| Records |
| Author |
Boray, J.C. |
| Title |
Experimental fascioliasis in Australia |
Type |
Journal Article |
| Year |
1969 |
Publication  |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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| Series Editor |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
0065-308X |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:4935272 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2744 |
| Permanent link to this record |
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| Author |
Menges, R.W.; Furcolow, M.L.; Selby, L.A.; Habermann, R.T.; Smith, C.D. |
| Title |
Ecologic studies of histoplasmosis |
Type |
Journal Article |
| Year |
1967 |
Publication |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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| Series Editor |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
0002-9262 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| 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. |
| Title |
PPARgamma in endothelial cells influences high fat diet-induced hypertension |
Type |
Journal Article |
| Year |
2005 |
Publication |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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| Series Editor |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
0895-7061 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:15831367 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
69 |
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| Author |
Morley, K.I.; Montgomery, G.W. |
| Title |
The genetics of cognitive processes: candidate genes in humans and animals |
Type |
Journal Article |
| Year |
2001 |
Publication |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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| Series Editor |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
0001-8244 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:11838530 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
4141 |
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| Author |
McClearn, G.E. |
| Title |
Behavioral genetics |
Type |
Journal Article |
| Year |
1971 |
Publication |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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| Series Editor |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
0005-7940 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:5105941 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
4150 |
| Permanent link to this record |
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| Author |
Arakawa, H.; Arakawa, K.; Blanchard, D.C.; Blanchard, R.J. |
| Title |
A new test paradigm for social recognition evidenced by urinary scent marking behavior in C57BL/6J mice |
Type |
Journal Article |
| Year |
2008 |
Publication |
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. |
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Place of Publication |
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Editor |
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Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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ISBN |
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Medium |
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Expedition |
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Conference |
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| Notes |
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Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
4639 |
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| Author |
Yamada, T.; Rojanasuphot, S.; Takagi, M.; Wungkobkiat, S.; Hirota, T. |
| Title |
Studies on an epidemic of Japanese encephalitis in the northern region of Thailand in 1969 and 1970 |
Type |
Journal Article |
| Year |
1971 |
Publication |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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| Series Editor |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
0006-2324 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:4400462 |
Approved |
no |
| Call Number |
Equine Behaviour @ team @ |
Serial |
2728 |
| Permanent link to this record |
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| Author |
Cheung, C.; Akiyama, T.E.; Ward, J.M.; Nicol, C.J.; Feigenbaum, L.; Vinson, C.; Gonzalez, F.J. |
| Title |
Diminished hepatocellular proliferation in mice humanized for the nuclear receptor peroxisome proliferator-activated receptor alpha |
Type |
Journal Article |
| Year |
2004 |
Publication |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
0008-5472 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:15172993 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
74 |
| Permanent link to this record |
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| Author |
Nicol, C.J.; Yoon, M.; Ward, J.M.; Yamashita, M.; Fukamachi, K.; Peters, J.M.; Gonzalez, F.J. |
| Title |
PPARgamma influences susceptibility to DMBA-induced mammary, ovarian and skin carcinogenesis |
Type |
Journal Article |
| Year |
2004 |
Publication |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
0143-3334 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:15073042 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
76 |
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| Author |
Crosby, M.B.; Zhang, J.; Nowling, T.M.; Svenson, J.L.; Nicol, C.J.; Gonzalez, F.J.; Gilkeson, G.S. |
| Title |
Inflammatory modulation of PPAR gamma expression and activity |
Type |
Journal Article |
| Year |
2006 |
Publication |
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 |
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Thesis |
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Place of Publication |
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Editor |
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| Language |
English |
Summary Language |
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Original Title |
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| Series Editor |
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Series Title |
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Abbreviated Series Title |
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| Series Volume |
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Series Issue |
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Edition |
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| ISSN |
1521-6616 |
ISBN |
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Medium |
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| Area |
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Expedition |
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Conference |
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| Notes |
PMID:16303334 |
Approved |
no |
| Call Number |
refbase @ user @ |
Serial |
67 |
| Permanent link to this record |
