degeneration.
 Axonal atrophy and swelling in organophosphorus-induced
 delayed neuropathy (OPIDN) were evaluated quantitatively using
 a computer-assisted image analyzer. Morphometric examinations
 on semi-thin sections and frozen sections stained with Nauta's
 method were demonstrated to be useful for objective evaluation
 of OPIDN in the rat.
 
 
 267                                   NAL Call. No.: 41.9 AM37
 Quantitative TC-99m-MDP joint scintigraphy in a lentivirus-
 induced arthritis of goats.
 Papageorges, M.; Gavin, P.R.; Barbee, D.D.; Sande, R.D.;
 Knowles, D.P.; Cheevers, W.P.
 Raleigh, N.C. : American College of Veterinary Radiology; 1991
 Mar. Veterinary radiology v. 32 (2): p. 82-86; 1991 Mar. 
 Includes references.
 
 Language:  English
 
 Descriptors: Goats; Scintigraphy; Technetium; Caprine
 arthritis encephalitis virus; Arthritis; Inflammation; Joints
 (animal); Histopathology; Animal models
 
 
 268                                  NAL Call. No.: RC262.C5N8
 A rationale for dietary intervention in postmenopausal breast
 cancer patients: an update.
 Cohen, L.A.; Rose, D.P.; Wynder, E.L.
 Hillsdale, N.J. : Lawrence Erlbaum Associates, Inc; 1993.
 Nutrition and cancer v. 19 (1): p. 1-10; 1993.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Mammary gland neoplasms; Nutritional
 intervention; Dietary fat; Nutrient intake; Risk; Women;
 Epidemiological surveys; Animal models; Feasibility studies;
 Literature reviews
 
 Abstract:  In 1982, we proposed a large-scale randomized
 prospective trial to test the hypothesis that decreasing
 dietary fat intake from 38% to 20% of total calories would
 increase the disease-free interval and/or five-year survival
 rate for postmenopausal breast cancer patients. We now review
 new evidence from epidemiological studies, laboratory animal
 model studies, and preliminary feasibility trials that has
 accumulated over the past decade, in support of such a trial,
 and suggest that a more appropriate dietary goal is a
 reduction in fat intake to 15% of total calories.
 
 
 269                                   NAL Call. No.: 442.9 SO1
 Reduced survival of neonates due to vitamin A deficiency
 during pregnancy in the guinea pig.
 Apgar, J.; Dulin, A.; Kramer, T.; Smith, J.C.
 Baltimore, Md. : Williams & Wilkins; 1991 May.
 Proceedings of the Society for Experimental Biology and
 Medicine v. 197 (1): p. 56-58; 1991 May.  Includes references.
 
 Language:  English
 
 Descriptors: Vitamin a deficiency; Pregnancy; Survival;
 Newborn animals; Guinea pigs; Animal models; Mineral nutrition
 
 Abstract:  Neonatal vitamin A stores are limited even in well-
 nourished full-term infants and are yet smaller in the
 premature infant. The object of this experiment was to
 determine whether vitamin A deficiency could be induced
 inpregnant guinea pigs and, if so, whether it would affect
 vitamin A status of the neonate.Adult (600 g) guinea pigs were
 fed a casein-agar diet that was vitamin A deficient
 (AD).Controls (vitamin A adequate) were orally dosed weekly
 with 2 mg of retinylpalmitate. Weight gains of dams and birth
 weights of neonates did not differ. No externalsigns of
 deficiency were observed. Six of eight AD and seven of eight
 vitamin A-adequatedams carried pregnancy to term (greater than
 or equal to Day 64). One AD dam died during delivery. Liver
 retinol concentrations were below the detection limit (<3
 microgram/g) for all AD neonatesand dams and in postpartum
 serum of AD dams. Of neonates born greater than or equal to
 Day64, 15 of 18 AD were dead or moribund compared with 4 of 22
 vitamin A adequate. The unexpectedly severeeffect on the
 neonate indicates that the guinea pig will be a sensitive
 modelfor investigating the affect of poor maternal vitamin A
 status on neonatal vitaminA-dependent functions. However, a
 less severe maternal deprivation should be used forsuch
 studies.
 
 
 270                                    NAL Call. No.: 381 B522
 Reduction of hyperlipidemia in the LA/N-corpulent rat by
 dietary fish oil containing n-3 fatty acids.
 Dolphin, P.J.; Amy, R.M.; Koeslag, D.G.; Limoges, B.F.;
 Russell, J.C. Amsterdam : Elsevier Science Publishers; 1988
 Oct14.
 Biochimica et biophysica acta : International journal of
 biochemistry and biophysics v. 962 (3): p. 317-329; 1988
 Oct14.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Obesity; Diet; Fish oils; Fatty acids;
 Hypertriglyceridemia
 
 Abstract:  The LA/N rat, when homozygous for the corpulent
 gene (cp/cp), is obese, hyperphageous, hyperinsulinemic,
 hypertriglyceridemic and prone to the development of vascular
 and myocardial lesions. The hypertriglyceridemia, which in 3-
 month-old cp/cp males is 282 +/- 42 mg/dl and in females, 512
 +/-83 mg/dl, results from the presence of a large
 triacylglycerol-rich VLDL. The moderate hypercholesterolemia
 in these animals is largely due to markedly elevated HDL
 levels, which reach 172 +/- 21 mg total lipid/dl in males and
 154 +/- 22 mg total lipid/dl in females. The LA/N-cp rat is
 thus an interesting animal model of endogenous
 hypertriglyceridemia in which to examine the hypolipidemic
 effects of pharmacological agents and also dietary oil
 supplements containing the n-3 fatty acids. In this study, 1-
 month-old male and female cp/cp rats were fed a normal low fat
 laboratory chow supplemented with either 10% olive oil or 10%
 redfish (Sebastes marinus) oil ad libitum for a period of 2
 months. The redfish oil contained 4.9 +/- 0.1% of its total
 fatty acids as eicosapentaenoic (20:5(n-3)) and 2.3 +/- 0.5%
 as docosahexaenoic acid (22:6(n-3)), the predominant fatty
 acids being gondoic (20:1(n-3)), 21.9 +/- 0.9% and cetoleic
 acid (22:1(n-11)), 21.7 +/- 1.7%, which are of dietary origin.
 Daily caloric was similar in the oil-fed versus control rats.
 However, the oil-fed animals weighed significantly more than
 the controls after 2 months of oil supplementation. Redfish
 oil reduced serum triacylglycerols by 54% in males and 45% in
 females after 2 months. VLDL levels, after the same time
 period, were reduced by 44% in males and 39% in females. HDL
 lipid mass was significantly reduced in both sexes (by 27% in
 males and 49% in females). However, the levels remained above
 those of male LA/N +/+ rats of the same age and Long-Evens
 rats. Olive oil feeding significantly reduced serum
 cholesterol, triacylglycerols and phospholipids in male but
 only cholesterol and phospholipids in female anim
 
 
 271                                   NAL Call. No.: 381 J8282
 Reevaluation and application of the dual-isoptope plasma ratio
 method for the measurement of intestinal cholesterol
 absorption in the hamster. Turley, S.D.; Herndon, M.W.;
 Dietschy, J.M.
 Bethesda, Md. : Lipid Research, inc., 1959-; 1994 Feb.
 Journal of lipid research v. 35 (2): p. 328-339; 1994 Feb. 
 Includes references.
 
 Language:  English
 
 Descriptors: Cholesterol; Intestinal absorption; Measurement;
 Isotope labeling; Blood plasma; Ratios; Biological techniques;
 Hamsters
 
 Abstract:  These experiments systematically evaluated the
 dual-isotope plasma ratio method for measuring intestinal
 cholesterol absorption in the hamster. It was found that while
 the ratio of the and 14C-labeled cholesterol in the plasma,
 relative to the respective dose of each that was given, became
 constant by 72 h after their administration, the percent
 cholesterol absorption was lower in animals that were fasted
 before dosing (35.7 +/- 5.5%) than in their fed controls (47.5
 +/- 3.7%). Furthermore, the percent absorption found 72 h
 after dosing varied greatly, depending on whether the
 intragastric dose of labeled cholesterol was administered in
 medium chain triglyceride (MCT) oil (46.2 +/- 2.3%), olive oil
 (63.9 +/- 11.2%), or safflower oil (74.6 +/- 4.5%). The level
 of absorption was not different between hamsters that had
 unrestricted (46.3 +/- 1.6%) and restricted (43.8 +/- 2.2%)
 access to their stools during the 72 h after dosing. Other
 experiments, using only hamsters in the fed state and MCT oil
 as the intragastric dosing medium, showed that the percent
 cholesterol absorption could be made to vary over a wide range
 using treatments known to produce such effects in humans.
 Thus, feeding either surfomer, cholestyramine, ursodeoxycholic
 acid, or CI-976, a new inhibitor of acyl-CoA:cholesterol
 acyltransferase, significantly blocked cholesterol absorption,
 whereas the addition of either cholic acid or increasing
 amounts of oil to the diet had the opposite effect. The
 modified dual-isotope plasma ratio method described here
 provides a simpler and more physiologic approach to the
 routine measurement of cholesterol absorption in the hamster
 and similar small animal models.
 
 
 272                                   NAL Call. No.: 44.8 J822
 Relationship of in vitro immune function with health and
 production in Holstein cattle.
 Weigel, K.A.; Freeman, A.E.; Kehrli, M.E. Jr; Thurston, J.R.;
 Kelley, D.H. Champaign, Ill. : American Dairy Science
 Association; 1992 Jun. Journal of dairy science v. 75 (6): p.
 1672-1679; 1992 Jun.  Includes references.
 
 Language:  English
 
 Descriptors: Dairy cows; Immune competence; Animal health; In
 vitro; Assays; Bovine mastitis; Costs; Regression analysis;
 Milk production; Disease resistance; Screening
 
 Abstract:  Eighty-seven lactating Holstein cows from the Iowa
 State University Breeding Research Herd were evaluated for 20
 in vitro measures of immune function. Principal component
 analysis was used to discard redundant assay variables such
 that the 11 remaining variables were more nearly independent
 than the original variables. Multiple linear regression in an
 animal model was used to determine the effects of these 11
 variables on lifetime production and on general udder, and
 reproductive health traits. A significant joint effect of the
 11 immune function variables on California mastitis test
 scores was observed. California mastitis test scores were
 positively correlated with antibody-dependent neutrophil
 cytotoxicity and negatively correlated with antibody-
 independent neutrophil cytotoxicity. Wisconsin mastitis test
 scores were also positively associated with antibody-dependent
 neutrophil cytotoxicity. Cytochrome c reduction was negatively
 associated with mammary and total health costs. A positive
 relationship between clinical mastitis and discarded milk and
 IgG2 was observed, and IgG1 was associated with increased
 quarter California mastitis test scores and increased
 production. Thus, certain in vitro immune function assays may
 serve as indicators of susceptibility to health problems in
 dairy cattle, particularly for traits associated with udder
 health.
 
 
 273                                   NAL Call. No.: 410.9 P94
 A reproducible method for producing and quantifying the stages
 of fracture repair.
 Bourque, W.T.; Gross, M.; Hall, B.K.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1992 Aug. Laboratory animal science v. 42 (4): p.
 369-374; 1992 Aug.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Bone fractures; Healing
 
 Abstract:  Male CD-1 mice, 4 to 6 months of age, were used to
 establish a reproducible model to study the stages of fracture
 repair. A custom-designed fracture apparatus was constructed,
 and trials with it demonstrated its capacity to reliably
 reproduce a closed fracture of the tibia. Dietary and sleep
 habits in the treated mice were the same as unfractured
 control mice. Four stages of fracture repair were documented
 and the duration of each stage was quantifiable and
 reproducible. The last stage of fracture repair was completed
 by 21 days postfracture. The reproducibility of the fracture,
 the reproducibility of the times and stages of fracture
 repair, the relatively short time to complete the fracture
 repair process, and the minimal discomfort which allowed the
 mice to maintain a normal daily routine, suggest that this is
 an ideal animal model for studying the fracture repair
 process.
 
 
 274                                   NAL Call. No.: Z6658.R47
 Research utilization of miniature swine.
 Wilmington, Mass.? : Charles River, [between 1988-1990?];
 1988-1990. 83 p. ; 28 cm.  Cover title.
 
 Language:  English
 
 Descriptors: Diseases; Animal models; Bibliography; Swine as
 laboratory animals; Bibliography; Swine; Physiology;
 Bibliography
 
 
 275                                     NAL Call. No.: QR1.I57
 Restricted ability of group B streptococcal C5a-ase to
 inactivate C5a prepared from different animal species.
 Bohnsack, J.F.; Chang, J.K.; Hill, H.R.
 Washington, D.C. : American Society for Microbiology; 1993
 Apr. Infection and immunity v. 61 (4): p. 1421-1426; 1993 Apr. 
 Includes references.
 
 Language:  English
 
 Descriptors: Streptococcus; Attractants; Inactivation; Strain
 differences
 
 Abstract:  Most strains of group B streptococci (GBS)
 elaborate a cell surface-associated enzyme that rapidly
 inactivates the human complement-derived chemoattractants C5a
 and C5a(desarg) by cleaving the His-Lys bond at positions 67
 and 68 in the C5a molecule. We have suggested that rapid
 inactivation of C5a and C5a(desarg) by this enzyme, called
 C5a-ase, can hinder the inflammatory response at sites of GBS
 infection. We tested the ability of GBS C5a-ase to inactivate
 C5a preparations from various animal species to determine the
 proper species for studying the role of GBS C5a-ase in the
 pathogenesis of GBS infections. Exposure of C5a preparations
 from humans, monkeys, and cows to GBS caused inhibition of C5a
 functional activity as measured by the ability of C5a to
 stimulate human polymorphonuclear leukocyte (PMN) adherence
 and human PMN chemotaxis. Bovine PMN chemotaxis to bovine C5a
 was also abolished after exposure of bovine C5a to GBS. In
 contrast, mouse, rat, guinea pig, rabbit, pig, and sheep C5a
 preparations retained full functional activity after exposure
 to GBS as measured by chemotaxis of human PMNs, PMNs from the
 same animal species, or both. These data suggest that there
 are structural differences between C5a proteins from different
 species which alter their susceptibility to GBS C5a-ase and
 indicate that most commonly used animal models of human GBS
 infection are inadequate for detection of a contribution of
 GBS C5a-ase to GBS virulence.
 
 
 276                                  NAL Call. No.: RA421.P684
 Retinoids or carotenoids: is there another choice?.
 Greenberg, E.R.
 Orlando, Fla. : Academic Press; 1993 Sep.
 Preventive medicine v. 22 (5): p. 723-727; 1993 Sep.  Paper
 presented at the Fourth International Conference on Prevention
 of Human Cancer: Nutrition and Chemoprevention Controversies,
 June 3-6, 1992, Tucson, Arizona.  Includes references.
 
 Language:  English
 
 Descriptors: Retinoids; Carotenoids; Carcinoma; Disease
 prevention; Toxicity; Epidemiological surveys; Diet; Clinical
 trials; Antioxidants; Vitamin supplements; Literature reviews
 
 Abstract:  Both retinoids and carotenoids decrease cancer
 occurrence in selected animal models of carcinogenesis, but
 the retinoids appear to have more potent activity against a
 wider variety of tumors. Future use of retinoids for cancer
 prevention will be limited, however, because of their toxic
 effects on bone and skin (among other organs). In contrast to
 retinoids, carotenoids seem to be free of important toxicity
 and this fact makes them more promising for use in the general
 adult population. However, the idea that carotenoids have a
 cancer-preventive effect in humans is based almost entirely on
 epidemiological studies of diet and serum which could simply
 reflect the effects of some other dietary constituents. In the
 search to explain the profoundly lower risk of death
 associated with eating a diet high in fruits, vegetables, and
 grains, there is a place for clinical trials testing one
 specific nutrient, such as beta-carotene, against one disease,
 such as lung cancer, but we should not rely exclusively on
 these narrowly focused studies. In addition, careful analyses
 of cohort studies may reveal broad patterns of diet that are
 associated with lower mortality. These diets can then be
 tested in clinical trials for their efficacy against a variety
 of causes of death and disability. For now, the most rational
 and prudent choice would be to consume a diet high in fruits,
 vegetables, and grains and not to take either supplemental
 antioxidants or retinoids until there is clear evidence of
 their effectiveness and safety.
 
 
 277                              NAL Call. No.: RC628.N48 1987
 Reversible impairment of glucose-induced insulin secretion in
 SHR/N-cp rats. Voyles, N.R.; Powell, A.M.; Timmers, K.I.;
 Wilkins, S.D.; Bhathena, S.J.; Hansen, C.; Michaelis, O.E. IV;
 Recant, L.
 Bethesda, Md. : National Institutes of Health; 1988.
 New models of genetically obese rats for studies in diabetes,
 heart disease, and complications of obesity : NIH workshop,
 June 18-19, 1987, summaries of workshop papers and current
 bibliography. p. 33-44; 1988.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Obesity; Diabetes; Rats
 
 
 278                                  NAL Call. No.: 389.8 AM34
 Review of clinical studies on cholesterol-lowering response to
 soy protein. Carroll, K.K.
 Chicago, Ill. : The Association; 1991 Jul.
 Journal of the American Dietetic Association v. 91 (7): p.
 820-827; 1991 Jul. Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Soy protein; Hypercholesterolemia;
 Triacylglycerols; Low density lipoprotein; Animal experiments;
 Man; Literature reviews; Cholesterol; Blood serum; Blood
 plasma; Dietary protein
 
 Abstract:  Experiments on animals have shown that soybean
 protein has hypocholesterolemic and antiatherogenic
 properties. In human beings, substitution of soy protein for
 dietary animal protein or addition of soy protein to the diet
 lowers total and low-density-lipoprotein cholesterol levels in
 individuals with hypercholesterolemia. Reductions of 20% or
 more have been obtained with diets high in protein (about 20%
 of total energy) and relatively low in fat. Triglycerides are
 also decreased, particularly in subjects with
 hypertriglyceridemia, but soy-protein diets appear to have
 little effect on high-density-lipoprotein cholesterol levels.
 Responses are similar in men and women, but may be greater in
 younger than in older subjects. The hypocholesterolemic effect
 is thought to be mainly attributable to the protein itself
 rather than to nonprotein components of soy-protein
 preparations. The mechanism of action is not known, and it may
 not be possible to explain the observed effects in human
 beings and in experimental animal models by the same
 mechanism. Although the hypocholesterolemic response to
 dietary soy protein has been observed by a number of European
 research groups, substitution of soy protein for animal
 protein in North American diets has generally had little
 effect, for reasons that are still not clear.
 
 
 279                                   NAL Call. No.: 389.8 J82
 A review of experimental studies of iodine deficiency during
 fetal development.
 Hetzel, B.S.; Mano, M.T.
 Bethesda, Md. : American Institute of Nutrition; 1989 Feb. The
 Journal of nutrition v. 119 (2): p. 145-151; 1989 Feb. 
 Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Maternal nutrition; Mineral deficiencies; Iodine;
 Hypothyroidism; Goiter; Cretinism; Fetus
 
 Abstract:  Iodine deficiency is now recognized as a major
 international public health problem. It is estimated that 800
 million people may be at risk of the effects of iodine
 deficiency. In humans, the effects occur at all stages of
 development: the fetus, the neonate, the child and adult. The
 effects are now denoted by the term iodine deficiency
 disorders (IDD). They include miscarriages, stillbirths,
 congenital anomalies, as well as the more familiar goiter,
 cretinism, impaired brain function, and hypothyroidism in
 children and adults. In domestic animals, reproductive failure
 has been reported with the production of aborted, stillborn
 and weak calves. Experimental studies in animal models have
 been reviewed to provide evidence of the mechanisms involved,
 particularly in relation to brain development. The findings in
 three different species (rat, sheep, monkey) indicate that the
 effects are mediated by a combination of maternal and fetal
 hypothyroidism, the effect of maternal hypothyroidism being
 earlier than the onset of fetal thyroid secretion. The
 findings suggest that iodine deficiency has an early effect on
 neuroblast multiplication and, if so, this could be important
 in the pathogenesis of the neurological form of endemic
 cretinism. The assessment of the full effects of iodine
 deficiency on the brain requires further studies in the
 postnatal period to determine the duration of these effects.
 
 
 280                                   NAL Call. No.: 410.9 P94
 The role of Branhamella catarrhalis in the "bloody-nose
 syndrome" of cynomolgus macaques.
 VandeWoude, S.J.; Luzarraga, M.B.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1991 Oct. Laboratory animal science v. 41 (5): p.
 401-406; 1991 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Macaca fascicularis; Branhamella; Respiratory
 diseases; Nose; Hemorrhage; Pathogens
 
 Abstract:  During a 15-month period, 25 cynomolgus macaques
 (Macaca fascicularis) at the Johns Hopkins University were
 observed to have nasal discharge. Fifteen (60%) of these
 animals had positive nasal cultures for Branhamella
 catarrhalis. Clinical signs associated with infection by this
 bacterium were sneezing, epistaxis, and mucohemorrhagic nasal
 discharge. Treatment with antibiotics resulted in prompt
 resolution of clinical signs. Post-therapeutic nasal cultures
 were negative for B. catarrhalis. Two groups of clinically
 normal, culture-negative, cynomolgus macaques were inoculated
 with natural isolates of B. catarrhalis which had been
 passaged in culture for various amounts of time. Five of the
 eight animals inoculated became culture-positive and had mild
 nasal discharge. Presence of blood on nasal swabs was
 indicative of infection with B. catarrhalis. Three of the
 inoculated animals had post-swabbing epistaxis. This report
 documents the role of B. catarrhalis as an upper respiratory
 pathogen in the cynomolgus monkey which causes mild self-
 limiting disease reminiscent of the so-called "Bloody-Nose
 Syndrome." In addition to the obvious clinical significance of
 this finding to primate clinicians, development of an animal
 model for human disease caused by this organism may be
 possible.
 
 
 281                                 NAL Call. No.: QP141.A1N88
 Role of omega-3 fatty acids in health and disease.
 Fernandes, G.; Venkatraman, J.T.
 Tarrytown, N.Y. : Pergamon Press; 1993.
 Nutrition research v. 13 (suppl.1): p. S19-S45; 1993.  Paper
 presented at the 5th International Meeting on Advances in
 Infantile Nutrition, November 12-14, 1992, Naples, Italy. 
 Includes references.
 
 Language:  English
 
 Descriptors: Polyenoic fatty acids; Dietary fat; Diet; Fish
 oils; Fat consumption; Trends; Monoenoic fatty acids;
 Nutrition physiology; Infant development; Elderly; Fat
 deficiencies; Cardiovascular diseases; Carcinoma; Autoimmune
 diseases; Immune response; Rheumatoid arthritis; Nutritional
 intervention; Supplements; Enteral feeding; Parenteral
 feeding; Drug toxicity; Literature reviews
 
 Abstract:  Dietary lipid interventions have an important role
 in modulating the onset of autoimmunity, cardiovascular
 diseases and cancer. Many studies carried out in the past have
 established the adverse effects of saturated fats in humans
 and in animal models. Based on these adverse effects, the
 consumption of vegetable oils containing both monounsaturated
 omega-9 and polyunsaturated fatty acids (rich in 18:2 omega-6)
 is rising significantly in the United States. The increased
 consumption of many vegetable oils particularly of omega-6
 series is however to be viewed as pro-inflammatory and is
 suspected as one of the possible causes for the gradual rise
 in certain malignant tumors, rheumatoid arthritis and
 autoimmune diseases primarily due to the increased production
 of pro-inflammatory cytokines although its increased usage has
 reduced cardiovascular disease nearly 30% in the United
 States. Diets based on omega-6 enriched oils can increase the
 level of linoleic acid in tissue phosphoglycerides and are
 able to reduce cholesterol levels, yet these lipids usually
 tend to elevate excessive arachidonic acid (20:4 omega-6)
 levels. In contrast, omega-3 fatty acid-enriched fish oil (FO)
 and/or omega-3 precursors from certain vegetable oils
 (linolenic acid, 18:3 omega-3) are found to provide protection
 against cardiovascular disease, rheumatoid arthritis, cancer
 and possibly against the severity of viral infections.
 Nutritional modification of cellular functions by dietary
 lipids with a balanced ratio of omega-6 and omega-3 fatty
 acids offers an attractive avenue to correct, modify and/or
 prevent many patho-physiological processes in health and
 disease state and to reduce toxicity of drugs in many
 patients. The mediation of such effects is thought to be
 primarily achieved through alterations of cellular membranes
 composition and other endogenous lipid stores which may modify
 the functional activity of various receptors on plasma
 membranes. In summary, the protective effects of omega-3
 lipids have been explained based on changes in eicosanoid
 synthesis and the reduced risk of sudden death from cardiac
 arrthyhmia, increased protection from ischemic myocardium,
 improved myocardial function and reduction of other
 cardiovascular and autoimmune disease risks. However, well-
 designed studies are still required to further define
 vegetable sources, both as a supplement to infant nutrition
 specifically for optimizing the development of cognitive
 function, and also as preventive measure for reducing the
 incidence of diseases of aging in rapidly growing elderly
 populations.
 
 
 282                                   NAL Call. No.: 389.8 J82
 The role of the cytokines, interferon alpha and tumor necrosis
 factor in the hypertriglyceridemia and wasting of AIDS.
 Grunfeld, C.; Feingold, K.R.
 Bethesda, Md. : American Institute of Nutrition; 1992 Mar. The
 Journal of nutrition v. 122 (3S): p. 749-753; 1992 Mar. 
 Proceedings of a symposium on "Nutrition, Immunomodulation and
 AIDS" held at the American Institute of Nutrition Annual
 Meeting, April 21-25, Atlanta, GA.  Literature review. 
 Includes references.
 
 Language:  English
 
 Descriptors: Acquired immune deficiency syndrome;
 Hypertriglyceridemia; Infections; Cachexia; Lipid metabolism;
 Immunological factors; Blood lipids; Interferon; Interleukins;
 Literature reviews
 
 Abstract:  The hypertriglyceridemia of infection is mediated
 by many of the cytokines that regulate the immune response,
 including the tumor necrosis factors, the interleukins and the
 interferons. In the acquired immunodeficiency syndrome (AIDS),
 hypertriglyceridemia is most likely due to increased
 circulating levels of interferon alpha. Both in AIDS and in
 animal models there is no direct association between the
 presence of hypertriglyceridemia and the syndrome of wasting.
 Rather, circulating lipoproteins may neutralize infectious
 organisms and therefore contribute to host defense.
 
 
 283                                 NAL Call. No.: QD415.A1B52
 Saturated fatty acid, but not cholesterol, regulates
 apolipoprotein AI gene expression by posttranscriptional
 mechanism.
 Srivastava, R.A.K.
 Marrickville, N.S.W., Australia : Academic Press; 1994 Sep.
 Biochemistry and molecular biology international v. 34 (2): p.
 393-402; 1994 Sep.  Includes references.
 
 Language:  English
 
 Descriptors: Dietary fat; Cholesterol; Saturated fats;
 Apolipoproteins; Gene expression; Genetic regulation; High
 density lipoprotein
 
 Abstract:  The aim of the present study was to investigate the
 regulation of the apoAI gene by dietary saturated fat and
 cholesterol Saturated fatty acids and cholesterol raise low
 density- and high density lipoprotein particles in humans
 Increased LDL is attributed to the down-regulation of LDL-
 receptor gene, but the mechanism of increased plasma HDL
 levels is unknown To study the mechanism of HDL elevation by
 saturated fat, male rats and male mice were employed as animal
 models. since they also raise their plasma HDL levels when fed
 high lipid diets Animals were divided in four groups and fed
 the following diets: control (5% corn oil); high cholesterol
 (05%): high fat (20% coconut oil). and high fat plus
 cholesterol diets The high cholesterol diet did not alter
 plasma and HDL-cholesterol levels However, the high fat diet
 increased HDL levels by 20% in rats and 55% in mice. A
 combination of saturated fat and cholesterol diet raised
 plasma HDL levels by 36 and 67% in rats and mice respectively.
 Plasma apoAI levels increased parallel to HDL concentrations.
 Mechanism of HDL elevation by saturated fat was investigated
 Hepatic and intestinal apoAI mRNA did not change with any of
 the test diets in mice. Rat hepatic apoAI mRNA was also
 unchanged by the high cholesterol diet, but was decreased on
 high fat and fat-cholesterol combination diets These results
 suggest that transcriptional regulation of the apoAI gene was
 not responsible for increased plasma apoAI and HDL The
 translational efficiency of apoAI on isolated polysomes was
 also measured, and it was found that apoAI synthesis increased
 about 20% on high fat and fat-cholesterol combination diets
 This partially explains the elevated levels of plasma HDL.
 Additional regulation through impaired catabolism of HDL
 particles by high fat diet feeding may be another pathway for
 increased HDL levels Unlike apoAI mRNA, the mRNA of other HDL
 apoproteins, apoAII and apoAIV, were increased by high fat and
 combination diet feeding These results suggest that saturated
 fatty acids regulate plasma HDL levels by translational and
 posttranslational mechanisms.
 
 
 284                                   NAL Call. No.: QH527.J68
 Seasonal affective disorders: animal models non fingo.
 Zucker, I.
 New York, N.Y. : Guilford Publications; 1988.
 Journal of biological rhythms v. 3 (2): p. 209-223. ill; 1988. 
 Includes references.
 
 Language:  English
 
 Descriptors: Laboratory animals; Animal behavior; Seasonal
 behavior; Research
 
 
 285                                   NAL Call. No.: 442.9 SO1
 Selenium and sulfur in antioxidant protective systems:
 relationships with vitamin E and malaria.
 Levander, O.A.
 Baltimore, Md. : Williams & Wilkins; 1992 Jun.
 Proceedings of the Society for Experimental Biology and
 Medicine v. 200 (2): p. 255-259; 1992 Jun.  Proceedings of a
 "Conference on Molecular and Comparative Nutrition," July
 22-24, 1991, National Institutes of Health, Bethesda,
 Maryland.  Includes references.
 
 Language:  English
 
 Descriptors: Selenium; Sulfur; Vitamin e; Antioxidants;
 Glutathione peroxidase; Hydrolases; Proteins; Fish oils;
 Qinghaosu; Nutrient deficiencies; Malaria; Mice; Animal models
 
 Abstract:  The metabolic relationships among the antioxidant
 nutrients selenium, sulfur, and vitamin E are particularly
 close. Selenium and vitamin E have long been known to spare
 one another in certain nutritional diseases of animals, and
 selenium has been considered to have a key antioxidant defense
 function as a component of glutathione peroxidase. However,
 the antioxidant role of glutathione peroxidase has been
 questioned and now proteins containing selenium have been
 identified: phospholipid hydroperoxide glutathione peroxidase,
 selenoprotein P, and iodothyronine deiodinase. Glutathione
 peroxidase activity independent of selenium resides in the
 glutathione S-transferases. Glutathione participates in both
 enzymatic and nonenzymatic antioxidant defense systems. Some
 low-molecular weight selenium compounds (e.g., ebselen)
 exhibit glutathione peroxidase-like action. Certain low
 molecular weight thiols decompose peroxides nonenzymatically
 (e.g., the ovothiols). Murine malaria appears to be a useful
 experimental model for investigating interrelationships of
 selenium and vitamin E. Vitamin E deficiency protects against
 the parasite, especially when the mice are concurrently fed
 peroxidizable fat such as fish or linseed oils. Selenium
 deficiency, on the other hand, has little or no protective
 effect against the parasite. Any practical utility of pro-
 oxidant diets in combating human malaria remains to be
 determined.
 
 
 286                                   NAL Call. No.: 389.8 J82
 Serum lipoprotein profiles in mice: effects of early over- and
 undernutrition. Aubert, R.; Camus, M.C.; Bourgeois, F.;
 Herzog, J.; Lemonnier, D. Bethesda, Md. : American Institute
 of Nutrition; 1988 Oct. The Journal of nutrition v. 118 (10):
 p. 1190-1196; 1988 Oct.  Includes references.
 
 Language:  English
 
 Descriptors: Overfeeding; Undernutrition; Litter size; Blood
 serum; Lipoproteins; Neonates; Mice
 
 Abstract:  Effects of early over- and undernutrition on
 lipoprotein profiles of adult Swiss male mice reared in
 litters of different sizes were investigated. Lipoproteins
 were isolated by density gradient ultracentrifugation and
 defined by chemical composition. Protein moieties were defined
 by their charges. The lipoprotein lipase (LPL) activity in
 epididymal adipose tissue, heart and diaphragm was measured.
 Early feeding patterns induced permanent body weight
 differences in adult mice. Serum phospholipid content was
 significantly higher in obese than in control mice.
 Overfeeding led to significantly higher activity of LPL in
 adipose tissue; inversely, undernutrition induced a lower LPL
 activity. There was a trend toward variations of lipoprotein
 concentrations in relation to litter size, with significant
 differences being observed only between obese and
 undernourished mice for LDL-HDL1 (low density lipoprotein-high
 density lipoprotein) and HDL1 concentrations. Compared with
 normally fed mice the most notable alterations in plasma
 lipoprotein composition were, in LDL-HDL2, greater cholesteryl
 ester in obese and less phospholipid in undernourished mice.
 In contrast, tetramethyl-urea-soluble apolipoprotein
 distribution was unaffected by litter size. Although moderate
 differences were observed in lipoprotein compositions and
 levels in over- or undernourished mice, further investigations
 of lipoprotein metabolism and metabolic abnormalities in this
 animal model are required.
 
 
 287                                  NAL Call. No.: QL55.A1I43
 SHHE/Mcc-cp rat: model of obesity, non-insulin-dependent
 diabetes, and congestive heart failure.
 McCune, S.A.; Baker, P.B.; Stills, H.F. Jr
 Washington, D.C. : Institute of Laboratory Animal Resources,
 National Research Council; 1990.
 I.L.A.R. news v. 32 (3): p. 23-27; 1990.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Obesity; Diabetes mellitus; Animal models;
 Heart diseases; Complications
 
 
 288                                 NAL Call. No.: Z7996.P85J6
 Simian & human retroviruses in nonhuman primates infection,
 disease & animal model studies : a bibliography, 1988-1989
 annual update..  Simian and human retroviruses in nonhuman
 primates
 Johnson-Delaney, Cathy A.
 University of Washington, Primate Information Center
 Seattle, Wash. : Primate Information Center, Regional Primate
 Research Center, University of Washington,; 1989.
 26 p. ; 28 cm.  Cover title.  September 1989.  Supported in
 part by Grant No. RR-00166 from the National Institutes of
 Health.  Includes index.
 
 Language:  English
 
 Descriptors: Primates; AIDS (Disease)
 
 
 289                                     NAL Call. No.: QR1.I57
 Site-directed mutagenesis of the alpha-toxin gene of
 Staphylococcus aureus: role of histidines in toxin activity in
 vitro and in a murine model. Menzies, B.E.; Kernodle, D.S.
 Washington, D.C., American Society for Microbiology; 1994 May.
 Infection and immunity v. 62 (5): p. 1843-1847; 1994 May. 
 Paper presented at the "33rd Interscience Conference on
 Antimicrobial Agents and Chemotherapy," Oct. 17-20, 1993, New
 Orleans, LA.  Includes references.
 
 Language:  English
 
 Descriptors: Staphylococcus aureus; Histidine; Toxins;
 Mutagenesis; Hemolysis; In vitro; Toxicity; Animal models;
 Mice
 
 Abstract:  Staphylococcus aureus alpha-toxin is a membrane-
 damaging exoprotein that oligomerizes to form transmembrane
 pores. Chemical modification of histidines with
 diethylpyrocarbonate has been shown to reduce the hemolytic
 activity of alpha-toxin, suggesting that one or more of the
 histidine residues is important for toxin function. To
 individually assess the functional importance of each of the
 four histidine (residues residues 35, 48, 144, and 259), we
 used oligonucleotide-directed mutagenesis of the cloned alpha-
 toxin gene to replace each histidine with leucine. The mutant
 toxins were expressed in S. aureus and evaluated for hemolytic
 activity in vitro and for lethality in an intraperitoneal
 murine model. Substitution of histidine 35 with leucine
 produced a mutant toxin (H35L) without hemolytic or lethal
 activity. Mutant toxins H48L, H144L, and H259L exhibited 7,
 16, and 46%, respectively, of the hemolytic activity of wild-
 type toxin. Immunoblotting of purified H35L toxin incubated
 with liposomal membranes demonstrated intact membrane binding
 and hexamer formation that was clearly detectable but reduced
 compared with that of the wild-type toxin. This suggests that
 hexamer formation alone is not sufficient for the expression
 of alpha-toxin activity. The nature of the defect underlying
 the lack of activity of the H35L mutant toxin remains to be
 elucidated but may involve failure of the hexamer to span the
 lipid bilayer to form a transmembrane pore or a change in the
 internal surface and permeability characteristics of the pore.
 
 
 290                                    NAL Call. No.: QL698.C7
 The Smyth chicken: a model for autoimmune amelanosis.
 Smyth, J.R. Jr
 Boca Raton, Fla. : CRC Press; 1989.
 Critical reviews in poultry biology v. 2 (1): p. 1-19; 1989. 
 Literature review.  Includes references.
 
 Language:  English
 
 Descriptors: Fowls; Mutations; Polygenic inheritance; Animal
 models; Melanins; Autoimmune diseases; Autoantibodies;
 Literature reviews
 
 
 291                                  NAL Call. No.: RC262.C5N8
 Soy intake and cancer risk: a review of the in vitro and in
 vivo data. Messina, M.J.; Persky, V.; Setchell, K.D.R.;
 Barnes, S.
 Hillsdale, N.J. : Lawrence Erlbaum Associates, Inc; 1994.
 Nutrition and cancer v. 21 (2): p. 113-131; 1994.  Includes
 references.
 
 Language:  English
 
 Descriptors: Soybean products; Carcinoma; Risk; Genistein;
 Estrogenic properties; Transduction; Research; Literature
 reviews
 
 Abstract:  International variations in cancer rates have been
 attributed, at least in part, to differences in dietary
 intake. Recently, it has been suggested that consumption of
 soyfoods may contribute to the relatively low rates of breast,
 colon, and prostate cancers in countries such as China and
 Japan. Soybeans contain a number of anticarcinogens, and a
 recent National Cancer Institute workshop recommended that the
 role of soyfoods in cancer prevention be investigated. In this
 review, the hypothesis that soy intake reduces cancer risk is
 considered by examining relevant in vitro, animal, and
 epidemiological data. Soybeans are a unique dietary source of
 the isoflavone genistein, which possesses weak estrogenic
 activity and has been shown to act in animal models as an
 antiestrogen. Genistein is also a specific inhibitor of
 protein tyrosine kinases; it also inhibits DNA topoisomerases
 and other critical enzymes involved in signal transduction. In
 vitro, genistein suppresses the growth of a wide range of
 cancer cells, with IC50 values ranging from 5 to 40 micromolar
 (1-10 micrograms/ml). Of the 26 animal studies of experimental
 carcinogenesis in which diets containing soy or soybean
 isoflavones were employed, 17 (65%) reported protective
 effects. No studies reported soy intake increased tumor
 development. The epidemiological data are also inconsistent,
 although consumption of nonfermented soy products, such as
 soymilk and tofu, tended to be either protective or not
 associated with cancer risk; however, no consistent pattern
 was evident with the fermented soy products, such as miso.
 Protective effects were observed for both hormone- and
 nonhormone-related cancers. While a definitive statement that
 soy reduces cancer risk cannot be made at this time, there is
 sufficient evidence of a protective effect to warrant
 continued investigation.
 
 
 292                                   NAL Call. No.: 410.9 P94
 Spinal dracunculiasis in an experimentally infected ferret.
 Broderson, J.R.; Eberhard, M.L.; Welch, B.G.; Bandt, F.H.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1991 Apr. Laboratory animal science v. 41 (2): p.
 180-182; 1991 Apr.  Includes references.
 
 Language:  English
 
 Descriptors: Ferrets; Dracunculus insignis; Disease models;
 Animal models; Morphology; Paralysis; Experimental infections;
 Spinal cord; Parasite migration
 
 
 293                                   NAL Call. No.: 410.9 P94
 Spontaneous and experimental infections in scid and scid/beige
 mice. Percy, D.H.; Barta, J.R.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1993 Apr. Laboratory animal science v. 43 (2): p.
 127-132; 1993 Apr.  Paper presented at a conference entitled
 "The Scid Mouse in Biomedical and Agricultural Research,"
 August 5-7, 1992, Guelph, Canada.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Mutants; Infections
 
 Abstract:  Severe combined immunodeficient (scid) mice are
 valuable animals to study a variety of logic and disease
 processes. Their capacity to support multiple tissue
 xenografts permits these mice to be used as intermediate
 models for host-specific, fastidious organisms for which a
 small animal model has not been available previously. However,
 because they are unable to mount a normal immune response,
 they are very susceptible to a variety of primary and
 opportunistic microbial pathogens. Fatal, naturally occurring
 infections with bacteria such as Proteus mirabilis,
 Streptococcus viridans, and Escherichia coli have been
 observed. In addition, based on observations after
 experimental or naturally occurring viral infections, scid and
 scid/beige mice have been shown to be very susceptible to
 infections with viruses such as mouse hepatitis virus, Sendai
 virus, and murine respiratory virus, with resulting mortality.
 Of the parasitic infections, Pneumocystis carinii is a
 relatively common contaminant of the respiratory tracts of
 scid mice and may complicate research projects, particularly
 experimental respiratory tract infections. In view of the
 enhanced susceptibility of these mice to infections of this
 type, it is essential that they be housed under optimal
 conditions, which include implementing stringent management
 practices and a functional barrier system.
 
 
 294                                   NAL Call. No.: QH573.N37
 Spontaneous hypercholesterolemia in pigs.
 Attie, A.D.; Aiello, R.J.; Cooper, S.T.; Uelmen, P.J.
 Berlin ; New York : Springer-Verlag : c1986-; 1993.
 NATO ASI series. Series H, Cell biology v. 73: p. 107-112;
 1993.  In the series analytic: Human apolipoprotein mutants.
 III. Diagnosis and treatment / edited by C.R. Sirtori, G.
 Franceschini and B.H. Brewer Jr.  Proceedings of a NATO
 Advanced Research Workshop held April 5-8, 1992, Limone sul
 Garda, Italy.  Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Hypercholesterolemia; Haplotypes; Alleles;
 Apolipoproteins; Low density lipoprotein; Receptors; Binding;
 Animal models
 
 
 295                                  NAL Call. No.: QL55.A1I43
 The spontaneously hypercholesterolemic pig as an animal model
 for human atherosclerosis.
 Attie, A.D.; Prescott, M.F.
 Washington, D.C. : Institute of Laboratory Animal Resources,
 National Research Council; 1988.
 I.L.A.R. news v. 30 (4): p. 5-12. ill; 1988.  Includes
 references.
 
 Language:  English
 
 Descriptors: Pigs; Disease models; Hypercholesterolemia;
 Atherosclerosis; Lipids; Cholesterol; Lipoproteins;
 Histopathology
 
 
 296                                  NAL Call. No.: 389.1 W892
 Studies of dietary supplementation with omega 3 fatty acids in
 patients with rheumatoid arthritis.
 Kremer, J.M.; Robinson, D.R.
 Basel : S. Karger; 1991.
 World review of nutrition and dietetics v. 66: p. 367-382;
 1991.  In the series analytic: Health effects of omega-3
 polyunsaturated fatty acids in seafoods / edited by A.
 Simopoulos, R. Kifer, R. Martin and S. Barlow. Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Rheumatoid arthritis; Eicosapentaenoic acid;
 Docosenoic acids; Fish oils; Supplements; Immune response;
 Pain; Assessment; Inflammation; Leukotrienes; Platelets;
 Interleukins; Mitogens; Eicosanoids; Literature reviews
 
 Abstract:  The purpose of this review is to summarize briefly
 the investigations employing omega-3 supplements in the animal
 model and then more thoroughly discuss subsequent clinical
 investigations in patients with rheumatoid arthritis. Data on
 the effects of omega-3 supplements on inflammatory and immune
 parameters is also summarized.
 
 
 297                                   NAL Call. No.: 448.8 P21
 Studies on a murine model of congenital toxoplasmosis:
 vertical disease transmission only occurs in BALB/c mice
 infected for the first time during pregnancy.
 Roberts, C.W.; Alexander, J.
 New York, N.Y. : Cambridge University Press; 1992 Feb.
 Parasitology v. 104 (pt.1): p. 19-23; 1992 Feb.  Includes
 references.
 
 Language:  English
 
 Descriptors: Toxoplasma gondii; Toxoplasmosis; Vertical
 transmission; Congenital infection; Animal models; Mice;
 Chronic infections; Pregnancy
 
 
 298                                  NAL Call. No.: QR360.A1J6
 Studies on glycoprotein 13 (gp13) of equid herpesvirus 1 using
 affinity-purified gp13, glycoprotein-specific monoclonal
 antibodies and synthetic peptides in a hamster model.
 Stokes, A.; Corteyn, A.H.; Pullen, L.A.; Doel, T.R.; Meredith,
 D.M.; Killington, R.A.; Halliburton, I.W.; Whittaker, G.R.;
 Wheldon, L.A.; Nicolson, L.
 Reading : Society for General Microbiology; 1991 Apr.
 The Journal of general virology v. 72 (pt.4): p. 923-931; 1991
 Apr.  Includes references.
 
 Language:  English
 
 Descriptors: Horses; Equine herpesvirus; Glycoproteins;
 Monoclonal antibodies; Animal models; Hamsters
 
 Abstract:  Hamsters were immunized with either an affinity-
 purified preparation of equid herpesvirus 1 (EHV-1)
 glycoprotein 13 (gp13) or synthetic peptides representing
 three sequences within the homologous glycoprotein of EHV-4,
 resulting in the production of antipeptide (in the case of
 peptide-immunized animals) or antivirus antibodies. The sera
 from gp13-immunized hamsters contained antibodies which showed
 virus-neutralizing activity and complement-mediated antibody
 lysis of EHV-1-infected target cells. These hamsters were
 protected from EHV-1 challenge. The characteristics of a panel
 of anti-gp13 monoclonal antibodies (P28, P17, 14H7, 16E4 and
 16H9) were assessed both in vivo and in vitro. 16E4 and P28
 showed high levels of complement-mediated neutralization of
 virus, complement-mediated lysis of virus-infected target
 cells and passive protection of hamsters. Furthermore, epitope
 mapping studies demonstrated that this glycoprotein contains a
 neutralizing epitope recognized by EHV-1-immune horse serum.
 The data imply that gp13 has potential as a candidate antigen
 for a molecular vaccine.
 
 
 299                                   NAL Call. No.: 447.8 AM3
 Studies on mechanisms of hepatic insulin resistance in
 cafeteria-fed rats. Davidson, M.B.; Garvey, D.
 Bethesda, Md. : American Physiological Society; 1993 Jan.
 American journal of physiology v. 264 (1,pt.1): p. E18-E23;
 1993 Jan. Includes references.
 
 Language:  English
 
 Descriptors: Obesity; Diet; Insulin; Resistance; Fatty acids;
 Oxidation; Lipolysis; Hyperinsulinemia; Metabolic inhibitors;
 Liver; Rats
 
 Abstract:  Whether hyperinsulinemia causes insulin resistance
 or vice versa is controversial. The development of
 hyperinsulinemia and insulin resistance was tracked in the
 cafeteria-fed rat to determine which occurred first. After 3
 days of cafeteria feeding the rats were obese, manifested a
 small but significant decrease in fasting glucose levels, and
 showed no change in fasting insulin levels, basal hepatic
 glucose production (HGP), insulin binding to hepatic
 membranes, and glucose utilization during a euglycemic
 hyperinsulinemic clamp, but the rats did demonstrate an
 increased glucose disappearance rate associated with an
 enhanced insulin response to intra-arterial glucose and
 hepatic insulin resistance during the clamp. After 7 days of
 cafeteria feeding, the results were similar except that
 fasting hyperglycemia and hyperinsulinemia, an enhanced basal
 HGP, and decreased insulin binding developed. After 6 wk of
 cafeteria feeding, both hepatic and peripheral insulin
 resistances were present. After 7 days of cafeteria feeding in
 rats given streptozotocin or etomoxir, an inhibitor of free
 fatty acid (FFA) oxidation, hepatic insulin resistance
 persisted despite elimination of hyperinsulinemia and
 reduction of FFA oxidation. These data do not support a causal
 role for either hyperinsulinemia or enhanced lipolysis of
 hypertrophied fat stores and subsequent FFA oxidation in the
 liver in the development of hepatic insulin resistance in this
 animal model of obesity.
 
 
 300                                   NAL Call. No.: 410.9 P94
 Subcutaneous abscess due to Salmonella adelaide in a grey
 collie with cyclic hematopoiesis.
 Moazed, T.C.; Deeb, B.J.; DiGiacomo, R.F.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1990 Nov. Laboratory animal science v. 40 (6): p.
 639-641; 1990 Nov.  Includes references.
 
 Language:  English
 
 Descriptors: Dogs; Salmonella; Abscesses; Hematopoiesis;
 Animal models; Case reports; Salmonellosis; Stress
 
 
 301                                 NAL Call. No.: QP141.A1N88
 Suppression of experimental allergic encephalomyelitis after
 dietary zinc deprivation in guinea pigs.
 Scelsi, R.; Franciotta, D.M.; Camana, C.; Savoldi, F.;
 Allegrini, M. Elmsford, N.Y. : Pergamon Press; 1989 Dec.
 Nutrition research v. 9 (12): p. 1345-1354; 1989 Dec. 
 Includes references.
 
 Language:  English
 
 Descriptors: Diet; Mineral deficiencies; Zinc; Immunology;
 Encephalitis; Guinea pigs
 
 Abstract:  The effects of different levels of zinc (Zn) in the
 diet were tested in the animal model of acute experimental
 allergic encephalomyelitis (EAE), which is considered a
 prototype for cell-mediated autoimmune disease of the central
 nervous system (CNS). Acute EAE was induced in guinea pigs
 maintained with normal, high and low levels of Zn in the diet.
 The animals fed normal and Zn-supplemented diets showed the
 same survival rates; the incidence and severity of the disease
 was similar for both groups. Zn-deficient animals exhibited
 the expected symptoms of Zn deficiency and after sensitization
 did not develop neurological signs of EAE; some of them
 presented only focal inflammatory alteration in CNS.
 
 
 302                                    NAL Call. No.: 41.8 J82
 Susceptibility of Balb/c, C57/B6 and C57/B10 mice to infection
 with Mycobacterium paratuberculosis.
 Chiodini, R.J.; Buergelt, C.D.
 London : Academic Press; 1993 Nov.
 Journal of comparative pathology v. 109 (4): p. 309-319; 1993
 Nov.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Mycobacterium paratuberculosis; Animal
 models
 
 
 303                                  NAL Call. No.: QR360.A1J6
 Swine-reconstituted SCID mice as a model for African swine
 fever virus infection.
 Revilla, Y.; Pena, L.; Mampaso, F.; Vinuela, E.; Martinez-
 Alonso, C. Reading : Society for General Microbiology; 1994
 Aug.
 The Journal of general virology v. 75 (pt.8): p 1983-1988;
 1994 Aug.  Includes references.
 
 Language:  English
 
 Descriptors: African swine fever virus; Mice; Animal models;
 Infection; Blood; Lymph nodes; Spleen; Monoclonal antibodies
 
 Abstract:  Injection of swine peripheral blood mononuclear
 cells into mice with severe combined immunodeficiency (SCID),
 resulted in the stable long-term establishment of a functional
 swine immune system (SCID-sw). Swine immunoglobulins were
 present in the serum of SCID-sw mice and swine cells were
 detected in the blood as well as in lymph nodes and spleen
 using monoclonal antibodies raised against cell
 subpopulations. Swine lymphocytes from reconstituted SCID mice
 responded in vitro to specific antigens or mitogens. When
 SCID-sw mice were challenged with African swine fever (ASF)
 virus. ASF virus-infected cells were detected in blood and
 spleen, and antiviral antibodies and virus-specific T cells
 were generated.
 
 
 304                                   NAL Call. No.: QL55.A1L3
 Sympathetic auricular chondritis in rats: a model of auto-
 immune disease?. Meingassner, J.G.
 London : Royal Society of Medicine Services; 1991 Jan.
 Laboratory animals v. 25 (1): p. 68-78; 1991 Jan.  Includes
 references.
 
 Language:  English
 
 Descriptors: Rats; Autoimmune diseases; Markers; Ear diseases;
 Pathology
 
 Abstract:  Following the unilateral implantation of metal ear
 tags in female Crl:CD(SD)BR-rats, chronic inflammatory lesions
 were observed in both auricles in 70% and 24% of the animals
 after 30 and 60 weeks, respectively. Involvement of the
 collateral auricles was identified only after diffuse
 inflammation of the ear tag-marked pinnae had developed.
 Histological examination revealed a multifocal granulomatous
 chondritis, characterized by progressive destruction of the
 cartilaginous plate and excessive regeneration of
 cartilaginous tissue. IgG and complement deposits were present
 in the matrix of the marginal area of regenerating cartilage
 and at the destruction sites of autochthonous cartilage. It is
 likely that the pinally-restricted chondritis was due to an
 autoimmune response initiated by a chronic inflammatory
 process at the insertion site of the ear tag. Since the
 respone was not due to immunity to type II collagen, this
 pathologic phenomenon in rats may provide a useful animal
 model to study autoimmunity involving other cartilaginous
 matrix molecules.
 
 
 305                                    NAL Call. No.: 41.8 AM3
 Systemic and pulmonary reactions in swine with endotoxemia and
 gram-negative bacteremia.
 Olson, N.C.; Kruse-Elliott, K.T.; Dodam, J.R.
 Schaumburg, Ill. : The Association; 1992 Jun15.
 Journal of the American Veterinary Medical Association v. 200
 (12): p. 1870-1884; 1992 Jun15.  Includes references.
 
 Language:  English
 
 Descriptors: Pigs; Circulatory disorders; Endotoxins; Toxemia;
 Gram negative bacteria; Bacterial diseases; Literature
 reviews; Physiopathology; Animal models
 
 
 306                                   NAL Call. No.: QL55.A1L3
 Systemic histopathology of rats with CCl(4)-induced hepatic
 cirrhosis. Doi, K.; Kurabe, S.; Shimazu, N.; Inagaki, M.
 London : Royal Society of Medicine Services; 1991 Jan.
 Laboratory animals v. 25 (1): p. 21-25; 1991 Jan.  Includes
 references.
 
 Language:  English
 
 Descriptors: Rats; Carbon tetrachloride; Histopathology;
 Animal models; Disease models; Cirrhosis
 
 Abstract:  Systemic histopathological examinations were
 carried out on rats with CCl4-induced hepatic cirrhosis.
 Moderate congestion in the spleen, prominent oedema and focal
 acinar cell degeneration in the pancreas, marked haemorrhage
 and phagocytosis of haemosiderin by macrophages in the
 pancreaticoduodenal lymph node, appearance of monocytes
 bearing haemosiderin-like granules in the pulmonary arteries
 and cardiac right atrium, and focal segmental
 glomerulosclerosis were consistently observed in rats with
 hepatic cirrhosis. In addition, a marked increase in number of
 target cells and the appearance of a small number of monocytes
 bearing haemosiderin-like granules were also commonly found in
 the peripheral blood smears of these animals. These findings
 are considered to be important in the use of the CCl4-induced
 model of hepatic cirrhosis in the rat.
 
 
 307                                     NAL Call. No.: QR1.I57
 T-lymphocyte response in a guinea pig model of tuberculous
 pleuritis. Phalen, S.W.; McMurray, D.N.
 Washington, D.C. : American Society for Microbiology; 1993
 Jan. Infection and immunity v. 61 (1): p. 142-145; 1993 Jan. 
 Includes references.
 
 Language:  English
 
 Descriptors: Guinea pigs; Animal models; Tuberculosis
 
 Abstract:  The ability to induce tuberculous pleuritis in
 Mycobacterium bovis BCG-vaccinated guinea pigs was
 investigated as a model of human disease. A pleural effusion
 of 5 to 10 ml was obtained 6 to 7 days after the bilateral
 pleural injection of a suspension of heat-killed M.
 tuberculosis cells. Histological lesions were indicative of
 granulomatous pleuritis. Comparative studies of T lymphocytes
 obtained from pleural fluid and peripheral blood revealed
 increased antigen-driven lymphoproliferation and E rosette
 formation in pleural effusion lymphocytes. The CD2+ T-
 lymphocyte population appeared to be expanded or concentrated
 in pleural fluid, suggesting a compartmentalization of
 antigen-reactive T lymphocytes. These data demonstrate that
 experimental tuberculous pleuritis with effusion, closely
 resembling the human disease, can be produced in BCG-
 vaccinated guinea pigs.
 
 
 308                           NAL Call. No.: RC347.5.T69  1994
 Toxin-induced models of neurological disorders.
 Woodruff, Michael L.; Nonneman, Arthur J.
 New York : Plenum Press,; 1994.
 xxi, 344 p. : ill. ; 24 cm.  Includes bibliographical
 references and index.
 
 Language:  English
 
 Descriptors: Neurotoxicology; Nervous system
 
 
 309                                    NAL Call. No.: 470 SCI2
 Transgenic animals.
 Jaenisch, R.
 Washington, D.C. : American Association for the Advancement of
 Science; 1988 Jun10.
 Science v. 240 (4858): p. 1468-1474; 1988 Jun10.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Gene expression; Genetic engineering;
 Genomes; Disease models; Neoplasms
 
 Abstract:  Astract: The ability to introduce foreign genes
 into the germ line and the successful expression of the
 inserted gene in the organism have allowed the genetic
 manipulation of animals on an unprecedented scale. The
 information gained from the use of the transgenic technology
 is relevant to almost any aspect of modern biology including
 developmental gene regulation, the action of oncogenes, the
 immune system, and mammalian development. Because specific
 mutations can be introduced into transgenic mice, it becomes
 feasible to generate precise animal models for human genetic
 diseases and to begin a systematic genetic dissection of the
 mammalian genome.
 
 
 310                                    NAL Call. No.: 500 N21P
 Transgenic mice overexpressing phosphoenolpyruvate
 carboxykinase develop non-insulin-dependent diabetes mellitus.
 Valera, A.; Pujol, A.; Pelegrin, M.; Bosch, F.
 Washington, D.C. : National Academy of Sciences,; 1994 Sep13.
 Proceedings of the National Academy of Sciences of the United
 States of America v. 91 (19): p. 9151-9154; 1994 Sep13. 
 Includes references.
 
 Language:  English
 
 Descriptors: Mice; Experimental diabetes; Diabetes; Diabetes
 mellitus; Transgenic animals; Gene transfer;
 Phosphoenolpyruvate carboxykinase; Gene expression;
 Gluconeogenesis; Liver; Hyperglycemia; Glucose; Carbohydrate
 metabolism; Liver cells
 
 Abstract:  An increase in hepatic gluconeogenesis is believed
 to be an important factor responsible for the fasting
 hyperglycemia detected in patients with non-insulin-dependent
 diabetes mellitus (NIDDM). Phosphoenolpyruvate carboxykinase
 (GTP) (PEPCK; EC 4.1.1.32) is a regulatory enzyme of
 gluconeogenesis. To study the role of the expression of PEPCK
 gene in the development of NIDDM, we have produced lines of
 transgenic mice expressing a PEPCK minigene under control of
 its own promoter. Transgenic mice were hyperglycemic and had
 higher serum insulin concentrations. In addition, alterations
 in liver glycogen content and muscle glucose transporter
 GLUT-4 gene expression were detected. The overexpression of
 the PEPCK gene led to an increase in glucose production from
 pyruvate in hepatocytes in primary culture. When
 intraperitoneal glucose tolerance tests were performed, blood
 glucose levels were higher than those detected in normal mice.
 This animal model shows that primary alterations in the rate
 of liver glucose production may induce insulin resistance and
 NIDDM.
 
 
 311                                  NAL Call. No.: 448.3 AC85
 Treatment of bovine leukaemia virus-infected sheep with
 suramin: an animal model for the development of antiretroviral
 compounds.
 Burkhardt, H.; Rosenthal, S.; Rosenthal, H.A.; Karge, E.; De
 Clercq, E. Praha : Academia, Publishing House of the
 Czechoslovak Academy of Sciences; 1989 Aug.
 Acta virologica v. 33 (4): p. 305-313; 1989 Aug.  Includes
 references.
 
 Language:  English
 
 Descriptors: Bovine oncovirus; Sheep; Drug therapy; Suramin;
 Models; Enzyme activity
 
 
 312                                   NAL Call. No.: QP901.A33
 Trophic stimulation of the ductular-islet cell axis: a new
 approach to the treatment of diabetes.
 Rosenberg, L.; Vinik, A.I.
 New York, N.Y. : Plenum Press; 1992.
 Advances in experimental medicine and biology v. 321: p.
 95-109; 1992.  In the series analytic: Pancreatic islet cell
 regeneration and growth / edited by A.I. Vinik. Proceedings of
 the Diabetic Institute Conference on Inslet Cell Regeneration
 and Growth, June 22-23, 1991, Norfolk, Virginia.  Includes
 references.
 
 Language:  English
 
 Descriptors: Diabetes mellitus; Pancreas islets; Cell
 differentiation; Cell growth; Regeneration; Animal models;
 Golden hamsters
 
 
 313                                    NAL Call. No.: 41.8 J82
 Tuberculosis in domesticated deer (Cervus elaphus): a large
 animal model for human tuberculosis.
 Buchan, G.S.; Griffin, J.F.T.
 London : Academic Press; 1990 Jul.
 Journal of comparative pathology v. 103 (1): p. 11-22. ill;
 1990 Jul. Includes references.
 
 Language:  English
 
 Descriptors: Red deer; Mycobacterium bovis; Histopathology;
 Immunodiagnosis; Lymphocyte transformation tests; Elisa; Skin
 tests; Stress; Immunological deficiency; Disease models;
 Animal models
 
 
 314                                    NAL Call. No.: 500 N21P
 Tumor necrosis factor alpha inhibits signaling from the
 insulin receptor. Hotamisligil, G.S.; Murray, D.L.; Choy,
 L.N.; Spiegelman, B.M. Washington, D.C. : National Academy of
 Sciences,; 1994 May24. Proceedings of the National Academy of
 Sciences of the United States of America v. 91 (11): p.
 4854-4858; 1994 May24.  Includes references.
 
 Language:  English
 
 Descriptors: Mice; Tumor necrosis factor; Insulin; Hormone
 receptors; Phosphorylation; Hormonal control; Adipocytes;
 Glucose; Active transport; Diabetes mellitus
 
 Abstract:  Insulin resistance is a common problem associated
 with infections and cancer and, most importantly, is the
 central component of non-insulin-dependent diabetes mellitus.
 We have recently shown that tumor necrosis factor (TNF) alpha
 is a key mediator of insulin resistance in animal models of
 non-insulin-dependent diabetes mellitus. Here, we investigate
 how TNF-alpha interferes with insulin action. Chronic exposure
 of adipocytes to low concentrations of TNF-alpha strongly
 inhibits insulin-stimulated glucose uptake. Concurrently, TNF-
 alpha treatment causes a moderate decrease in the insulin-
 stimulated autophosphorylation of the insulin receptor (IR)
 and a dramatic decrease in the phosphorylation of IR substrate
 1, the major substrate of the IR in vivo. The IR isolated from
 TNF-alpha-treated cells is also defective in the ability to
 autophosphorylate and phosphorylate IR substrate 1 in vitro.
 These results show that TNF-alpha directly interferes with the
 signaling of insulin through its receptor and consequently
 blocks biological actions of insulin.
 
 
 315                                    NAL Call. No.: 41.8 P27
 Ultraviolet radiation-induced skin tumors in a South American
 opossum (Monodelphis domestica).
 Kusewitt, D.F.
 Lawrence, Kan. : American College of Veterinary Pathologists;
 1991 Jan. Veterinary pathology v. 28 (1): p. 55-65. ill; 1991
 Jan.  Includes references.
 
 Language:  English
 
 Descriptors: Monodelphis domestica; Skin diseases; Neoplasms;
 Ultraviolet radiation; Histopathology; Sarcoma; Melanoma;
 Papillomas; Carcinoma; Animal models; Disease models
 
 
 316                               NAL Call. No.: SF95.A1C6 v.6
 Use of animal models for research in human nutrition.
 Beynen, Anton C.,_1953-; West, C. E.
 Basel ; New York : Karger,; 1988.
 190 p. ; 25 cm. (Comparative animal nutrition ; v. 6). 
 Includes bibliographies and index.
 
 Language:  English
 
 Descriptors: Nutritionally induced diseases; Animal models;
 Animal nutrition
 
 
 317                                   NAL Call. No.: SF95.A1C6
 Use of animals for the study of relations between nutrition
 and infectious diseases.
 Beisel, W.R.
 Basel : Karger; 1988.
 Comparative animal nutrition v. 6: p. 33-55; 1988.  In the
 series analytic: Use of Animal Models for Research in Human
 Nutrition / edited by A.C. Beynen and C.E. West.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Malnutrition; Infectious diseases;
 Fatal infections; Mineral deficiencies; Synergism; Antagonism;
 Species differences; Pathogens; Strain differences; Vitamin
 deficiencies; Deficiency diseases; Immune response;
 Endotoxins; Literature reviews
 
 
 318                                   NAL Call. No.: SF95.A1C6
 Use of animals in elucidating the regulation of metabolism of
 amino acids with particular reference to branched chain amino
 acids.
 Goodwin, G.W.; Harris, R.A.
 Basel : Karger; 1988.
 Comparative animal nutrition v. 6: p. 14-30; 1988.  In the
 series analytic: Use of Animal Models for Research in Human
 Nutrition / edited by A.C. Beynen and C.E. West.  Literature
 review.  Includes references.
 
 Language:  English
 
 Descriptors: Rats; Animal models; Amino acid metabolism;
 Branched chain amino acids; Catabolism; Oxidoreductases;
 Enzyme activity; Dietary protein; Liver cells; Biotechnology;
 Dna probes
 
 
 319                                  NAL Call. No.: RC372.3.S5
 The use of animals in research related to epilepsy and other
 disorders in which convulsions may occur.
 Silcock, Sheila
 Sussex, UK? : RSPCA,; 1989.
 49 p. ; 30 cm.  Cover title.  August 1989.  Includes
 bibliographical references (p. 44-49).
 
 Language:  English
 
 Descriptors: Epilepsy; Animal models in research; Convulsions
 
 
 320                                   NAL Call. No.: SF95.A1C6
 The use of animals in studying the effects of diet on
 gallstone formation. Liepa, G.U.; Gorman, M.A.; Duffy, A.M.
 Basel : Karger; 1988.
 Comparative animal nutrition v. 6: p. 149-173; 1988.  In the
 series analytic: Use of Animal Models for Research in Human
 Nutrition / edited by A.C. Beynen and C.E. West.  Includes
 references.
 
 Language:  English
 
 Descriptors: Animal models; Biliary calculi; Bile; Hamsters;
 Cholesterol metabolism; Dietary protein; Blood serum;
 Laboratory animals; Mice; Dietary fat; Primates
 
 
 321                                 NAL Call. No.: QD415.A1B58
 The use of gene targeting to develop animal models for human
 genetic diseases. Melton, D.W.
 Colchester : The Society; 1990 Dec.
 Transactions - Biochemical Society v. 18 (6): p. 1035-1039.
 ill; 1990 Dec. Includes references.
 
 Language:  English
 
 Descriptors: Transgenics; Genetic engineering; Animals;
 Models; Genetic disorders; Therapy
 
 
 322                            NAL Call. No.: R853.A53U84 1989
 The use of laboratory animals in biomedical research
 significance for human and animal health : information
 package..  Information package; the use of laboratory animals
 in biomedical research
 National Association for Biomedical Research (U.S.)
 Washington : DC? : National Association for Biomedical
 Research?,; 1989. 174 p. : ill. ; 28 cm.  Cover title. 
 January 1989.  Includes bibliographical references.
 
 Language:  English
 
 Descriptors: Animal experimentation; Animal models in
 research; Medicine; Diseases; Animal welfare
 
 
 323                                   NAL Call. No.: 448.3 Ap5
 Virulence of an Escherichia coli O157:H7 sorbitol-positive
 mutant. Fratamico, P.M.; Buchanan, R.L.; Cooke, P.H.
 Washington : American Society for Microbiology; 1993 Dec.
 Applied and environmental microbiology v. 59 (12): p.
 4245-4252; 1993 Dec. Includes references.
 
 Language:  English
 
 Descriptors: Escherichia coli; Sorbitol; Carbohydrate
 metabolism; Fermentation; Mutants; Virulence; Pathogenicity;
 Experimental infections; Rabbits; Diarrhea; Foodborne
 diseases; Pathogens
 
 Abstract:  Virulence and pathogenicity of an Escherichia coli
 O157:H7 sorbitol-positive mutant were investigated with an
 infant rabbit animal model as well as a battery of in vitro
 assays. Total cell lysate protein profiles, outer membrane
 protein profiles, plasmid profiles, and levels of cytotoxic
 activity against Vero cells were similar in the wild-type and
 mutant strains. Both adhered to intestinal epithelial cells in
 culture and reacted with fluorescein isothiocyanate-labeled
 antiserum against E. coli O157:H7. The mutant appeared to be
 similar to the wild type in all respects except in its ability
 to ferment sorbitol. [14C]sorbitol uptake and sorbitol-6-
 phosphate dehydrogenase activities were notably increased in
 the mutant strain. Diarrhea developed in rabbits administered
 the wild-type strain and in those fed the sorbitol-positive
 mutant. There was greater bacterial attachment and mucosal
 damage in the cecum and large intestine than in the small
 intestine. Scanning electron microscopy revealed bacteria
 adhering as single cells and as aggregates closely associated
 with mucus. Mucosal lesions consisted of areas of tissue
 necrosis with sloughing of epithelial cells. By transmission
 electron microscopy, electron-dense necrotic epithelial cells
 were visible in areas where bacteria were present, and
 epithelial cell debris containing bacteria was observed
 between the villar luminal surfaces. Light microscopy of
 epithelial cells of intestinal sections of infected rabbits
 revealed noticeable vacuolation and spherical, pyknotic
 nuclei. These data indicate that the sorbitol-negative
 phenotype is not associated with the pathogenicity of E. coli
 O157:H7.
 
 
 324                                    NAL Call. No.: 500 N21P
 Vitamin C prevents cigarette smoke-induced leukocyte
 aggregation and adhesion to endothelium in vitro.
 Lehr, H.A.; Frei, B.; ARfors, K.E.
 Washington, D.C. : National Academy of Sciences,; 1994 Aug02.
 Proceedings of the National Academy of Sciences of the United
 States of America v. 91 (16): p. 7688-7692; 1994 Aug02. 
 Includes references.
 
 Language:  English
 
 Descriptors: Hamsters; Ascorbic acid; Protection; Tobacco
 smoking; Cigarettes; Smoke; Leukocytes; Adhesion; Endothelium;
 Blood vessels
 
 Abstract:  A common feature of cigarette-smoke (CS)-associated
 diseases such as atherosclerosis and pulmonary emphysema is
 the activation, aggregation, and adhesion of leukocytes to
 micro- and macrovascular endothelium. A previous study, using
 a skinfold chamber model for intravital fluorescence
 microscopy in awake hamsters, has shown that exposure of
 hamsters to the smoke generated by one research cigarette
 elicits the adhesion of fluorescently labeled leukocytes to
 the endothelium of arterioles and small venules. By the
 combined use of intravital microscopy and scanning electron
 microscopy, we now demonstrate in the same animal model that
 (i) CS-induced leukocyte adhesion is not confined to the
 microcirculation, but that leukocytes also adhere singly and
 in clusters to the aortic endothelium; (ii) CS induces the
 formation in the bloodstream of aggregates between leukocytes
 and platelets; and (iii) CS-induced leukocyte adhesion to micro-
  and macrovascular endothelium and leukocyte-platelet
 aggregate formation are almost entirely prevented by dietary
 or intravenous pretreatment with the water-soluble antioxidant
 vitamin C (venules, 21.4 +/- 11.0 vs. 149.6 +/- 38.7
 leukocytes per mm(2), P < 0.01; arterioles, 8.5 +/- 4.2 vs.
 54.3 +/- 21.6 leukocytes per mm(2),P < 0.01; aortas, 0.8 +/-
 0.4 vs. 12.4 +/- 5.6 leukocytes per mm(2), P < 0.01; means +/-
 SD of n = 7 animals, 15 min after CS exposure). No inhibitory
 effect was observed by pretreatment of the animals with the
 lipid-soluble antioxidants vitamin E or probucol. The
 protective effects of vitamin C on CS-induced leukocyte
 adhesion and aggregation were seen at vitamin C plasma levels
 (55.6 +/- 22.2 micromolar, n = 7) that can easily be reached
 in humans by dietary means or supplementation, suggesting that
 vitamin C effectively contributes to protection from CS-
 associated cardiovascular and pulmonary diseases in humans.
 
 
 325                                    NAL Call. No.: 500 N484
 Vitamin E and cancer prevention in an animal model.
 Wang, Y.M.; Purewal, M.; Nixon, B.; Li, D.H.; Soltysiak-
 Pawluczuk, D. New York, N.Y. : The Academy; 1989.
 Annals of the New York Academy of Sciences v. 570: p. 383-390;
 1989.  In the series analytic: Vitamin E--biochemistry and
 health implications / edited by A.T. Diplock, L.J. Machlin, L.
 Packer and W.A. Pryor.  Includes references.
 
 Language:  English
 
 Descriptors: Carcinoma; Diet studies; Disease prevention;
 Disease surveys; Vitamin e; Human nutrition research; Rats
 
 
 326                                  NAL Call. No.: 389.1 W892
 Vitamins and hypertension.
 Dakshinamurti, K.; Lal, K.J.
 Basel : S. Karger; 1992.
 World review of nutrition and dietetics v. 69: p. 40-73; 1992. 
 In the series analytic: Nutrients in the control of metabolic
 diseases / edited by A.P. Simopoulos.  Includes references.
 
 Language:  English
 
 Descriptors: Hypertension; Pyridoxine; Vitamin d; Vitamin e;
 Vitamin deficiencies; Blood pressure; Animal models; Calcium;
 Nutrition physiology; Literature reviews
 
 Abstract:  Based on the evidence presented in this review, the
 authors offer the following conclusions: 1) Among the
 vitamins, pyridoxine and cholecalciferol seem to have
 significant influences on blood pressure regulation. 2) The
 effect of vitamin E seems to be indirect based on the
 maintenance of integrity of membranes. 3) Vitamin D is
 directly involved in regulation of calcium homeostasis.
 Conditions associated with a deficiency of vitamin D or its
 conversion to the active form, would have profound effect on
 calcium absorption and, thus, indirectly on regulation of
 blood pressure.
 
 
 327                                    NAL Call. No.: 500 N484
 Vitamins and the immune system.
 Beisel, W.R.
 New York, N.Y. : The Academy; 1990.
 Annals of the New York Academy of Sciences v. 587: p. 5-8;
 1990.  In the series analytic: Micronutrients and immune
 functions / edited by A. Bendich and Ranjit K. Chandra. 
 Includes references.
 
 Language:  English
 
 Descriptors: Ascorbic acid; Pyridoxine; Retinol; Vitamin e;
 Human nutrition research; Immune response; Immunology; Trace
 elements; Mice; Animal models
 
 
 328                                   NAL Call. No.: 442.9 SO1
 Vitamin A status: relationship to immunity and the antibody
 response. Ross, A.C.
 Baltimore, Md. : Williams & Wilkins; 1992 Jul.
 Proceedings of the Society for Experimental Biology and
 Medicine v. 200 (3): p. 303-320; 1992 Jul.  Literature review. 
 Includes references.
 
 Language:  English
 
 Descriptors: Retinol; Retinoic acid; Vitamin a deficiency;
 Cell mediated immunity; Humoral immunity; Antibody formation;
 Antigens; Natural killer cells; Infections; Immunization;
 Animal models; Literature reviews
 
 
 329                                   NAL Call. No.: 389.8 J82
 Weanling rats display bioperiodicity of growth and food intake
 rates. Mercer, L.P.; Haijazi, H.; Hidevgi, M.
 Bethesda, Md. : American Institute of Nutrition; 1993 Aug. The
 Journal of nutrition v. 123 (8): p. 1356-1362; 1993 Aug. 
 Includes references.
 
 Language:  English
 
 Descriptors: Growth; Growth rate; Biological rhythms; Casein;
 Valine; Methionine; Weight gain; Experimental diets; Animal
 models; Rats
 
 Abstract:  Bioperiodicities in biological phenomena have long
 been studied to gain insight into the dynamics of living
 organisms. However, apparent periodicities in rates of growth
 and food intake have often been either ignored or attributed
 to random error. We have found that such periodicities are not
 random but take the form of infradian rhythms (period > 28 h),
 with multiple periods including circasemiseptan (period = 3.5
 d). in the reported experiments, we examine the existence of
 periodic, oscillatory phenomena in growth and eating patterns
 of rats. The cosinor model of Halberg was used to establish
 the occurrence of rhythms and quantify rhythm characteristics
 of components identified in least squares spectra. The four
 parameters of the rhythm were found to be altered by
 concentrations of the limiting dietary nutrient in that they
 had different spectral signatures. Existence of such
 oscillations in growth rates and food intake rates could have
 important consequences in designing feeding and growth
 experiments for achieving optimal physiological responses as
 well as providing possible insights into eating disorders.
 
 
 330                                   NAL Call. No.: 410.9 P94
 Xenogeneic PBL-scid mice: their potential and current
 limitations. Greenwood, J.D.
 Cordova, Tenn. : American Association for Laboratory Animal
 Science; 1993 Apr. Laboratory animal science v. 43 (2): p.
 151-155; 1993 Apr.  Paper presented at a conference entitled
 "The Scid Mouse in Biomedical and Agricultural Research,"
 August 5-7, 1992, Guelph, Canada.  Includes references.
 
 Language:  English
 
 Descriptors: Animal models; Mice; Lymphocytes
 
 Abstract:  The hu-PBL-scid has been constructed by
 intraperitoneal inoculation of lymphocytes from human
 peripheral blood into immunodeficient scid mice. Such scid
 mouse-human chimeras have proven useful as in vivo animal
 models for studies on human lymphocyte development and
 differentiation from pluripotent stem cells. Further, the hu-
 PBL-scid mouse provides a readily accessible model for the
 examination of immune cell function and involvement in
 autoimmune and infectious disease processes. In response to
 the growing need for model systems to examine the immune
 system and disease pathogenesis in agriculturally important
 animals, PBL engraftment of scid mice has expanded to include
 the bovine and equine species. This review discusses the
 properties and potential uses of the xenogeneic PBL-
 reconstituted scid mouse.
 

Author Index

 Abileah, S. 222
 Ackermann, M.R. 185
 Adams, J.L. 234
 Adams, Robert J. 150
 Adlam, C. 23
 Ahern-Rindell, A.J. 249
 Aiello, R.J. 294
 Ailhaud, G. 245
 Albertini, A. 250
 Alder, V.A. 79
 Alexander, J. 297
 Allegrini, M. 301
 Allen, G.P. 171
 Alziari, S. 225
 Amy, R.M. 208, 270
 Aoki, F.Y. 67
 Apgar, J. 269
 Arai, T. 189
 Arbeeny, C.M. 122
 Arendonk, J.A.M. van 114
 ARfors, K.E. 324
 Arp, L.H. 148
 Asano, T. 66
 Attie, A.D. 294, 295
 Aubert, R. 286
 Aukema, H.M. 127
 Austin, L.L. 194
 Austin-Lafrance, R.J. 261
 Azmi, M. 201
 Bacchus, C. 48
 Bacon, W.L. 64
 Baker, George T. 260
 Baker, P.B. 287
 Bandt, F.H. 292
 Bannatyne, R.M. 231
 Barbee, D.D. 267
 Barnes, S. 291
 Barr, R.J. 74
 Barr, S.C. 136
 Barrett, D.S. 115
 Barrett-Connor, E. 103
 Barsh, G.S. 244
 Barta, J.R. 293
 Basson, N.J. 143
 Baumal, R. 56
 Bautista, J.R. 49
 Beard, J.L. 52, 235
 Beatty, R.J. 167
 Beausoleil, N. 156
 Beisel, W.R. 317, 327
 Bell, J.D. 195
 Bell, J.G. 121
 Belton, P.S. 195
 Berdanier, C.D. 95
 Bergquist, K.E. 122
 Beynen, A.C. 65
 Beynen, Anton C., 108
 Beynen, Anton C.,_1953- 316
 Beziat, F. 225
 Bhathena, S.J. 119, 277
 Bishop, S.A. 149
 Blanchette-Mackie, E.J. 93
 Blenden, D.C. 223
 Blondeau, J.M. 67
 Bloom, F.E. 236
 Bodo, M. 160
 Boffa, G.M. 250
 Bohnsack, J.F. 275
 Boothe, D.M. 111
 Boothe, H.W. 111
 Bosch, F. 310
 Bosshard, N.U. 157
 Bourgeois, F. 286
 Bourque, W.T. 273
 Bovee, K.C. 217
 Bradley, A. 184
 Bray, G.A. 252
 Brennan, M.F. 13
 Breslow, J. 210
 Bridenstine, R.T. 133
 Briner, J. 157
 Broderson, J.R. 292
 Bronzino, J.D. 261
 Brown, F. 166
 Bruss, M.L. \u University of California, Davis, CA 219
 Buchan, G.S. 313
 Buchanan, R.L. 323
 Buergelt, C.D. 302
 Bunch, T. 166
 Burgin, C.W. 167
 Burkhardt, H. 311
 Burns, R.A. 121
 Burny, A. 50
 Buselmaier, W. 48
 Butler, D.G. 147
 Butterworth, R.F. 263
 Byham, L.D. 100
 Calnek, B.W. 70
 Camana, C. 301
 Camus, M.C. 286
 Cantor, Jerome O. 88
 Capellan, J.M. 231
 Capodicasa, E. 71
 Carapetis, R. 14
 Carbone, K.M. 49
 Caroldi, S. 71
 Carraway, J.H. 209
 Carroll, K.K. 278
 Carswell, N. 119
 Carter, J.W. 144
 Caskey, C.T. 184
 Cerda, J.J. 167
 Cha, Y.S. 58
 Chambon, C. 36
 Chang, J.K. 275
 Chao, F.F. 93
 Charnock, J.S. 38
 Chastin, I. 36
 Cheevers, W.P. 267
 Chen, M.L. 222
 Chen, M.T. 130
 Cheng, P. 231
 Chiodini, R.J. 302
 Chowdhury, J.R. \u Albert Einstein College of Medicine, Bronx,
 NY 170
 Chowdhury, N.R. 170
 Choy, L.N. 314
 Christman, J.K. 222
 Chu, H. 69
 Ciresi, R. 173
 Clabough, D.L. 152
 Clark, A.M. 113
 Clarkson, R.B. 82
 Clarkson, T.B. 26
 Clifford, A.J. 116
 Clingerman, K. 28
 Coates, F. 156
 Coghlan, L. 174
 Cohen, L.A. 268
 Conboy, H.S. 152
 Condorelli, E. 250
 Conner, B.H. 110
 Connolly, J.M. 104
 Connor, J.D. 52
 Connor, W.E. 141
 Contreras, R.J. 107
 Cooke, P.H. 323
 Cooley, A.J. 234
 Cooper, D.R. 200
 Cooper, S.T. 294
 Cornelius, C.E. 154
 Cornelius, C.E. \u University of California, Davis, CA 153
 Cornelius, Charles E. 22
 Corrier, D.E. 111
 Corteyn, A.H. 298
 Cotsonis, G.A. 227
 Cotter, P.A. 54
 Cox, I.J. 195
 Crabble, J.C. 162
 Cranwell, P.D. 257
 Cray, W.C. Jr 37
 Cremer, K.J. 35
 Cringle, S.J. 79
 Crusberg, T.C. 140
 Cruse, Julius M.,_1937- 62
 Cullen, J.M. 111
 Curello, S. 250
 Cyr, D. 263
 Czuprynski, C.J. 234
 D'Aquino, M. 118
 Dakshinamurti, K. 326
 Daley, E. 156
 Daoust, L. 202
 Davidson, M.B. 299
 Davis, N.L. 42
 De Clercq, E. 311
 Dean, E.A. 148
 DeCarli, L.M. 25
 Deeb, B.J. 300
 Deming, E.J. 15
 DeRousseau, C. Jean 248
 Deyl, Zdenek 221
 Di Felice, M. 118
 Diamond, Herbert S., 87
 Dickens, B.F. 93
 Dietrich, H.M. 181
 Dietschy, J.M. 271
 DiGiacomo, R.F. 300
 DiGirolamo, M. 227
 Diker, F.S. 146
 Diker, K.S. 146
 Dionne, S. 202
 Dizik, M. 222
 Dodam, J.R. 305
 Doel, T.R. 298
 Doi, K. 306
 Dolphin, P.J. 270
 Donovan, S.M. \u University of Illinois, Urbana, IL 169
 Dooley, T.P. 142
 Douglas, S.D. 243
 Doyle, R.E. 233
 Dubielzig, R.R. 61
 Dubreuil, J.D. 262
 Duffy, A.M. 320
 Dukes, I.D. 89
 Dulin, A. 269
 Dunaway, G.A. 94
 Easter, R.A. 203
 Eberhard, M.L. 292
 Edelsteinova, S. 131
 Efendic, S. 192
 Elder, J.H. 236
 Elliott, S.C. 223
 Engstrand, L. 199
 Erdmann, G. 206
 Esparza, J. 17
 Evermann, J.F. 77
 Farber, J.M. 156
 Farese, R.V. 200
 Faribrother, J.M. 262
 Faustman, D. 2
 Fearon, K.C.H. 215
 Feingold, K.R. 282
 Fenstermacher, E.A. 217
 Fernandes, G. 281
 Ferrari, R. 250
 Ferre, P. 91
 Fettman, M.J. 9
 Field, H.J. 201
 Findon, G. 255
 Fishlock, R.C. 14
 Fisler, J.S. \u University of California, Los Angeles, CA 53
 Focht, S.J. 164
 Fong, I.W. 231
 Ford, C.W. 135
 Fosmire, G.J. 164
 Fournier, J. 156
 Fowke, J.H. 198
 Fox, H.S. 236
 Fragonas, E. 137
 Fraker, P. 242
 Fraker, P.J. 191
 Franciotta, D.M. 301
 Frangakis, C.J. 89
 Fratamico, P.M. 323
 Freedland, R.A. 154
 Freeman, A.E. 272
 Frei, B. 324
 Freinkel, N. 97
 Friedlander, N.J. 103
 Friedman, A. 193
 Frigeri, L.G. 244
 Fu, Y. 2
 Fukui, M. 66
 Fukumoto, H. 211
 Gabriel, E. 160
 Gabrielson, D.A. 78
 Galler, J. 261
 Gamble, W. 93
 Garofalo, C. 202
 Garvey, D. 299
 Garvy, B.A. 191
 Gavin, P.R. 267
 Gentili, V. 118
 Gerlach, R.F. 7
 Geske, R. 184
 Gibson, B.M. 143
 Giebink, G.S. 206
 Giguere, R. 263
 Gilbert, R.O. 185
 Gill, A.M. 244
 Gillett, N.A. 7
 Gitzelmann, R. 157
 Glade, M.J. 129
 Glavin, G.B. 67
 Glowa, J. 4
 Gluckman, J. C. 32
 Gnudi, L. 5
 Godeas, C. 137
 Gold, P.W. 4
 Goodwin, G.W. 318
 Gorman, M.A. 320
 Goto, N. 196
 Gragtmans, N.J. 220
 Granato, D. 83
 Grand, R.J. 182
 Grandolfo, M. 137
 Grant, G.L. 152
 Grant, K.A. 44
 Green, R.A. 111
 Greenberg, E.R. 276
 Greenwald, G.F. 42
 Greenwald, Robert A.,_1943- 87
 Greenwel, P. 34
 Greenwood, J.D. 330
 Griffin, C.E. 74
 Griffin, J.F.T. 313
 Gross, M. 273
 Gruber, J. 35
 Grunfeld, C. 282
 Guarnieri, G. 250
 Guberski, D.L. 96
 Guo, J. 2
 Guo, Z.M. 63, 265
 Gustavsson, S. 199
 Guthrie, M.J. 116
 Gwathmey, J.K. 229
 Haijazi, H. 329
 Hall, B.K. 273
 Hall-Craggs, M. 232
 Halliburton, I.W. 298
 Halsted, C.H. 8, 73
 Hamilton, H.L. 234
 Hampson, D.J. 254
 Hancock, M.L. 125
 Hansen, C. 277
 Hansen, C.T. 92, 119, 213
 Hansen, R.J. \u University of California, Davis, CA 43
 Hara, C. 155
 Hara, K.S. 256
 Harada, T. 266
 Harris, M.C. 243
 Harris, R.A. 318
 Harvey, J.W. 94
 Haskins, M.E. 176
 Hayden, J.E. 176
 Hayes, K.C. 106
 Haziroglu, R. 146
 Hegstad, R.L. 9
 Heisler, O.R. 208
 Hendrickx, A.G. 121
 Heng, J. 132
 Henriksen, S.J. 236
 Herberg, L. 16
 Herndon, M.W. 271
 Herzog, J. 286
 Hetzel, B.S. 279
 Hidevgi, M. 329
 Higgins, B. 233
 Hill, H.R. 275
 Hirose, H. 45
 Ho, C.C. 116
 Ho, Y.K. 116
 Hoeg, J.M. 1
 Hollifield, V. 213
 Holmes, R.A. 136
 Holub, B.J. 127
 Hope, J. 195
 Horzinek, Marian C. 18
 Hosie, M.J. 90
 Hosokawa, S. 238
 Hotamisligil, G.S. 314
 How, S.J. 123
 Howard, R.B. 69
 Hsu, B.Y.L. 217
 Huang, L.C. 200
 Huether, G. 12
 Hufford, C.D. 113
 Hyun, B.H. 237
 Iglauer, Franz 138
 Ikeda, H. 3, 211
 Imura, H. 211
 Inagaki, M. 306
 Ingram, Donald K. 260
 Institute of Laboratory Animal Resources (U.S.), Committee on
 Immunologically Compromised Rodents 188
 Inui, K. 266
 Inzana, T.J. 186
 Ip, C. 84
 Itakura, C. 168
 Ito, K. 85
 Jackson, W.D. 182
 Jaenisch, R. 309
 Janig, W. 145
 Jayo, J.M. 128
 Jenkins, W.L. 111
 Jevcak, J.J. 220
 Jezyk, P.F. 176
 Jiao, S. 3
 Johnson, B.J.B. 42
 Johnson, D.E. 232
 Johnson, J.H. 45
 Johnson, R. 51
 Johnson-Delaney, Cathy A. 288
 Johnston, M.R. 69
 Johnston, R.E. 42
 Johnston, S.D. 9
 Jones, B.C. 52
 Jones, J. 119
 Jones, P. 184
 Jones, P.W. 254
 Jorgensen, A. 199
 Kahn, B.B. 5
 Kamimura, E. 134
 Kanarek, R.B. 24, 109
 Kanety, H. 183
 Kaplan, J.R. 128
 Karasik, A. 183
 Karge, E. 311
 Kasahara, K. 205
 Kasai, N. 134
 Katoh, T. 168
 Kaufman, L.N. 130
 Kausche, F.M. 148
 Kawaguchi, A. 238
 Kawaoka, Y. 139
 Kayyali, U.S. 198
 Keen, C.L. 121
 Kehrli, M.E. Jr 185, 272
 Kelley, D.H. 272
 Kennedy, B.W. 119
 Kerkhofs, P. 50
 Kernodle, D.S. 289
 Kettmann, R. 50
 Khan, A. 192
 Khosla, P. 106
 Killington, R.A. 298
 Kinebuchi, H. 117
 King, L.E. 191
 King, S. 107
 Klei, T.R. 136
 Kliegman, R.M. 132
 Klimes, I. 131
 Klumpp, S.A. 82
 Knowles, D.P. 267
 Koeslag, D.G. 207, 270
 Koh, G. 211
 Kondapalli, R. 170
 Konietzko, S. 206
 Koo, S.I. 144
 Korpela, H. 175
 Koskela, M. 206
 Kovacsova, B. 131
 Kozarsky, K.F. 194
 Kramer, T. 269
 Kremer, J.M. 296
 Krinsky, N.I. 60
 Kristek, F. 131
 Kritchevsky, D. 98
 Kruse-Elliott, K.T. 305
 Kruth, H.S. 93
 Kubo, M. 3
 Kumazawa, A. 85
 Kurabe, S. 306
 Kurata, K. 126
 Kurihara, K. 85
 Kuriyama, M. 165
 Kuroda, J. 168
 Kusewitt, D.F. 315
 Kutner, M.H. 227
 Kuznetsov, A. 89
 Kvam, B.J. 137
 Kyselovic, J. 131
 Laboratory Animals Information Service Centre (India) 19
 Lacy, P.E. 177
 Ladiges, W.C. 10, 55
 Ladiges, W.C. \u University of Washington, Seattle, WA 11
 Lal, K.J. 326
 Lallier, R. 262
 Lancaster, M.E. 89
 Lariviere, S. 262
 Larner, J. 200
 Larson, J.A. 29
 Leach, F. 5
 Lee, Y. 45, 112
 LeFebvre, R.B. 264
 Lehr, H.A. 324
 Leiter, E.H. 240
 Lemonnier, D. 286
 Lepage, G. 202
 Lerner, D.L. 236
 Letvin, Norman L. 32
 Levander, O.A. 285
 Levine, J.F. 152
 Levy, E. 202
 Lewis, R. E. 62
 Lewis, S.M. 209
 Li, D.H. 325
 Li, F. 2
 Licinio, J. 4
 Lieber, C.S. 25
 Liepa, G.U. 320
 Limoges, B.F. 270
 Litschi, B. 157
 Liu, C.T. 63, 265
 Lloyd, D.H. 123
 Lockatell, C.V. 232
 Lonnerdal, B. 121
 Lotti, M. 71
 Lowseth, L.A. 7
 Lucke, V.M. 149
 Lund, A. 190
 Lunenfeld, B. 183
 Lusis, A.J. 53
 Luskey, K.L. 112
 Lust, G. 258
 Lutz, H. 157
 Luzarraga, M.B. 280
 Lysons, R.J. 254
 M.D. Anderson Cancer Center, Science-Park Research Division
 230
 Maeda, H. 68, 205
 Mahoney, S.G. 217
 Maita, K. 266
 Makar, A.B. 159
 Mammerickx, M. 50
 Mampaso, F. 303
 Mannen, H. 196
 Mano, M.T. 279
 Manuck, S.B. 128
 Marcell, T. 69
 Marks-Kaufman, R. 24
 Marlar, A.B. 61
 Marrano, P. 56
 Marsh, P.A. 119
 Martinez-Alonso, C. 303
 Mason, P.W. 166
 Masoro, E.J. 241
 Masuda, K. 211
 Matsubara, K. 3
 Matsuda, J. 66
 Matsuo, T. 3
 Matsuzawa, Y. 3
 McCaleb, M.L. 218
 McCann, R.A. 220
 McClearn, G.E. 164
 McConnell, I. 195
 McCracken, K.J. 246
 McCune, S.A. 287
 McGarry, J.D. 45
 McInnes, R.R. 56
 McIntosh, G.H. 76
 McKinley, D.R. 194
 McMurray, D.N. 307
 McNamara, P.D. 217
 Medina, C.A. 191
 Meingassner, J.G. 304
 Melton, D.W. 321
 Mendis, S. 133
 Menzies, B.E. 289
 Menzies, C. 81
 Mercer, L.P. 329
 Meredith, D.M. 298
 Mertz, R.J. 89
 Messina, M.J. 291
 Metz, J. 75
 Mhaskar, Y. 94
 Michaelis, O.E. IV 119, 277
 Michalak, A. 263
 Mikami, T. 238
 Miller, J.F. 54
 Miller, K. 216
 Miller, P.E. 61
 Miller, T.E. 255
 Mitchel, R.E.J. 220
 Mitkova, A. 131
 Mitsumori, K. 266
 Miura, K. 168
 Miyoshi, I. 134
 Moazed, T.C. 300
 Montgomery, C. Jr 184
 Moon, H.W. 148
 Moore, T.B. 198
 Morel, F. 225
 Moretto, A. 71
 Morgan, J.H. 254
 Morgane, P.J. 261
 Morrison, D.P. 220
 Moshe, S. 183
 Mote, C.R. 15
 Moughan, P.J. 257
 Mozrzymas, J.W. 137
 Muggenburg, B.A. 7
 Muller, P.K. 160
 Mulvin, D. 69
 Murnane, R.D. 249
 Murphy, J.W. 220
 Murray, D.L. 314
 Murray, P.K. 171
 Mutwiri, G.K. 147
 Myers, Laurie A. 47
 Nagatani, M. 168
 Nagy, J.I. 67
 Nakagwa, M. 66
 Nakayama, M. 85
 Narama, I. 68, 168
 Nardini, M. 118
 Nashold, B.S. Jr 151
 National Association for Biomedical Research (U.S.) 322
 Nederlandse Centrale Organisatie voor Toegepast-
 Natuurwetenschappelijk Onderzoek 18
 Neef, N.A. 254
 Nelson, L.M. 1
 Nestor, K.E. 64
 Neuringer, M. 141
 Newby, F.D. 227
 Nicklin, S. 216
 Nicolson, L. 298
 Nieuwland, M.G.B. 114
 Niewiesk, Stefan 253
 Nirtles, M.J. 257
 Nishikawa, T. 68
 Nishimura, M. 68
 Niu, C. 160
 Nixon, B. 325
 Nonneman, Arthur J. 308
 Nose, M. 237
 Notbohm, H. 160
 Nozaki, Y. 238
 O'Connor, D.L. 203
 Odaka, H. 3
 Odle, J. 169
 Oehme, F.W. 115
 Ogawa, N. 155
 Ogilvie, G.K. 9
 Ogura, A. 66
 Ohneda, M. 45
 Ohyama, H. 126
 Oki, Y. 189
 Okuyama, H. 224
 Okwueze, M.I. 41
 Olmsted, R.A. 236
 Olson, N.C. 305
 Olsvik, O. 190
 Opgenorth, T.J. 41
 Orthen-Gambill, N. 109
 Osanai, T. 134
 Osborne, M.T. 120
 Ostenson, C.G. 192
 Osweiler, G. 159
 Otis, E.J. 176
 Ouding, R.J. 142
 Ovelmen-Levitt, J. 151
 Ozaki, K. 68
 Pace, M.J. 53
 Pahud, J.J. 83
 Panneton, W.M. 233
 Paoletti, S. 137
 Papageorges, M. 267
 Pasini, E. 250
 Paulson, D.J. 57
 Pedraza, M. 257
 Pelegrin, M. 310
 Pena, L. 303
 Penicaud, L. 91
 Penn, D. 59
 Percy, D.H. 293
 Persky, V. 291
 Peters, C.J. 63
 Phalen, S.W. 307
 Philbrick, D.J. 127
 Philipson, L.H. 89
 Phillips, T.J. 162
 Phillips, T.R. 236
 Picciano, M.F. 203
 Pieber, T.R. 112
 Pinard, M.H. 114
 Pisters, P.W.T. 13
 Podbielski, F.J. 133
 Pollesello, P. 137
 Potgieter, L.N.D. 15
 Powell, A.M. 277
 Powell, N. 42
 Prescott, M.F. 295
 Price, R.E. 174
 Prieur, D.J. 249
 Probert, W.S. 264
 Pronczuk, A. \u Brandeis University, Waltham, MA 106
 Prospero-Garcia, O. 236
 Puaoi, D.L. 236
 Pujol, A. 310
 Pullen, L.A. 171, 298
 Purewal, M. 325
 Qian, C.G. 63
 Qureshi, I.A. 263
 Racz, Paul 32
 Radcliffe, J.D. 80
 Randall, J.C. 198
 Raper, S.E. 194
 Rapp-Gabrielson, V.J. 78
 Rasmussen, M.A. 37
 Ratnakumari, L. 263
 Rea, C.T. 217
 Recant, L. 119, 277
 Reddy, B.S. 99, 102
 Rehg, J.E. 125
 Reider, E. 166
 Reisbick, S. 141
 Renegar, K.B. 197
 Revilla, Y. 303
 Reznik, Gerd 40
 Richardson, R.J. 198
 Rives, L. 107
 Robbins, F.L. 167
 Roberts, C.W. 297
 Robins, E.D. 1
 Robinson, D.R. 296
 Roe, M.W. 89
 Roebuck, B.D. 101
 Rogers, A.E. 110
 Rohrbach, M.S. 256
 Roitelman, J. 112
 Rojkind, M. \u Albert Einstein College of Medicine, Bronx, NY
 34
 Romeo, J.P. 233
 Roos, M.A. 203
 Rose, D.P. 104, 268
 Rosenberg, L. 312
 Rosendal, S. 147
 Rosenkrantz, W.S. 74
 Rosenthal, H.A. 311
 Rosenthal, S. 311
 Ross, A.C. 328
 Rossi, R.P. 69
 Rossitch, E. Jr 151
 Rothuizen, J. 259
 Rowe, L.C. 255
 Rowsell, H.C. 20
 Roy, C.C. 202
 Rubin, E.M. 39
 Rubin, S.A. 49
 Runciman, W.B. 14
 Russell, J.C. 207, 208, 270
 Ruzzier, F. 137
 Sachan, D.S. 58
 Saegusa, T. 168
 Sahin, G. 159
 Saint Paul, N. 225
 Saito, T. 237
 Samuel, J.E. 148
 Sanchez, M.S. 135
 Sandaradura, S. 72
 Sande, R.D. 267
 Sanders, T.A.B. 72
 Sasaki, M. 189
 Sato, M. 180
 Satterfield, W. 174
 Saudek, C.D. 251
 Savoldi, F. 301
 Scaccini, C. 118
 Scanlon, P.D. 256
 Scapellato, M.L. 71
 Scelsi, R. 301
 Schamber, G.J. 78
 Schellekens, H. 21
 Schellekens, Huub 18
 Scheynius, A. 199
 Schmidt-Sommerfeld, E. 59
 Schroeder, M.A. 256
 Schuller, Hildegard M. 40
 Schutz, M.M. 163
 Schwan, A. 199
 Schwarz, K. 83
 Sebokova, E. 131
 Segal, S. 217
 Seino, Y. 211
 Setchell, K.D.R. 291
 Shafrir, E. 183
 Shamoto, M. 238
 Sheikhnejad, G. 222
 Shelton, M. 81
 Shepherd, P.R. 5
 Shimazu, N. 306
 Shiraishi, N. 117
 Shively, C.A. 26, 128
 Shock, Nathan Wetherill, 260
 Shrago, E. 130
 Shuster, D.E. 185
 Silcock, Sheila 319
 Simopoulos, A.P. 247
 Sklan, D. 193
 Smith, C.P. 29, 30, 31
 Smith, D.J. 39
 Smith, G.P. 33
 Smith, J.C. 269
 Smith, J.F. 42
 Smith, M.O. 58
 Smith, W.C. 257
 Smyth, J.R. Jr 290
 Snoswell, A.M. 14
 Soares, J.H. Jr 120
 Soltysiak-Pawluczuk, D. 325
 Spencer, B. 89
 Spennetta, T. 130
 Spiegelman, B.M. 314
 Spycher, M.A. 157
 Sredy, J. 218
 Srivastava, R.A.K. 283
 Stamp-Cole, M. 142
 Standaert, M.L. 200
 Starc, T. 137
 Stein, D.T. 112
 Stephens, L.C. 174
 Stevenson, Donald E. 230
 Stills, H.F. Jr 287
 Stinson, Sherman F.,_1946- 40
 Stokes, A. 171, 298
 Stokes, C.R. 149
 Storb, R. 55
 Storts, R.W. 81
 Stramm, L. 176
 Strandberg, J.D. 251
 Stratford-Perricaudet, L.D. 194
 Stratum, P. van 124
 Strobel, S. 158
 Stump, K.C. 251
 Su, E.N. 79
 Sugano, Michihiro,_1933- 108
 Sullivan, M.P. 167
 Sundberg, John P. 172
 Superti-Furga, A. 157
 Suzuki, S. 200
 Svec, P. 131
 Swanson, J. 28
 Swanson, J.C. 27
 Swindle, M. Michael 150
 Swindle, M.M. 251
 Tagaya, O. 238
 Taguchi, T. 117
 Tahiliani, A.G. 57
 Takahashi, H. 127
 Takano, K 66
 Tanaka, S. 180
 Taniguchi, T. 180
 Tarui, S. 3
 Tashijan, R.J. 140
 Tephly, T.R. 159
 Thibault, L. 202
 Thienpont, E. 50
 Thomas, E.D. 55
 Thomas, J. A._1933- 47
 Thorner, P.S. 56
 Thurston, J.R. 272
 Timmers, K.I. 277
 Todd, J. 186
 Todhunter, R.J. 258
 Tokunaga, K. 3
 Tomassi, G. 118
 Tomita, T. 237
 Tonkiss, J. 261
 Torres-Anjel, M.J. 223
 Toyota, T. 200
 Tozzo, E. 5
 Trott, D.J. 254
 Trpis, M. 6
 Tshikuka, J.G. 223
 Tsuchitani, M. 168
 Tsuji, S. 196
 Turley, S.D. 271
 Uelmen, P.J. 294
 Unger, R.H. 45
 University of Washington, Primate Information Center 288
 Usui, T. 189
 Vail, D.M. 9
 Vaishnav, S. 184
 Valera, A. 310
 Van Wyk, C.W. 143
 VandeWoude, S.J. 280
 Vari, R.C. 41
 Venkatraman, J.T. 281
 Verschuren, P.M. 124
 Vinik, A.I. 312
 Vinuela, E. 303
 Virmani, K. 179
 Vittur, F. 137
 Vles, R.O. 124
 Vogler, G.A. 233
 Volz-Lingenhol, A. 225
 Von Bernuth, R.D. 15
 Von Geldern, T.W. 41
 Voyles, N.R. 119, 277
 Vrana, A. 131
 Waggie, K.S. 213
 Wainfan, E. 222
 Wakabayashi, T. 85, 126
 Wakamiya, M. 184
 Wakasugi, N. 237
 Walker, B.E. 239
 Walker, M.A. 81
 Walker-Smith, J.A. 161
 Waltrip, R.W. II 49
 Walzem, R.L. 43
 Wang, Y. 204
 Wang, Y.M. 325
 Wang, Z. 200
 Warden, C.H. 53
 Wargovich, M.J. 174
 Warren, J.W. 232
 Wasteson, Y. 190
 Watanabe, K. 155
 Watson, B.J. 233
 Watson, R.R. 204
 Wattleton, T. 107
 Weide, L.G. 177
 Weigel, K.A. 272
 Weingand, K.W. 26
 Weingard, K.W. 226
 Weir, V.A. 81
 Weise, D. 111
 Welch, B.G. 292
 West, C. E. 316
 West, C.E. 65
 Wheeler, S.L. 9
 Wheldon, L.A. 298
 Whipp, S.C. 37
 Whittaker, G.R. 298
 Widhalm, K. 179
 Wiesmann, U. 157
 Wilkins, S.D. 277
 Willems, L. 50
 Williams, A. 107
 Williams, S.C.R. 195
 Willis, L.V. 42
 Wilson, J.M. 194
 Wissler, R.W. 133
 Wolf, E. 160
 Wolfe, G.L. 244
 Wong, M.L. 4
 Woodruff, Michael L. 308
 Woods, P.R. 81
 Worley, J.F. III 89
 Wu, Bing-quan,_1930- 187
 Wu, X. 184
 Wu-Owens, J. 213
 Wynder, E.L. 268
 Yager, J. 147
 Yamada, K. 200
 Yamaguchi, T. 127
 Yamamoto, T. 211
 Yamasaki, K. 86
 Yamashita, T. 134
 Yamatsu, K. 238
 Yamazaki, K. 85, 126
 Yan, G. 2
 Yancey, R.J. Jr 135
 Yang, C. 160
 Yang, H. 5
 Yang, Y. 200
 Yano, H. 211
 Yasuda, K. 211
 Yen, T.T. 244
 Yokomizo, Y. 180
 Yoshida, H. 165
 Yoshida, M.C. 134
 Yoshikawa, Y. 86
 Young, E.A. 214
 Young, G.P. 105
 Young, J.B. 178
 Young, J.N. 151
 Youson, J.H. \u University of Toronto, Ontario, Canada 46
 Yu, D.Y. 79
 Zaalberg, J. 124
 Zeligman, B.E. 69
 Zeller, K.R. 212
 Zevenbergen, J.L. 124
 Zhang, C. 200
 Zheng, Jie 187
 Zheng, K. 56
 Zicha, Joseph 221
 Zijpp, A.J. van der 114
 Zucker, I. 284
 

Subject Index

 Abnormal behavior 49
 Abnormalities 97
 Abortion 186
 Abscesses 300
 Absorption 257
 Acetyl coenzyme a 130
 Acetylcholinesterase 71, 115, 198
 Acquired immune deficiency syndrome 17, 113, 204, 223, 282
 Active transport 5, 314
 Activity 155
 Acute infections 67
 Adenine 116
 Adenoviridae 194
 Adhesion 324
 Adipocytes 5, 200, 227, 314
 Adipose tissue 5, 91, 109, 227
 Adrenalectomy 252
 Adults 191
 Adverse effects 258
 Aedes mediovittatus 6
 African swine fever virus 303
 Age 117, 152
 Age differences 7, 94, 177
 Aging 7, 85, 112, 227, 260
 AIDS (Disease) 18, 288
 Alcoholism 8, 34, 44, 73, 162
 Alleles 2, 294
 Allergens 83
 Aluminum 164
 Alzheimer's disease 52, 164
 Amino acid metabolism 13, 318
 Amino acid sequences 56
 Amino acids 12, 179
 Angiotensin 107
 Animal behavior 224, 284
 Animal breeding 92, 181
 Animal diseases 28, 31
 Animal experimentation 322
 Animal experiments 21, 33, 38, 44, 95, 144, 162, 216, 228,
 233, 235, 246, 278
 Animal fat 76
 Animal health 233, 272
 Animal husbandry 233
 Animal models 1, 2, 6, 7, 9, 10, 11, 12, 15, 16, 25, 26, 29,
 30, 34, 35, 36, 37, 38, 39, 40, 43, 44, 45, 46, 49, 51, 52,
 53, 54, 56, 57, 58, 61, 62, 63, 65, 67, 68, 69, 70, 73, 75,
 76, 77, 79, 81, 82, 85, 87, 87, 91, 92, 93, 94, 95, 98, 99,
 100, 101, 104, 106, 107, 109, 111, 112, 114, 115, 116, 119,
 123, 126, 130, 131, 135, 136, 139, 141, 142, 143, 145, 146,
 148, 149, 150, 151, 152, 153, 154, 155, 157, 161, 162, 163,
 164, 167, 168, 170, 173, 174, 176, 178, 179, 180, 183, 184,
 185, 186, 187, 187, 188, 189, 191, 192, 194, 195, 196, 197,
 200, 201, 205, 207, 208, 209, 210, 212, 214, 217, 218, 219,
 220, 221, 222, 224, 227, 228, 229, 230, 231, 232, 234, 237,
 238, 240, 242, 243, 244, 248, 249, 254, 257, 258, 259, 261,
 262, 265, 266, 267, 268, 269, 274, 277, 285, 287, 289, 290,
 292, 294, 297, 298, 300, 302, 303, 305, 306, 307, 312, 313,
 315, 316, 317, 318, 320, 326, 327, 328, 329, 330
 Animal models in research 19, 319, 322
 Animal nutrition 316
 Animal physiology 224
 Animal protein 76
 Animal proteins 5, 205
 Animal research 21
 Animal testing alternatives 10, 11
 Animal welfare 27, 87, 322
 Animals 23, 27, 28, 321
 Anorexia 4, 215
 Anorexia nervosa 33, 155
 Antagonism 317
 Antagonists 41
 Antibacterial properties 264
 Antibiotics 113, 135, 255
 Antibodies 158, 206
 Antibody formation 49, 114, 186, 264, 328
 Antifungal properties 113
 Antigens 158, 161, 328
 Antimicrobial properties 113
 Antioxidants 118, 204, 276, 285
 Aphthovirus 166
 Apolipoproteins 3, 39, 210, 283, 294
 Appetite 24
 Application methods 78
 Arochlor 144
 Arprinocid 125
 Arteries 86
 Arthritis 87, 137, 267
 Ascorbic acid 324, 327
 Assays 272
 Assessment 296
 Atherogenic diet 26, 167
 Atherosclerosis 39, 82, 108, 208, 226, 295
 Atlases 40, 40, 40, 40
 Atresia 46
 Attenuation 42
 Attractants 275
 Autoantibodies 290
 Autoimmune diseases 2, 62, 95, 181, 240, 247, 281, 290, 304
 Autoimmunity 2, 62, 158
 Azoxymethane 174
 B lymphocytes 191
 Bacteria 199
 Bacterial antigens 190
 Bacterial count 135
 Bacterial diseases 21, 232, 305
 Bacterial proteins 54
 Bacteroids 254
 Beta-galactosidase 194
 Beta-glucuronidase 157
 Bibliographies 27, 28, 29, 30, 31
 Bibliography 274, 274, 274
 Bile 320
 Bile ducts 46
 Bile pigments 170
 Biliary calculi 320
 Bilirubin 153, 154, 170
 Binding 294
 Bioavailability 12
 Biochemistry 75
 Biological rhythms 329
 Biological techniques 271
 Biotechnology 47, 318
 Bladder 232
 Blastomere 48
 Blood 303
 Blood cholesterol 108
 Blood coagulation 20
 Blood composition 106
 Blood flow 20
 Blood glucose 251
 Blood lipids 1, 45, 118, 133, 282
 Blood picture 52
 Blood plasma 3, 63, 72, 82, 106, 112, 115, 118, 130, 141, 271,
 278
 Blood pressure 86, 107, 131, 326
 Blood proteins 108
 Blood serum 7, 9, 122, 152, 206, 278, 286, 320
 Blood sugar 9, 16, 79, 95
 Blood vessels 324
 Bo RNAdisease virus 49
 Body fat 5, 128, 227
 Body weight 64, 107, 130, 155, 227
 Bone density 120
 Bone diseases 160
 Bone fractures 273
 Bone marrow 191
 Bone marrow transplant 55
 Bone strength 129, 160
 Bordetella bronchiseptica 54
 Borrelia burgdorferi 264
 Bovine leukosis 185
 Bovine mastitis 23, 146, 163, 272
 Bovine oncovirus 50, 51, 311
 Brain 52, 63, 71, 81, 198, 236, 252, 261
 Brain disorders 12
 Branched chain amino acids 318
 Branhamella 280
 Breast feeding 83
 Breed differences 163
 Breeding value 114, 163
 Broilers 58
 Brown fat 5
 Brugia malayi 6
 Brugia pahangi 6
 Bulimia nervosa 33
 Bulls 185
 Cabt 163
 Cachexia 9, 13, 147, 215, 282
 Calcium 76, 120, 129, 137, 326
 Calcium ions 89
 Caloric intake 84, 102, 241
 Calorie-restricted diets 214
 Calories 101
 Calves 185
 Campylobacter 146
 Cancer 187, 230
 Candida albicans 143
 Candidosis 143
 Caprine arthritis encephalitis virus 267
 Carbohydrate metabolism 5, 95, 130, 211, 310, 323
 Carbohydrate metabolism disorders 9, 109
 Carbohydrates 98
 Carbon tetrachloride 34, 306
 Carcinogenesis 84, 98, 99, 101, 102, 220, 222, 230
 Carcinogenicity testing 230
 Carcinogens 110, 174, 220
 Carcinoma 13, 60, 76, 102, 215, 222, 276, 281, 291, 315, 325
 Cardiomyopathy 136, 229
 Cardiovascular diseases 57, 228, 281
 Carnitine 14, 58, 59
 Carotenoids 60, 276
 Cartilage 137
 Case reports 157, 300
 Casein 80, 329
 Cat 74
 Catabolism 318
 Cataract 61
 Catecholamines 235
 Catheters 232
 Cats 43, 90, 149, 157, 176, 236
 Cattle 37, 147, 186
 Cell culture 166
 Cell differentiation 312
 Cell growth 312
 Cell lines 166
 Cell mediated immunity 328
 Cell membranes 100
 Cell ultrastructure 68
 Cells 191
 Cellular immunity 62
 Central nervous system 52, 224, 236
 Cerebral cortex 151
 Cerebrospinal fluid 63, 236
 Ceroid 81
 Characterization 262
 Chediak-higashi syndrome 68
 Chicken housing 181
 Chicks 173, 193
 Child development 12
 Children 161
 Chimeras 48
 Chinchillas 206
 Chlorpyrifos 71, 198
 Cholecalciferol 120
 Cholesterol 1, 72, 82, 86, 93, 106, 122, 133, 144, 167, 271,
 278, 283, 295
 Cholesterol acyltransferase 3
 Cholesterol metabolism 106, 194, 320
 Chondrocytes 137
 Chronic course 25, 73
 Chronic infections 297
 Cigarettes 324
 Ciprofloxacin 135
 Circulatory disorders 305
 Cirrhosis 259, 306
 Clinical trials 100, 276
 Clones 42
 Cloxacillin 135
 Coconut oil 133
 Coffee 72
 Collagen 56, 160
 Colon 76, 99, 102, 105, 174
 Colonization 254
 Colonizing ability 54
 Colostrum 152
 Complementary
 DNA 194
 Complications 287
 Composition 127, 164
 Computed tomography 81, 128
 Computer simulation 228
 Congenital infection 297
 Congresses 187, 187, 187, 187, 230, 230, 230, 230, 230
 Contamination 15
 Convulsions 85, 319
 Cooking oils 36
 Copper 117
 Coronary vessels 86
 Correlation 130
 Costs 272
 Cotton 256
 Cottonseed protein 80
 Cows 43, 219
 Cretinism 279
 Cricetulus barabensis 16
 Cross immunity 123
 Cross immunization 123
 Cryptosporidium 125
 Culling 185
 Cycling 107
 Cytochrome b 225
 Cytokines 204, 215
 Cytosine 166
 Cytosol 205
 Dairy cattle 51
 Dairy cows 163, 272
 Death 191
 Deficiency 194, 222
 Deficiency diseases 14, 36, 73, 317
 Degeneration 81
 Deletions 166, 225
 Demyelination 75
 Dermatophilus congolensis 123
 Diabetes 2, 79, 91, 96, 97, 168, 244, 247, 251, 277, 310
 Diabetes mellitus 3, 16, 41, 45, 89, 95, 122, 183, 189, 192,
 200, 211, 218, 228, 287, 310, 312, 314
 Diagnosis 81, 161, 179, 249
 Diarrhea 190, 323
 Diet 3, 25, 57, 60, 72, 76, 84, 107, 127, 133, 164, 175, 193,
 203, 222, 247, 257, 270, 276, 281, 299, 301
 Diet studies 325
 Diet treatment 179, 215
 Dietary carbohydrate 16, 109, 119, 130
 Dietary fat 16, 38, 76, 84, 98, 99, 100, 101, 102, 103, 104,
 109, 118, 124, 130, 239, 268, 281, 283, 320
 Dietary protein 76, 80, 98, 278, 318, 320
 Dietary proteins 241
 Diethylstilbestrol 239
 Diets 144, 167, 226
 Digesta 190
 Digestion 257
 Digestive tract 161
 Digestive tract mucosa 182
 Digoxin 229
 Diploidy 48
 Disease course 86, 136, 180
 Disease models 1, 9, 10, 11, 15, 17, 20, 21, 27, 28, 29, 31,
 48, 51, 61, 66, 69, 77, 78, 82, 93, 96, 111, 117, 134, 136,
 137, 140, 143, 145, 146, 147, 148, 149, 156, 164, 165, 167,
 168, 174, 176, 181, 184, 189, 220, 223, 226, 228, 229, 234,
 237, 238, 251, 292, 295, 306, 309, 313, 315
 Disease prevalence 37, 61
 Disease prevention 60, 76, 90, 125, 224, 247, 258, 264, 276,
 325
 Disease resistance 243, 272
 Disease surveys 325
 Disease transmission 15, 77
 Disease vectors 6
 Diseases 19, 22, 30, 40, 150, 221, 224, 230, 248, 274, 322
 Distribution 128
 Dna hybridization 190
 Dna methylation 222
 Dna probes 318
 Docosenoic acids 141, 247, 296
 Dogs 7, 9, 55, 56, 74, 94, 111, 136, 176, 217, 258, 259, 300
 Domestic animals 197
 Dosage 258
 Dosage effects 123, 198
 Down's syndrome 48
 Dracunculus insignis 292
 Drinking behavior 44
 Drosophila melanogaster 116
 Drosophila subobscura 225
 Drug combinations 135
 Drug effects 24, 125, 135, 258
 Drug therapy 74, 122, 215, 258, 311
 Drug toxicity 281
 Dry period 135
 Dusts 256
 Ear diseases 304
 Eating patterns 132
 Edema 148
 Eicosanoids 100, 296
 Eicosapentaenoic acid 247, 296
 Elderly 191, 281
 Elderly nutrition 241
 Electrocardiograms 136
 Elisa 123, 313
 Embryonic stem cells 184
 Encephalitis 49, 301
 Encephalopathy 259
 Endocrine glands 191
 Endocrine system 189
 Endoplasmic reticulum 89
 Endothelium 324
 Endotoxins 305, 317
 Energy expenditure 252
 Energy intake 103, 130
 Energy metabolism 137, 178, 215, 263
 Enteral feeding 182, 281
 Enteritis 147
 Enterotoxemia 148
 Enterotoxins 190, 262
 Enzyme activity 89, 94, 115, 116, 157, 198, 200, 311, 318
 Enzyme deficiencies 157, 263
 Enzymes 254, 258
 Epidemiological surveys 268, 276
 Epidemiology 51, 223
 Epidermal growth factor 169
 Epilepsy 319
 Epinephrine 63, 178
 Epithelium 74
 Equine herpesvirus 201, 298
 Equine infectious anemia 140
 Equine infectious anemia virus 140
 Equine influenzavirus 139
 Erythrocytes 94, 115
 Escherichia 37
 Escherichia coli 37, 148, 190, 262, 323
 Essential fatty acids 141, 202
 Esterases 71, 115, 198
 Estradiol 1
 Estrogenic properties 291
 Estrogens 196
 Estrous cycle 155
 Ethanol 25, 58, 110
 Evolution 247
 Exercise 101, 109, 128
 Exons 56
 Experimental atherosclerosis 26, 93, 144, 210
 Experimental diabetes 45, 89, 183, 200, 310
 Experimental diets 91, 141, 329
 Experimental infection 6, 146, 147, 197, 231
 Experimental infections 49, 67, 135, 139, 292, 323
 Experiments 232
 Fanconi syndrome 217
 Fasting 132, 153, 154
 Fat absorption 202
 Fat consumption 281
 Fat deficiencies 141, 202, 281
 Fat metabolism 109
 Fatal infections 139, 317
 Fatty acids 45, 99, 101, 104, 106, 127, 141, 270, 299
 Fatty liver 43, 219
 Fatty liver hemorrhagic syndrome 43
 Feasibility studies 268
 Feces 190
 Feed conversion efficiency 109
 Feed intake 16, 109
 Feedback 252
 Feeding behavior 24, 155
 Feet 67
 Feline immunodeficiency virus 90, 236
 Feline oncovirus 223
 Female animals 155, 239
 Fermentation 323
 Ferrets 61, 292
 Ferritin 52
 Fetal alcohol syndrome 173
 Fetus 173, 279
 Fiber 76, 102, 105
 Filariasis 6
 Fimbriae 190
 Fish oils 38, 99, 101, 127, 131, 141, 270, 281, 285, 296
 Foals 152
 Folic acid 8, 73, 159, 203
 Food 108
 Food allergies 83, 158, 161
 Food composition tables 247
 Food intake 80, 155
 Food intolerance 216
 Food restriction 155, 241
 Food supplements 131
 Foodborne diseases 156, 323
 Foreign bodies 232
 Formates (salts) 159
 Formic acid 159
 Fowls 70, 71, 114, 181, 290
 Fsh 1
 Fulvic acids 160
 Furazolidone 229
 Ganglia 67
 Gangliosidosis 249
 Gastric ulcer 155
 Gastritis 199
 Gastroenteritis 161
 Gastrointestinal diseases 37, 182
 Gene expression 2, 4, 194, 211, 222, 225, 283, 309, 310
 Gene therapy 194
 Gene transfer 194, 310
 Genes 42, 180, 190, 211, 225, 244
 Genetic correlation 163
 Genetic defects 185
 Genetic disorders 321
 Genetic engineering 39, 166, 309, 321
 Genetic factors 179
 Genetic gain 163
 Genetic markers 91
 Genetic models 53, 162
 Genetic regulation 162, 283
 Genetic resistance 163
 Genetic trend 114
 Genetic variation 50
 Genistein 291
 Genomes 225, 309
 Gerbils 167
 Germfree state 143
 Glomerular filtration rate 41
 Glomerulonephritis 66, 149
 Glomerulopathy 237
 Glomerulus 238
 Glucagon 119
 Glucocorticoids 191
 Gluconeogenesis 310
 Glucose 5, 89, 95, 130, 192, 211, 310, 314
 Glucose tolerance 5, 9, 91
 Glutathione peroxidase 285
 Glycerate 2,3-bis(phosphate) 79
 Glycerol-3-phosphate acyltransferase 200
 Glycogen 168
 Glycogenosis 94
 Glycolysis 137
 Glycoproteins 42, 171, 298
 Glycosaminoglycans 176, 258
 Gnotobiotic animals 254
 Goats 267
 Goiter 36, 279
 Golden hamsters 312
 Gonadotropins 1
 Gram negative bacteria 305
 Granules 68
 Granuloma 180
 Growth 227, 329
 Growth factors 104
 Growth rate 80, 329
 Guinea pigs 63, 78, 167, 255, 256, 265, 269, 301, 307
 Haemophilus 78
 Haemophilus somnus 186
 Hair 172
 Hamsters 72, 166, 167, 171, 271, 298, 320, 324
 Handbooks, manuals, etc 87, 87
 Handling 233
 Haplotypes 294
 Healing 273
 Health risk assessment 47
 Heart 57, 86
 Heart diseases 175, 207, 247, 287
 Heart rate 38, 107
 Heat stability 160, 262
 Hematology 79
 Hematopoiesis 300
 Hemodialysis 14
 Hemodynamics 41
 Hemoglobin 79
 Hemolysis 289
 Hemorrhage 20, 280
 Hens 43, 71, 198
 Hepatitis 111, 126, 134, 259
 Hereditary diseases 56, 131, 176, 177, 181, 194, 238
 Heritability 114, 163
 Herpes simplex virus 67
 Herpetoviridae 171
 High density lipoprotein 39, 133, 283
 Histidine 289
 Histidinemia 179
 Histocompatibility antigens 2
 Histology 7, 147
 Histopathology 61, 66, 68, 86, 155, 168, 174, 180, 189, 229,
 238, 249, 266, 267, 295, 306, 313, 315
 HIV infections 32
 Holstein-friesian 185
 Homologous recombination 184
 Hormonal control 200, 314
 Hormone receptors 183, 314
 Hormones 104, 189
 Horses 129, 137, 140, 258, 298
 Host specificity 77
 Human behavior 52
 Human diseases 15, 36, 37, 51, 55, 165, 209
 Human immunodeficiency virus 17, 204, 223
 Human milk 158, 169, 257
 Human nutrition research 33, 65, 131, 235, 250, 261, 325, 327
 Humoral immunity 328
 Hydrolases 285
 Hyperbilirubinemia 153, 154, 238
 Hypercholesteremia 108
 Hypercholesterolemia 1, 106, 122, 194, 278, 294, 295
 Hyperglycemia 45, 218, 310
 Hyperinsulinemia 16, 130, 183, 226, 299
 Hyperlipemia 1, 86, 93, 167, 194
 Hyperphenylalaninemia 12
 Hyperplasia 5
 Hypersensitivity 83
 Hypertension 107, 247, 326
 Hyperthermia 220
 Hypertriglyceridemia 131, 270, 282
 Hyperuricemia 184
 Hypoglycemia 132
 Hypoplasia 259
 Hypothalamic lesions 91
 Hypothalamus 1, 4
 Hypothyroidism 279
 Identification 185
 Iga 206
 Igg 152, 206
 Igm 206
 Immune competence 272
 Immune response 42, 83, 158, 193, 197, 201, 204, 242, 281,
 296, 317, 327
 Immune serum 206
 Immunity 100
 Immunization 264, 328
 Immunodiagnosis 190, 313
 Immunohistochemistry 189
 Immunological deficiency 147, 313
 Immunological deficiency syndromes 187, 188
 Immunological diseases 74
 Immunological factors 63, 282
 Immunology 187, 187, 188, 242, 301, 327
 Immunopathology 49, 191
 Immunosuppression 125
 Immunosuppressive agents 74
 In vitro 198, 272, 289
 In vivo 21
 Inactivation 275
 Inbred strains 143
 Incidence 64, 95, 124, 177, 185
 Induced mutations 39
 Induced resistance 143
 Infant development 281
 Infant formulas 121
 Infant nutrition 243
 Infants 257
 Infection 15, 90, 156, 303
 Infections 161, 282, 293, 328
 Infectious diseases 243, 317
 Infectivity 166
 Inflammation 49, 247, 267, 296
 Influenza 197
 Influenzavirus 197
 Inhibition 115, 198, 258
 Inoculation 199
 Inoculum 156
 Inoculum density 156
 Inositol phosphates 200
 Insulin 3, 9, 16, 91, 95, 112, 119, 130, 169, 183, 200, 211,
 226, 251, 299, 314
 Insulin secretion 16, 45, 89, 192
 Insulin-like growth factor 169
 Intake 106
 Interactions 24
 Interferon 21, 282
 Interleukins 282, 296
 Intestinal absorption 3, 121, 161, 202, 271
 Intestinal microorganisms 254
 Intestinal mucosa 158
 Intramuscular injection 255
 Intraperitoneal injection 78
 Intravenous injection 149
 Iodine 36, 279
 Ion transport 137
 Iron 52, 203, 235
 Irrigation 15
 Isoenzymes 94
 Isolation 206
 Isotope labeling 271
 Isotypes 206
 Japanese quails 64
 Joints (animal) 267
 Karyotypes 48
 Kidney diseases 127, 212
 Kidneys 41, 56, 86, 127, 168, 177, 217
 Kinetics 13, 198
 Laboratory animals 20, 28, 44, 65, 162, 241, 284, 320
 Lactation 84, 129, 135, 203
 Lactic acid 9
 Lampreys 46
 Latent infections 67, 148
 Lawns and turf 15
 Laying performance 64
 Lentivirinae 77
 Lesions 151, 236
 Lethal dose 198
 Leukemia 51
 Leukocytes 115, 324
 Leukotrienes 296
 Lh 1
 Life cycle 46
 Ligaments 64
 Line differences 64, 114
 Linoleic acid 84, 106, 224
 Linolenic acid 224
 Lipid metabolism 43, 130, 205, 219, 282
 Lipid metabolism disorders 45
 Lipid peroxidation 118
 Lipids 91, 93, 186, 295
 Lipogenesis 205
 Lipolysis 299
 Lipoproteins 3, 202, 286, 295
 Lipotropic factors 222
 Lipoxygenase 100
 Liquid diets 25
 Listeria monocytogenes 156
 Literature reviews 8, 16, 38, 39, 43, 46, 51, 52, 57, 65, 73,
 75, 77, 84, 90, 91, 95, 98, 100, 102, 103, 109, 158, 161, 163,
 169, 178, 179, 182, 191, 197, 204, 212, 215, 219, 223, 243,
 244, 247, 250, 252, 257, 258, 259, 261, 268, 276, 278, 281,
 282, 290, 291, 296, 305, 317, 326, 328
 Litter size 286
 Live vaccines 42, 123
 Liver 8, 25, 46, 130, 174, 176, 180, 183, 205, 211, 219, 230,
 299, 310
 Liver cells 194, 310, 318
 Liver diseases 34, 46, 170
 Livestock 36, 77
 Loci 244
 Long chain fatty acids 219
 Long term experiments 232
 Louisiana 136
 Low density lipoprotein 1, 39, 118, 133, 194, 278, 294
 Lungs 69, 88
 Lymph nodes 303
 Lymphadenitis 23
 Lymphocyte transformation 135
 Lymphocyte transformation tests 313
 Lymphocytes 100, 330
 Lymphoma 9, 74, 213
 Lysine 160
 Lysosomes 165, 249
 Macaca fascicularis 156, 280
 Macaca mulatta 141
 Magnetic separation 190
 Maize oil 133
 Major histocompatibility complex 2
 Malabsorption 73
 Malaria 285
 Male animals 227
 Males 128
 Malnutrition 12, 73, 182, 243, 317
 Mammary gland neoplasms 84, 103, 110, 124, 268
 Mammary glands 146
 Man 12, 37, 43, 57, 71, 77, 197, 212, 278
 Mares 152
 Markers 304
 Mastitis 135
 Maternal antibodies 152
 Maternal effects 97, 179
 Maternal immunity 152
 Maternal nutrition 129, 132, 279
 Maturation 239
 Measurement 112, 265, 271
 Medical anthropology 248
 Medical research 10, 11, 228, 233
 Medical treatment 152
 Medicine 322
 Melanins 290
 Melanoma 142, 315
 Membranes 195, 217
 Men 13, 133
 Menopause 103
 Mental ability 52
 Mental stress 128
 Meriones unguiculatus 106
 Messenger
 RNA 211, 225
 Metabolic disorders 116, 244, 263
 Metabolic inhibitors 299
 Metabolic studies 214
 Metabolism 58, 73, 91, 116, 132, 159, 179, 203, 218, 247
 Metabolites 116, 120, 195, 198
 Methanol 159
 Methionine 329
 Methodology 221, 221
 Methylation 75
 Mice 2, 5, 39, 48, 49, 53, 66, 85, 89, 117, 124, 127, 135,
 139, 142, 146, 147, 164, 166, 172, 177, 180, 184, 186, 187,
 195, 196, 201, 210, 213, 220, 224, 230, 231, 232, 234, 237,
 240, 244, 255, 263, 264, 273, 285, 286, 289, 293, 297, 302,
 303, 309, 310, 314, 320, 327, 330
 Mice as laboratory animals 172
 Microtus arvalis 189
 Milk 206, 257
 Milk production 272
 Milk yield 163
 Mineral content 52
 Mineral deficiencies 52, 160, 175, 191, 235, 279, 301, 317
 Mineral metabolism 164, 235
 Mineral nutrition 269
 Mineral supplements 120
 Minerals 241
 Miniature pigs 174
 Mitochondrial
 DNA 225
 Mitochondrial genetics 225
 Mitogens 296
 Models 14, 23, 24, 33, 55, 83, 97, 171, 199, 311, 321
 Molecular biology 51
 Molecular genetics 210
 Monitoring 69
 Monkeys 82, 128
 Monoclonal antibodies 171, 298, 303
 Monodelphis domestica 315
 Monoenoic fatty acids 281
 Morbidity 78, 212
 Morphology 227, 292
 Mortality 78, 155, 212, 251
 Mucopolysaccharidosis 157, 176
 Multiple genes 53
 Multiple sclerosis 52
 Muscle contraction 38
 Muscles 183
 Muscular hypertrophy 229
 Muskrats 233
 Mutagenesis 289
 Mutants 42, 54, 66, 184, 237, 238, 293, 323
 Mutations 42, 50, 56, 185, 244, 290
 Mycobacterium bovis 313
 Mycobacterium paratuberculosis 147, 180, 234, 302
 Mycoses 231
 Myocardial ischemia 250
 Myristic acid 106
 N-nitrosodimethylamine 111
 Nadh dehydrogenase 225
 Natural killer cells 100, 328
 Necrosis 234
 Neonatal development 169
 Neonates 59, 121, 132, 158, 243, 286
 Neoplasms 10, 11, 64, 69, 70, 80, 99, 100, 101, 104, 105, 174,
 239, 247, 309, 315
 Nephritis 56
 Nephropathy 184
 Nephrosis 177
 Nephrotic syndrome 66
 Nervous system 308
 Nervous system diseases 71, 115, 139, 145, 151, 198, 204, 266
 Neuroleptics 52
 Neurons 81, 249, 266
 Neuropeptides 4
 Neurophysiology 235, 261
 Neurosecretory systems 235
 Neurotoxicology 308
 Neurotoxins 71, 266
 Neurotransmitters 12, 52, 252
 Neutrophils 135, 204, 243
 Newborn animals 269
 Nitrogen 86
 Nitrogen balance 13
 Nitrous oxide 75
 Norepinephrine 63, 178
 Normal values 79
 Norway 190
 Nose 280
 Nuclear magnetic resonance spectroscopy 195
 Nucleotide sequences 50, 56, 185
 Nutrient balance 8, 252
 Nutrient deficiencies 59, 242, 247, 285
 Nutrient intake 103, 128, 129, 241, 268
 Nutrient nutrient interactions 76
 Nutrient requirements 65, 182
 Nutrient sources 247
 Nutrient transport 95, 202, 217
 Nutrient uptake 217
 Nutrition 24, 153, 224
 Nutrition physiology 8, 52, 65, 178, 191, 214, 242, 246, 247,
 252, 281, 326
 Nutrition research 191
 Nutritional assessment 182
 Nutritional disorders 33
 Nutritional intervention 102, 268, 281
 Nutritional state 191, 204, 242
 Nutritionally induced diseases 316
 Nutritive ratio 109
 Obesity 3, 45, 53, 57, 91, 92, 95, 104, 107, 109, 112, 119,
 132, 178, 205, 211, 218, 227, 244, 245, 246, 252, 270, 277,
 287, 299
 Olive oil 118
 Oncovirinae 77
 Opportunistic infections 113, 143
 Oral administration 115, 148, 158, 255
 Oral contraceptives 82
 Organophosphorus compounds 115, 266
 Osteoarthritis 248, 258
 Osteoporosis 120
 Ovariectomy 120
 Ovaries 1
 Overfeeding 183, 286
 Oviducts 64
 Oxidation 204, 299
 Oxidoreductases 184, 263, 318
 Oxygen 250
 Pain 296
 Palmitic acid 106
 Pancreas 16, 101
 Pancreas islets 45, 89, 95, 189, 312
 Pancreatectomy 251
 Papillomas 315
 Papio 25
 Paralysis 292
 Parasite migration 292
 Parasites 21
 Parenteral feeding 182, 281
 Parkinson's disease 52
 Pathogenesis 23, 26, 42, 43, 45, 77, 112, 147
 Pathogenicity 37, 139, 254, 323
 Pathogens 280, 317, 323
 Pathology 165, 304
 Pathology, Experimental 221
 Peptides 41, 169, 234
 Perilla 224
 Phagocytes 191
 Pharmacokinetics 71, 255
 Phenotypes 42, 53, 54, 114, 244, 254
 Phosphatidylcholines 93
 Phosphatidylinositols 200
 Phosphoenolpyruvate carboxykinase 310
 Phosphofructokinase 94
 Phospholipids 86, 141
 Phosphorus 137
 Phosphorylation 314
 Physical activity 4
 Physiology 274
 Physiology, Experimental 221
 Physiopathology 36, 63, 73, 218, 305
 Phytate 121
 Pichinde virus 63, 265
 Pigeons 26, 144
 Piglets 190, 257
 Pigs 15, 26, 115, 148, 159, 175, 199, 203, 226, 251, 254, 262,
 294, 295, 305
 Pituitary 1
 Pituitary hormones 16
 Pituitary-gonadal axis 1
 Plant extracts 113
 Plant oils 224
 Plasma membranes 5
 Platelets 296
 Polychlorinated biphenyls 144
 Polydipsia 141
 Polyenoic fatty acids 38, 247, 281
 Polygenic inheritance 290
 Polypeptides 112
 Porcine enterovirus 15
 Portal vein 259
 Postmortem examinations 81
 Postpartum period 129
 Potassium 137
 Poults 229
 Pregnancy 84, 97, 129, 132, 203, 269, 297
 Prenatal period 239, 261
 Primates 26, 248, 288, 320
 Progesterone 1
 Proline 160
 Promoters 194, 220
 Propranolol 229
 Prostate 7, 104
 Protection 324
 Protein deficiencies 261
 Protein energy malnutrition 191
 Protein intake 212
 Protein kinase 183
 Protein metabolism 12, 215
 Protein secretion 212
 Protein synthesis 12
 Proteins 195, 285
 Proteinuria 237
 Protozoal infections 21
 Psammomys obesus 183
 Puerperium 261
 Purification 262
 Pyridoxine 326, 327
 Pyrophosphatases 89
 Qinghaosu 285
 Quails 120
 Quarantine 233
 Rabbits 1, 26, 59, 93, 122, 123, 194, 206, 255, 323
 Rabies virus 223
 Radiography 69
 Radioimmunoassay 112
 Ratios 271
 Rats 3, 4, 16, 25, 36, 40, 41, 45, 57, 67, 68, 69, 76, 79, 80,
 86, 91, 92, 96, 101, 107, 109, 110, 112, 118, 119, 120, 121,
 125, 126, 130, 131, 132, 134, 143, 145, 151, 155, 165, 168,
 170, 187, 191, 193, 200, 205, 207, 208, 211, 218, 222, 224,
 227, 238, 243, 250, 255, 262, 266, 270, 277, 287, 299, 304,
 306, 318, 325, 329
 Rats as laboratory animals 40
 Receptors 1, 41, 194, 294
 Recessive genes 237
 Recombinant
 DNA 194
 Recombination 166
 Recordings 136
 Red deer 313
 Regeneration 312
 Regression analysis 106, 272
 Regulation 158, 200, 252
 Relaxin 169
 Renal failure 86, 212
 Renal function 212
 Repetitive
 DNA 50
 Replication 137
 Reporter genes 194
 Research 113, 284, 291
 Resistance 211, 299
 Respiration 265
 Respiratory diseases 23, 256, 280
 Restricted feeding 98
 Retinoic acid 328
 Retinoids 276
 Retinol 193, 327, 328
 Retroviridae 35
 Retrovirus infections 32
 Reviews 99, 101, 104
 Rhesus monkeys 121
 Rheumatism 87
 Rheumatoid arthritis 281, 296
 Rhinitis 23
 Risk 15, 51, 84, 103, 104, 268, 291
 Rna 166
 Rodents 188
 Rodents as laboratory animals 188
 Safflower oil 141, 224
 Saimiri boliviensis 153
 Saimiri sciureus 154
 Salmonella 300
 Salmonellosis 300
 Sarcoma 315
 Saturated fats 130, 283
 Schistosomiasis 34
 Scintigraphy 267
 Scrapie 195
 Screening 113, 185, 272
 Seasonal behavior 284
 Selection criteria 163
 Selection differential 114
 Selection index 163
 Selection methods 181
 Selection responses 64, 114
 Selenium 160, 175, 285
 Serotonin 12, 63
 Serotypes 78
 Serum albumin 149
 Sex 117
 Sex differences 82
 Sex hormones 134
 Sex linkage 56
 Sheep 14, 23, 50, 81, 219, 249, 311
 Skeletal muscle 130, 211
 Skin 172, 220
 Skin diseases 153, 315
 Skin tests 313
 Smoke 324
 Smooth muscle 64
 Sodium 217
 Somatic cell count 163
 Sorbitol 323
 Source fat 241
 Soy milk 121
 Soy protein 278
 Soybean oil 118
 Soybean products 291
 Species differences 65, 191, 317
 Specific dynamic action 109
 Sphingomyelins 93
 Spinal cord 292
 Spirochaetales 254
 Spleen 180, 303
 Spread 77
 Sri lanka 133
 Staphylococcus aureus 135, 289
 Starvation 182
 Strain differences 49, 50, 54, 78, 96, 146, 164, 180, 275, 317
 Streptococcus 275
 Stress 82, 107, 155, 204, 250, 300, 313
 Structural genes 2, 50, 56, 184, 210, 225
 Subcutaneous injection 67, 117, 255
 Sulfur 285
 Supplements 38, 58, 160, 281, 296
 Suramin 311
 Surface antigens 264
 Surgery 250
 Surgery, Experimental 150
 Survival 116, 269
 Susceptibility 6, 180
 Swine 274
 Swine as laboratory animals 274
 Sympathetic nervous system 178, 252
 Symptoms 149, 156, 157, 165, 249
 Synergism 317
 T lymphocytes 2, 158, 193, 201
 Targeted mutagenesis 184
 Technetium 267
 Temperature 235
 Testes 7
 Testosterone 7
 Thalamus 81
 Therapy 321
 Thrombosis 20
 Thymus gland 191
 Thyroid diseases 181
 Tissues 52, 141, 164
 Tobacco smoking 82, 324
 Tongue 143
 Tongue lesions 143
 Toxemia 305
 Toxicity 25, 75, 115, 116, 117, 159, 164, 170, 174, 198, 266,
 276, 289
 Toxicology 115, 266
 Toxins 289
 Toxoplasma gondii 297
 Toxoplasmosis 297
 Trace elements 98, 327
 Transcription 225
 Transduction 54, 291
 Transfection 166
 Transfer RNA 225
 Transferases 153, 170
 Transferrin 52
 Transgenic animals 5, 39, 210, 310
 Transgenics 321
 Transport 43
 Treatment 74, 170
 Trends 281
 Triacylglycerol lipase 165
 Triacylglycerols 86, 167, 202, 219, 278
 Trichosporon beigelii 231
 Triglycerides 133
 Triolein 118
 Trisomy 48
 Trypanosoma cruzi 136
 Trypanosomiasis 136
 Tuberculosis 307
 Tumor necrosis factor 135, 314
 Tumors 40, 230
 Tumors in animals 40
 U.S.A. 162, 163
 Ultrastructure 189, 266
 Ultraviolet radiation 315
 Undernutrition 286
 Unsaturated fatty acids 118
 Urea 86
 Uric acid 184
 Urination disorders 196
 Vaccination 90, 123, 197
 Vaccine development 90
 Vaccines 90, 186
 Vacuoles 176
 Valine 329
 Vascular diseases 207, 259
 Venezuelan equine encephalitis virus 42
 Vertical transmission 297
 Very low density lipoprotein 118, 210
 Veterans 73
 Viral diseases 77, 95
 Viral proteins 50
 Virulence 42, 54, 78, 139, 166, 323
 Vision disorders 141
 Vitamin a deficiency 269, 328
 Vitamin b12 75
 Vitamin d 120, 326
 Vitamin deficiencies 8, 75, 193, 317, 326
 Vitamin deficiency 250
 Vitamin e 76, 126, 204, 250, 285, 325, 326, 327
 Vitamin supplements 204, 276
 Vitamins 65, 98, 241
 Waste water 15
 Weight 7, 64, 86
 Weight gain 132, 329
 Weight reduction 57
 Women 13, 103, 268
 X chromosome 56
 Xanthine dehydrogenase 116
 Yersinia pseudotuberculosis 254
 Young adults 133
 Zinc 121, 191, 301
 Zoonoses 51
 

The Animal Welfare Information Center, http://www.nal.usda.gov/awic/contact.php
http://www.nal.usda.gov/awic/pubs/oldbib/qb9514.htm, April 17, 1998