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Author Boray, J.C. openurl 
  Title Experimental fascioliasis in Australia Type Journal Article
  Year 1969 Publication (up) Advances in Parasitology Abbreviated Journal Adv Parasitol  
  Volume 7 Issue Pages 95-210  
  Keywords Adaptation, Biological; Adaptation, Physiological; Animal Nutrition Physiology; Animals; Animals, Laboratory; Australia; Cattle; *Cattle Diseases/pathology; Climate; *Disease Vectors; Ecology; Electron Transport; Estivation; Fasciola hepatica/enzymology/*growth & development/metabolism/physiology; Fascioliasis/epidemiology/immunology/*prevention & control/veterinary; Glycolysis; Guinea Pigs; Horses; Humans; Larva/growth & development/physiology; Marsupialia; Metamorphosis, Biological; Mice; New Guinea; New Zealand; Parasite Egg Count; Rats; Seasons; Sheep; *Sheep Diseases/pathology  
  Abstract  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0065-308X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:4935272 Approved no  
  Call Number Equine Behaviour @ team @ Serial 2744  
Permanent link to this record
 

 
Author Menges, R.W.; Furcolow, M.L.; Selby, L.A.; Habermann, R.T.; Smith, C.D. openurl 
  Title Ecologic studies of histoplasmosis Type Journal Article
  Year 1967 Publication (up) American Journal of Epidemiology Abbreviated Journal Am J Epidemiol  
  Volume 85 Issue 1 Pages 108-119  
  Keywords Adolescent; Adult; Animals; Antibodies/*analysis; Carnivora; Cats; Cattle; Child; Child, Preschool; Dogs; Ecology; Female; Fluorescent Antibody Technique; Histoplasma/isolation & purification; Histoplasmin; Histoplasmosis/*epidemiology/*immunology; Horses; Humans; Infant; Infant, Newborn; Kansas; Male; Marsupialia; Mice; Middle Aged; Missouri; Rabbits; Skin Tests; *Soil Microbiology; Swine  
  Abstract  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0002-9262 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:5334640 Approved no  
  Call Number Equine Behaviour @ team @ Serial 2747  
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Author Nicol, C.J.; Adachi, M.; Akiyama, T.E.; Gonzalez, F.J. doi  openurl
  Title PPARgamma in endothelial cells influences high fat diet-induced hypertension Type Journal Article
  Year 2005 Publication (up) American journal of hypertension : journal of the American Society of Hypertension Abbreviated Journal Am J Hypertens  
  Volume 18 Issue 4 Pt 1 Pages 549-556  
  Keywords Administration, Oral; Animals; Antihypertensive Agents/pharmacology; Blood Pressure/drug effects; Diabetes Mellitus, Type 2/physiopathology; Dietary Fats/*administration & dosage/pharmacology; Dose-Response Relationship, Drug; Endothelial Cells/*metabolism; Female; Heart Rate/drug effects; Hypertension/*etiology; Ligands; Male; Mice; Mice, Knockout; PPAR gamma/*metabolism; Sodium Chloride/administration & dosage/pharmacology; Thiazolidinediones/pharmacology  
  Abstract BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands improve human hypertension. However, the mechanism and site of this effect remains unknown, confounded by PPARgamma expression in many cell types, including endothelial cells (ECs). METHODS: To evaluate the vascular role of PPARgamma we used a conditional null mouse model. Specific disruption of PPARgamma in ECs was created by crossing Tie2-Cre+ transgenic (T2T+) and PPARgamma-floxed (fl/fl) mice to generate PPARgamma (fl/fl)T2T+ (PPARgamma E-null) mice. Conscious 8- to 12-week-old congenic PPARgamma (fl/fl)Cre- (wild type) and PPARgamma E-null mice were examined for changes in systolic blood pressure (BP) and heart rate (HR), untreated, after 2 months of salt-loading (drinking water), and after treatment for 3 months with high fat (HF) diet alone or supplemented during the last 2 weeks with rosiglitazone (3 mg/kg/d). RESULTS: Untreated PPARgamma E-nulls were phenotypically indistinguishable from wild-type littermates. However, compared to similarly treated wild types, HF-treated PPARgamma E-nulls had significantly elevated systolic BP not seen after normal diet or salt-loading. Despite sex-dependent baseline differences, salt-loaded and HF-treated PPARgamma E-nulls of either sex had significantly elevated HR versus wild types. Interestingly, rosiglitazone improved serum insulin levels, but not HF diet-induced hypertension, in PPARgamma E-null mice. CONCLUSIONS: These results suggest that PPARgamma in ECs not only is an important regulator of hypertension and HR under stressed conditions mimicking those arising in type 2 diabetics, but also mediates the antihypertensive effects of rosiglitazone. These data add evidence supporting a beneficial role for PPARgamma-specific ligands in the treatment of hypertension, and suggest therapeutic strategies targeting ECs may prove useful.  
  Address Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0895-7061 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:15831367 Approved no  
  Call Number refbase @ user @ Serial 69  
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Author Morley, K.I.; Montgomery, G.W. openurl 
  Title The genetics of cognitive processes: candidate genes in humans and animals Type Journal Article
  Year 2001 Publication (up) Behavior Genetics Abbreviated Journal Behav Genet  
  Volume 31 Issue 6 Pages 511-531  
  Keywords Animals; *Chromosome Mapping; Drosophila melanogaster; Genetic Markers/*genetics; Humans; Intelligence/*genetics; Mental Retardation/genetics; Mice; Phenotype; Quantitative Trait, Heritable  
  Abstract It has been hypothesized that numerous genes contribute to individual variation in human cognition. An extensive search of the scientific literature was undertaken to identify candidate genes which might contribute to this complex trait. A list of over 150 candidate genes that may influence some aspect of cognition was compiled. Some genes are particularly strong candidates based on evidence for involvement in cognitive processes in humans, mice, and Drosophila melanogaster. This survey confirms that many genes are associated with cognitive variation and highlights the potential importance of animal models in the study of human cognition.  
  Address Genetic Epidemiology Laboratory, Queensland Institute of Medical Research, Brisbane, Australia  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0001-8244 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:11838530 Approved no  
  Call Number Equine Behaviour @ team @ Serial 4141  
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Author McClearn, G.E. openurl 
  Title Behavioral genetics Type Journal Article
  Year 1971 Publication (up) Behavioral Science Abbreviated Journal Behav Sci  
  Volume 16 Issue 1 Pages 64-81  
  Keywords Amino Acid Metabolism, Inborn Errors; Animals; Aptitude; Behavior, Animal; Chromosome Aberrations; Cognition; Cytogenetics; Female; *Genetics, Behavioral; Genetics, Population; Humans; Intelligence; Mental Retardation; Mice; Models, Biological; Personality; Phenylketonurias; Pregnancy; Research; Schizophrenia; Sex Chromosome Aberrations; Twins  
  Abstract  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0005-7940 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:5105941 Approved no  
  Call Number Equine Behaviour @ team @ Serial 4150  
Permanent link to this record
 

 
Author Arakawa, H.; Arakawa, K.; Blanchard, D.C.; Blanchard, R.J. url  doi
openurl 
  Title A new test paradigm for social recognition evidenced by urinary scent marking behavior in C57BL/6J mice Type Journal Article
  Year 2008 Publication (up) Behavioural Brain Research Abbreviated Journal Behav. Brain. Res.  
  Volume 190 Issue 1 Pages 97-104  
  Keywords Social recognition; Urine marking; Familiarity; Context recognition; C57BL/6J mice  
  Abstract Olfaction is a major sensory element in intraspecies recognition and communication in mice. The present study investigated scent marking behaviors of males of the highly inbred C57BL/6J (C57) strain in order to evaluate the ability of these behaviors to provide clear and consistent measures of social familiarity and response to social signals. C57 males engage in scent marking when placed in a chamber with a wire mesh partition separating them from a conspecific. Male mice (C57 or outbred CD-1 mice) showed rapid habituation of scent marking (decreased marking over trials) with repeated exposure at 24-h intervals, to a stimulus animal of the C57 or CD-1 strains, or to an empty chamber. Subsequent exposure to a genetically different novel mouse (CD-1 after CD-1 exposure, or CD-1 after C57 exposure) or to a novel context (different shaped chamber) produced recovery of marking, while responses to a novel but genetically identical mouse (C57 after C57 exposure) or to the empty chamber did not. This finding demonstrated that male mice differentiate familiar and novel conspecifics as expressed by habituation and recovery of scent marking, but neither C57 or CD-1 mice can differentiate new vs. familiar C57 males; likely due to similarities in their odor patterns. The data also indicate that scent marking can differentiate novel from familiar contexts.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number Equine Behaviour @ team @ Serial 4639  
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Author Yamada, T.; Rojanasuphot, S.; Takagi, M.; Wungkobkiat, S.; Hirota, T. openurl 
  Title Studies on an epidemic of Japanese encephalitis in the northern region of Thailand in 1969 and 1970 Type Journal Article
  Year 1971 Publication (up) Biken Journal Abbreviated Journal Biken J  
  Volume 14 Issue 3 Pages 267-296  
  Keywords Adolescent; Adult; Animals; Arboviruses/immunology; Buffaloes; Cattle; Chickens; Child; Child, Preschool; Cross Reactions; Culicidae; Dengue Virus/immunology; Disease Outbreaks; Ducks; Ecology; Encephalitis Virus, Japanese/immunology/isolation & purification; Encephalitis, Japanese/cerebrospinal fluid/*epidemiology/immunology/microbiology/mortality; Female; Hemagglutination Inhibition Tests; Hemorrhagic Fevers, Viral/epidemiology; Horses; Humans; Infant; Male; Mice; Neutralization Tests; Swine; Thailand  
  Abstract  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0006-2324 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:4400462 Approved no  
  Call Number Equine Behaviour @ team @ Serial 2728  
Permanent link to this record
 

 
Author Cheung, C.; Akiyama, T.E.; Ward, J.M.; Nicol, C.J.; Feigenbaum, L.; Vinson, C.; Gonzalez, F.J. doi  openurl
  Title Diminished hepatocellular proliferation in mice humanized for the nuclear receptor peroxisome proliferator-activated receptor alpha Type Journal Article
  Year 2004 Publication (up) Cancer research Abbreviated Journal Cancer Res  
  Volume 64 Issue 11 Pages 3849-3854  
  Keywords Animals; Anticholesteremic Agents/pharmacology; Carcinogens/pharmacology; Cell Division; DNA Replication/drug effects; Fatty Acids/metabolism; Hepatocytes/cytology/drug effects/metabolism/*physiology; Humans; Mice; Mice, Transgenic; Oxidation-Reduction; Peroxisome Proliferators/pharmacology; Pyrimidines/pharmacology; Receptors, Cytoplasmic and Nuclear/genetics/*physiology; Species Specificity; Transcription Factors/genetics/*physiology  
  Abstract Lipid-lowering fibrate drugs function as agonists for the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha). Sustained activation of PPARalpha leads to the development of liver tumors in rats and mice. However, humans appear to be resistant to the induction of peroxisome proliferation and the development of liver cancer by fibrate drugs. The molecular basis of this species difference is not known. To examine the mechanism determining species differences in peroxisome proliferator response between mice and humans, a PPARalpha-humanized mouse line was generated in which the human PPARalpha was expressed in liver under control of the tetracycline responsive regulatory system. The PPARalpha-humanized and wild-type mice responded to treatment with the potent PPARalpha ligand Wy-14643 as revealed by induction of genes encoding peroxisomal and mitochondrial fatty acid metabolizing enzymes and resultant decrease of serum triglycerides. However, surprisingly, only the wild-type mice and not the PPARalpha-humanized mice exhibited hepatocellular proliferation as revealed by elevation of cell cycle control genes, increased incorporation of 5-bromo-2'-deoxyuridine into hepatocyte nuclei, and hepatomegaly. These studies establish that following ligand activation, the PPARalpha-mediated pathways controlling lipid metabolism are independent from those controlling the cell proliferation pathways. These findings also suggest that structural differences between human and mouse PPARalpha are responsible for the differential susceptibility to the development of hepatocarcinomas observed after treatment with fibrates. The PPARalpha-humanized mice should serve as models for use in drug development and human risk assessment and to determine the mechanism of hepatocarcinogenesis of peroxisome proliferators.  
  Address Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0008-5472 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:15172993 Approved no  
  Call Number refbase @ user @ Serial 74  
Permanent link to this record
 

 
Author Nicol, C.J.; Yoon, M.; Ward, J.M.; Yamashita, M.; Fukamachi, K.; Peters, J.M.; Gonzalez, F.J. doi  openurl
  Title PPARgamma influences susceptibility to DMBA-induced mammary, ovarian and skin carcinogenesis Type Journal Article
  Year 2004 Publication (up) Carcinogenesis Abbreviated Journal Carcinogenesis  
  Volume 25 Issue 9 Pages 1747-1755  
  Keywords 9,10-Dimethyl-1,2-benzanthracene/*toxicity; Animals; DNA Primers/chemistry; Disease Susceptibility; Female; Heterozygote; Humans; Mammary Neoplasms, Experimental/chemically induced/*pathology; Mice; Ovarian Neoplasms/chemically induced/*pathology; RNA, Messenger/genetics/metabolism; Receptors, Cytoplasmic and Nuclear/genetics/*physiology; Reverse Transcriptase Polymerase Chain Reaction; Skin Neoplasms/chemically induced/*pathology; Survival Rate; Transcription Factors/genetics/*physiology; Zinc Fingers  
  Abstract Peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear receptor superfamily, plays a role in adipocyte differentiation, type II diabetes, macrophage response to inflammation and is suggested to influence carcinogen-induced colon cancer. Studies done in vitro and in vivo also revealed that PPARgamma ligands might promote differentiation and/or regression of mammary tumors. To directly evaluate the role of PPARgamma in mammary carcinogenesis, PPARgamma wild-type (+/+) or heterozygous (+/-) mice were administered 1 mg 7,12-dimethylbenz[a]anthracene (DMBA) by gavage once a week for 6 weeks and followed for a total of 25 weeks. Compared with congenic PPARgamma(+/+) littermate controls, PPARgamma(+/-) mice had early evidence for increased susceptibility to DMBA-mediated carcinogenesis based on a 1.6-fold increase in the percentage of mice with skin papillomas, as well as a 1.7-fold increase in the numbers of skin papillomas per mouse (P < 0.05). Similarly, PPARgamma(+/-) mice also had a 1.5-fold decreased survival rate (P = 0.059), and a 1.7-fold increased incidence of total tumors per mouse (P < 0.01). Moreover, PPARgamma(+/-) mice had an almost 3-fold increase in mammary adenocarcinomas (P < 0.05), an over 3-fold increase in ovarian granulosa cell carcinomas (P < 0.05), an over 3-fold increase in malignant tumors (P < 0.02) and a 4.6-fold increase in metastatic incidence. These results are the first to demonstrate an increased susceptibility in vivo of PPARgamma haploinsufficiency to DMBA-mediated carcinogenesis and suggest that PPARgamma may act as a tumor modifier of skin, ovarian and breast cancers. The data also support evidence suggesting a beneficial role for PPARgamma-specific ligands in the chemoprevention of mammary, ovarian and skin carcinogenesis.  
  Address Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0143-3334 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:15073042 Approved no  
  Call Number refbase @ user @ Serial 76  
Permanent link to this record
 

 
Author Crosby, M.B.; Zhang, J.; Nowling, T.M.; Svenson, J.L.; Nicol, C.J.; Gonzalez, F.J.; Gilkeson, G.S. doi  openurl
  Title Inflammatory modulation of PPAR gamma expression and activity Type Journal Article
  Year 2006 Publication (up) Clinical immunology Abbreviated Journal Clin Immunol  
  Volume 118 Issue 2-3 Pages 276-283  
  Keywords Age Factors; Animals; Cell Line, Transformed; Cells, Cultured; Female; Inflammation Mediators/*physiology; Kidney/metabolism; Mesangial Cells/metabolism; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred MRL lpr; Mice, Knockout; Nitric Oxide/biosynthesis; Nitric Oxide Synthase Type II/biosynthesis/genetics; PPAR gamma/*biosynthesis/*genetics/metabolism; Up-Regulation/immunology  
  Abstract Nitric oxide (NO) production increases with age in the lupus-prone MRL/lpr mouse, paralleling disease activity. One mechanism for excess NO production in MRL/lpr mice may be a defect in down-regulatory mechanisms of the iNOS pathway. A potential modulator of NO is the nuclear hormone receptor peroxisome proliferation activated receptor gamma (PPARgamma). We demonstrate that renal PPARgamma protein expression was altered as disease progressed in MRL/lpr mice, which paralleled increased iNOS protein expression. Additionally, MRL/lpr-derived primary mesangial cells expressed less PPARgamma than BALB/c mesangial cells and produced more NO in response to LPS and IFNgamma. Furthermore, PPARgamma activity was reduced in mesangial cells following exposure to inflammatory mediators. This activity was restored with the addition of a NOS enzyme inhibitor. These results indicate that the activation of inflammatory pathways may lead to reduced activity and expression of PPARgamma, further exacerbating the disease state.  
  Address Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1521-6616 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:16303334 Approved no  
  Call Number refbase @ user @ Serial 67  
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