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Author |
Sufit, E.; Houpt, K.A.; Sweeting, M. |
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Title |
Physiological stimuli of thirst and drinking patterns in ponies |
Type |
Journal Article |
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Year |
1985 |
Publication |
Equine veterinary journal |
Abbreviated Journal |
Equine Vet J |
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Volume |
17 |
Issue |
1 |
Pages |
12-16 |
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Keywords |
Animals; Blood Proteins/analysis; Drinking Behavior/drug effects/*physiology; Furosemide/pharmacology; Horses/*physiology; Male; Osmolar Concentration; Osmotic Pressure; Sodium Chloride/pharmacology; Thirst/drug effects/*physiology; Time Factors; Water Deprivation/physiology |
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Abstract |
The stimuli that elicit thirst were studied in four ponies. Nineteen hours of water deprivation produced an increase in plasma protein from 67 +/- 0.1 g/litre to 72 +/- 2 g/litre, a mean (+/- se) increase in plasma sodium from 139 +/- 3 to 145 +/- 2 mmol/litre and an increase in plasma osmolality from 297 +/- 1 to 306 +/- 2 mosmol/litre. Undeprived ponies drank 1.5 +/- 0.9 kg/30 mins; 19 h deprived ponies drank 10.2 +/- 2.5 kg/30 mins and corrected the deficits in plasma protein, plasma sodium and plasma osmolality as well as compensating for the water they would have drunk during the deprivation period. In order to determine if an increase in plasma osmolality would stimulate thirst, 250 ml of 15 per cent sodium chloride was infused intravenously. The ponies drank when osmolality increased 3 per cent and when plasma sodium rose from 136 +/- 3 mmol/litre to 143 +/- 3 mmol/litre. Ponies infused with 15 per cent sodium chloride drank 2.9 +/- 0.7 kg; those infused with 0.9 per cent sodium chloride drank 0.7 +/- 0.5 kg. In order to determine if a decrease in plasma volume would stimulate thirst, ponies were injected with 1 or 2 mg/kg bodyweight (bwt) frusemide. Plasma protein rose from 68 +/- 2 g/litre pre-injection to 75 +/- 2 g/litre 1 h after 1 mg/kg bwt frusemide and to 81 +/- 1 g/litre 1 h after 2 mg/kg bwt frusemide.(ABSTRACT TRUNCATED AT 250 WORDS) |
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0425-1644 |
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PMID:3979367 |
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refbase @ user @ |
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56 |
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Author |
Houpt, K.A.; Wolski, T.R. |
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Title |
Stability of equine hierarchies and the prevention of dominance related aggression |
Type |
Journal Article |
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Year |
1980 |
Publication |
Equine veterinary journal |
Abbreviated Journal |
Equine Vet J |
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Volume |
12 |
Issue |
1 |
Pages |
15-18 |
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Keywords |
*Aggression; Animals; *Behavior, Animal; Feeding Behavior; Female; *Hierarchy, Social; *Horses; Humans; Male; Maternal Behavior; *Social Dominance |
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The dominance hierarchy of a herd of 10 Thoroughbred mares was determined twice, at an interval of 18 months, using paired feeding tests. Each mare's rank was correlated significantly between the 2 tests. This indicated that the hierarchy within the herd was stable. The offspring of dominant and subordinate mares were also tested for dominance in their own age groups. The offspring of dominant mares tended to be near the top of the hierarchy while those of middle and low ranking mares were not consistently found in the middle or bottom of their own hierarchies. Paired feeding tests were carried out on 8 ponies. During tests the time that each pony spent eating and the ponies' aggressive interactions were recorded. Two situations were used. Each pony-pair was tested when both ponies were in the same paddock and also when they were separated by a rail fence. The subordinate ponies spent significantly more time eating and the domonant pony was significantly less aggressive, when the pony-pair was separated by a fence than when they were in one paddock. It was concluded that the dominance hierarchies of adult horse groups changed very little over time and that the foals of dominant mares will tend to be dominant in their own age groups. Management practices can be used to reduce aggression and consequent injury that may arise in group feeding situations. |
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0425-1644 |
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PMID:7189148 |
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refbase @ user @ |
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59 |
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Author |
Houpt, K.A. |
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Title |
Animal behavior as a subject for veterinary students |
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Journal Article |
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Year |
1976 |
Publication |
The Cornell veterinarian |
Abbreviated Journal |
Cornell Vet |
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Volume |
66 |
Issue |
1 |
Pages |
73-81 |
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Keywords |
Aggression; Animals; *Behavior, Animal; Cats; Chickens; Dogs; Education, Veterinary; Goats; Horses; Humans; Maternal Behavior; Mice; New York; Sexual Behavior, Animal; Sheep; Sleep; Social Behavior; Social Dominance; Swine |
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Knowledge of animal behavior is an important asset for the veterinarian; therefore a course in veterinary animal behavior is offered at the New York State College of Veterinary Medicine as an elective. The course emphasizes the behavior of those species of most interest to the practicing veterinarian: cats, dogs, horses, cows, pigs and sheep. Dominance heirarchies, animal communication, aggressive behavior, sexual behavior and maternal behavior are discussed. Play, learning, diurnal cycles of activity and sleep, and controls of ingestive behavior are also considered. Exotic and zoo animal behaviors are also presented by experts in these fields. The critical periods of canine development are related to the optimum management of puppies. The behavior of feral dogs and horses is described. The role of the veterinarian in preventing cruelty to animals and recognition of pain in animals is emphasized. Whenever possible behavior is observed in the laboratory or on film. |
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0010-8901 |
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PMID:767053 |
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no |
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Call Number |
refbase @ user @ |
Serial |
61 |
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Author |
Nicol, C.J.; Adachi, M.; Akiyama, T.E.; Gonzalez, F.J. |
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Title |
PPARgamma in endothelial cells influences high fat diet-induced hypertension |
Type |
Journal Article |
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Year |
2005 |
Publication |
American journal of hypertension : journal of the American Society of Hypertension |
Abbreviated Journal |
Am J Hypertens |
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Volume |
18 |
Issue |
4 Pt 1 |
Pages |
549-556 |
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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 |
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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. |
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Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA |
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0895-7061 |
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PMID:15831367 |
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refbase @ user @ |
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69 |
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Guo, G.L.; Moffit, J.S.; Nicol, C.J.; Ward, J.M.; Aleksunes, L.A.; Slitt, A.L.; Kliewer, S.A.; Manautou, J.E.; Gonzalez, F.J. |
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Title |
Enhanced acetaminophen toxicity by activation of the pregnane X receptor |
Type |
Journal Article |
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Year |
2004 |
Publication |
Toxicological sciences : an official journal of the Society of Toxicology |
Abbreviated Journal |
Toxicol Sci |
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Volume |
82 |
Issue |
2 |
Pages |
374-380 |
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Keywords |
Acetaminophen/pharmacokinetics/*toxicity; Analgesics, Non-Narcotic/pharmacokinetics/*toxicity; Animals; Aryl Hydrocarbon Hydroxylases/biosynthesis; Biotransformation; Blotting, Northern; Chromatography, High Pressure Liquid; Cytochrome P-450 CYP3A; Membrane Proteins; Mice; Mice, Knockout; Oxidoreductases, N-Demethylating/biosynthesis; Pregnenolone Carbonitrile/pharmacology; Receptors, Cytoplasmic and Nuclear/*drug effects; Receptors, Steroid/*drug effects; Sulfhydryl Compounds/metabolism |
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The pregnane X receptor (PXR) is a ligand-activated transcription factor and member of the nuclear receptor superfamily. Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Therefore, it was hypothesized that activation of PXR plays a major role in APAP-induced hepatotoxicity. Pretreatment with the PXR activator, pregnenolone 16alpha-carbonitrile (PCN), markedly enhanced APAP-induced hepatic injury, as revealed by increased serum ALT levels and hepatic centrilobular necrosis, in wild-type but not in PXR-null mice. Further analysis showed that following PCN treatment, PXR-null mice had lower CYP3A11 expression, decreased NAPQI formation, and increased maintenance of hepatic glutathione content compared to wild-type mice. Thus, these results suggest that PXR plays a critical role in APAP-induced hepatic toxicity, probably by inducing CYP3A11 expression and hence increasing bioactivation. |
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Laboratory of Metabolism, CCR, NCI, NIH, Bethesda, Maryland 20892, USA |
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1096-6080 |
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PMID:15456926 |
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no |
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refbase @ user @ |
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71 |
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Author |
Jeong, S.; Han, M.; Lee, H.; Kim, M.; Kim, J.; Nicol, C.J.; Kim, B.H.; Choi, J.H.; Nam, K.-H.; Oh, G.T.; Yoon, M. |
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Title |
Effects of fenofibrate on high-fat diet-induced body weight gain and adiposity in female C57BL/6J mice |
Type |
Journal Article |
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Year |
2004 |
Publication |
Metabolism: clinical and experimental |
Abbreviated Journal |
Metabolism |
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Volume |
53 |
Issue |
10 |
Pages |
1284-1289 |
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Keywords |
Adipose Tissue/*anatomy & histology/drug effects; Animals; Antilipemic Agents/*pharmacology; Body Composition/*drug effects; Body Weight/drug effects; Dietary Fats/*pharmacology; Eating/drug effects; Fatty Acids/metabolism; Female; Gene Expression Regulation/drug effects; Leptin/metabolism; Liver/metabolism; Mice; Mice, Inbred C57BL; Ovariectomy; Procetofen/*pharmacology; RNA, Messenger/biosynthesis/genetics; Receptors, Cytoplasmic and Nuclear/biosynthesis/genetics/metabolism; Transcription Factors/biosynthesis/genetics/metabolism; Weight Gain/*drug effects |
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Our previous study suggested that fenofibrate affects obesity and lipid metabolism in a sexually dimorphic manner in part through the differential activation of hepatic peroxisome proliferator-activated receptor alpha (PPARalpha) in male and female C57BL/6J mice. To determine whether fenofibrate reduces body weight gain and adiposity in female sham-operated (Sham) and ovariectomized (OVX) C57BL/6J mice, the effects of fenofibrate on not only body weight, white adipose tissue (WAT) mass, and food intake, but also the expression of both leptin and PPARalpha target genes were measured. Compared to their respective low-fat diet-fed controls, both Sham and OVX mice exhibited increases in body weight and WAT mass when fed a high-fat diet. Fenofibrate treatment decreased body weight gain and WAT mass in OVX, but not in Sham mice. Furthermore, fenofibrate increased the mRNA levels of PPARalpha target genes encoding peroxisomal enzymes involved in fatty acid beta-oxidation, and reduced apolipoprotein C-III (apo C-III) mRNA, all of which were expressed at higher levels in OVX compared to Sham mice. However, leptin mRNA levels were found to positively correlate with WAT mass, and food intake was not changed in either OVX or Sham mice following fenofibrate treatment. These results suggest that fenofibrate differentially regulates body weight and adiposity due in part to differences in PPARalpha activation, but not to differences in leptin production, between female OVX and Sham mice. |
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Department of Life Sciences, Mokwon University, Taejon, Korea |
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0026-0495 |
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PMID:15375783 |
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no |
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refbase @ user @ |
Serial |
72 |
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Author |
Crosby, M.B.; Svenson, J.L.; Zhang, J.; Nicol, C.J.; Gonzalez, F.J.; Gilkeson, G.S. |
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Title |
Peroxisome proliferation-activated receptor (PPAR)gamma is not necessary for synthetic PPARgamma agonist inhibition of inducible nitric-oxide synthase and nitric oxide |
Type |
Journal Article |
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Year |
2005 |
Publication |
The Journal of pharmacology and experimental therapeutics |
Abbreviated Journal |
J Pharmacol Exp Ther |
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Volume |
312 |
Issue |
1 |
Pages |
69-76 |
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Keywords |
Animals; Cell Line; Gene Expression/drug effects; Macrophages/drug effects/metabolism; Mice; Mice, Inbred C57BL; Nitric Oxide/*metabolism; Nitric Oxide Synthase/*metabolism; Nitric Oxide Synthase Type II; PPAR delta/metabolism; PPAR gamma/*agonists/deficiency; Thiazolidinediones/pharmacology |
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Peroxisome proliferation-activated receptor (PPAR)gamma agonists inhibit inducible nitric-oxide synthase (iNOS), tumor necrosis factor-alpha, and interleukin-6. Because of these effects, synthetic PPARgamma agonists, including thiazolidinediones, are being studied for their impact on inflammatory disease. The anti-inflammatory concentrations of synthetic PPARgamma agonists range from 10 to 50 microM, whereas their binding affinity for PPARgamma is in the nanomolar range. The specificity of synthetic PPARgamma agonists for PPARgamma at the concentrations necessary for anti-inflammatory effects is thus in question. We report that PPARgamma is not necessary for the inhibition of iNOS by synthetic PPARgamma agonists. RAW 264.7 macrophages possess little PPARgamma, yet lipopolysaccharide (LPS)/interferon (IFN)gamma-induced iNOS was inhibited by synthetic PPARgamma agonists at 20 microM. Endogenous PPARgamma was inhibited by the transfection of a dominant-negative PPARgamma construct into murine mesangial cells. In the transfected cells, synthetic PPARgamma agonists inhibited iNOS production at 10 microM, similar to nontransfected cells. Using cells from PPARgamma Cre/lox conditional knockout mice, baseline and LPS/IFNgamma-induced nitric oxide levels were higher in macrophages lacking PPARgamma versus controls. However, synthetic PPARgamma agonists inhibited iNOS at 10 microM in the PPARgamma-deficient cells, similar to macrophages from wild-type mice. These results indicate that PPARgamma is not necessary for inhibition of iNOS expression by synthetic PPARgamma agonists at concentrations over 10 microM. Intrinsic PPARgamma function, in the absence of synthetic agonists, however, may play a role in inflammatory modulation. |
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Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA |
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0022-3565 |
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PMID:15356214 |
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refbase @ user @ |
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73 |
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Nicol, C.J.; Yoon, M.; Ward, J.M.; Yamashita, M.; Fukamachi, K.; Peters, J.M.; Gonzalez, F.J. |
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Title |
PPARgamma influences susceptibility to DMBA-induced mammary, ovarian and skin carcinogenesis |
Type |
Journal Article |
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Year |
2004 |
Publication |
Carcinogenesis |
Abbreviated Journal |
Carcinogenesis |
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25 |
Issue |
9 |
Pages |
1747-1755 |
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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 |
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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. |
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Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA |
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0143-3334 |
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PMID:15073042 |
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no |
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Call Number |
refbase @ user @ |
Serial |
76 |
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Permanent link to this record |
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Nicol, C.J.; Potzsch, C.; Lewis, K.; Green, L.E. |
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Matched concurrent case-control study of risk factors for feather pecking in hens on free-range commercial farms in the UK |
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Journal Article |
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Year |
2003 |
Publication |
British poultry science |
Abbreviated Journal |
Br Poult Sci |
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Volume |
44 |
Issue |
4 |
Pages |
515-523 |
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*Aggression; Analysis of Variance; Animal Husbandry/methods; Animals; Case-Control Studies; Chickens/*physiology; Feathers; Female; Multivariate Analysis; Odds Ratio; Regression Analysis; Species Specificity |
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1. The aim of the study was to compare the management and husbandry of free-range flocks in the UK where feather pecking was either present (case) or absent (control). 2. One hundred flocks were enrolled into a concurrent case-control study: 50 where birds had recently started feather pecking, and 50 matched control flocks where birds of the same age had not started feather pecking. 3. Information was obtained from a detailed interview with the flock manager, and by direct inspection of the flock, house and range. 4. Initial univariate analyses revealed that case flocks were more likely to comprise ISA Brown than Lohmann, were more likely to be restricted from litter areas to prevent floor eggs, and were less likely to use the outside range. 5. Cluster analysis indicated that feather pecking was not associated with any particular husbandry system. 6. The only influential risk factor significant in the multivariable conditional logistic regression analysis was use of the outdoor range. The risk of feather pecking was reduced 9-fold in flocks where more than 20% of birds used the range on sunny days (odds ratio = 0.12). Use of the range was positively associated with the presence of trees and/or hedges on the range. |
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Department of Clinical Veterinary Science, University of Bristol, England. c.j.nicol@bris.ac.uk |
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0007-1668 |
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PMID:14584840 |
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79 |
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Author |
Albentosa, M.J.; Kjaer, J.B.; Nicol, C.J. |
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Strain and age differences in behaviour, fear response and pecking tendency in laying hens |
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Journal Article |
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2003 |
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British poultry science |
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Br Poult Sci |
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44 |
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3 |
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333-344 |
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Age Factors; Aggression/*physiology; Animal Husbandry; Animals; *Behavior, Animal; Breeding; Chickens/genetics/*physiology; Fear/*physiology; Feathers/*injuries; Female; Housing, Animal; Population Density; Social Behavior |
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Abstract |
1. Behaviours associated with a high or low tendency to feather peck could be used as predictors of feather pecking behaviour in selective breeding programmes. This study investigated how strain and age at testing influenced responses in behavioural tests. 2. Four layer-type strains (ISA Brown, Columbian Blacktail, Ixworth and a high feather pecking (HP) and a low feather pecking (LP) line of White Leghorn) were reared in 6 same-strain/line pens of 8 birds from one day old. Birds in half the pens were given an open field test, a novel object test and a test with loose feather bundles between 4 and 12 weeks of age and a tonic immobility (TI) test at 13 weeks of age. All pens were tested with fixed feather bundles at 26 weeks, and undisturbed behaviour in the home pens was videoed at 1 and 27 weeks of age. Daily records of plumage damage were used as an indicator of feather pecking activity in the home pens. 3. Strain did not influence novel object test, open field test or loose feather test behaviour, although age effects in all three tests indicated a reduction in fearfulness and/or an increase in exploratory behaviour with increasing age. 4. White Leghorns showed longer TI durations than the other strains but less pecking at fixed feather bundles than ISA Browns and Columbian Blacktails. 5. There were few associations between behaviour in the 5 different tests, indicating that birds did not have overall behavioural traits that were consistent across different contexts. This suggests hens cannot easily be categorised into different behavioural 'types', based on their test responses and casts doubt on the usefulness of tests as predictors of feather pecking. |
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Centre for Behavioural Biology, Division of Farm Animal Science, University of Bristol, Langford, Bristol, England. MAlbentosa@lincoln.ac.uk |
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0007-1668 |
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PMID:13677322 |
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refbase @ user @ |
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80 |
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