| |
Records |
Links |
|
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. |
|
| |
Title |
Effects of fenofibrate on high-fat diet-induced body weight gain and adiposity in female C57BL/6J mice |
Type |
Journal Article |
| |
Year  |
2004 |
Publication |
Metabolism: clinical and experimental |
Abbreviated Journal |
Metabolism |
|
| |
Volume |
53 |
Issue |
10 |
Pages |
1284-1289 |
|
| |
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 |
|
| |
Abstract |
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. |
|
| |
Address |
Department of Life Sciences, Mokwon University, Taejon, Korea |
|
| |
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 |
0026-0495 |
ISBN |
|
Medium |
|
|
| |
Area |
|
Expedition |
|
Conference |
|
|
| |
Notes |
PMID:15375783 |
Approved |
no |
|
| |
Call Number |
refbase @ user @ |
Serial |
72 |
|
| Permanent link to this record |
| |
|
| |
|
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 |
|
| |
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. |
|
| |
Title |
Development, direction, and damage limitation: social learning in domestic fowl |
Type |
Journal Article |
| |
Year |
2004 |
Publication |
Learning & behavior : a Psychonomic Society publication |
Abbreviated Journal |
Learn Behav |
|
| |
Volume |
32 |
Issue |
1 |
Pages |
72-81 |
|
| |
Keywords |
Adaptation, Psychological; Age Factors; Animals; Behavior, Animal; *Chickens; *Feeding Behavior; *Food Preferences; *Imitative Behavior; Imprinting (Psychology); *Learning; Maternal Behavior; Reinforcement (Psychology); *Social Environment; *Social Facilitation |
|
| |
Abstract |
This review highlights two areas of particular interest in the study of social learning in fowl. First, the role of social learning in the development of feeding and foraging behavior in young chicks and older birds is described. The role of the hen as a demonstrator and possible teacher is considered, and the subsequent social influence of brood mates and other companions on food avoidance and food preference learning is discussed. Second, the way in which work on domestic fowl has contributed to an understanding of the importance of directed social learning is examined. The well-characterized hierarchical social organization of small chicken flocks has been used to design studies which demonstrate that the probability of social transmission is strongly influenced by social relationships between birds. The practical implications of understanding the role of social learning in the spread of injurious behaviors in this economically important species are briefly considered. |
|
| |
Address |
Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol, England. c.j.nicol@bristol.ac.uk |
|
| |
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 |
1543-4494 |
ISBN |
|
Medium |
|
|
| |
Area |
|
Expedition |
|
Conference |
|
|
| |
Notes |
PMID:15161142 |
Approved |
no |
|
| |
Call Number |
refbase @ user @ |
Serial |
75 |
|
| Permanent link to this record |
| |
|
| |
|
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 |
|
| |
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 |
Harman, F.S.; Nicol, C.J.; Marin, H.E.; Ward, J.M.; Gonzalez, F.J.; Peters, J.M. |
|
| |
Title |
Peroxisome proliferator-activated receptor-delta attenuates colon carcinogenesis |
Type |
Journal Article |
| |
Year |
2004 |
Publication |
Nature medicine |
Abbreviated Journal |
Nat Med |
|
| |
Volume |
10 |
Issue |
5 |
Pages |
481-483 |
|
| |
Keywords |
Animals; Azoxymethane/toxicity; Colonic Neoplasms/etiology/genetics/*prevention & control; Colonic Polyps/etiology/genetics/pathology/prevention & control; Disease Models, Animal; Mice; Mice, Knockout; Mice, Mutant Strains; Phenotype; Receptors, Cytoplasmic and Nuclear/deficiency/genetics/*physiology; Transcription Factors/deficiency/genetics/*physiology |
|
| |
Abstract |
Peroxisome proliferator-activated receptor-delta (PPAR-delta; also known as PPAR-beta) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-delta in colon carcinogenesis using PPAR-delta-deficient (Ppard(-/-)) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-delta. In contrast to previous reports suggesting that activation of PPAR-delta potentiates colon polyp formation, here we show that PPAR-delta attenuates colon carcinogenesis. |
|
| |
Address |
Department of Veterinary Science and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. jmp21@psu.edu |
|
| |
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 |
1078-8956 |
ISBN |
|
Medium |
|
|
| |
Area |
|
Expedition |
|
Conference |
|
|
| |
Notes |
PMID:15048110 |
Approved |
no |
|
| |
Call Number |
refbase @ user @ |
Serial |
77 |
|
| Permanent link to this record |
| |
|
| |
|
Author |
Wells, P.G.; Bhuller, Y.; Chen, C.S.; Jeng, W.; Kasapinovic, S.; Kennedy, J.C.; Kim, P.M.; Laposa, R.R.; McCallum, G.P.; Nicol, C.J.; Parman, T.; Wiley, M.J.; Wong, A.W. |
|
| |
Title |
Molecular and biochemical mechanisms in teratogenesis involving reactive oxygen species |
Type |
Journal Article |
| |
Year |
2005 |
Publication |
Toxicology and applied pharmacology |
Abbreviated Journal |
Toxicol Appl Pharmacol |
|
| |
Volume |
207 |
Issue |
2 Suppl |
Pages |
354-366 |
|
| |
Keywords |
|
|
| |
Abstract |
Developmental pathologies may result from endogenous or xenobiotic-enhanced formation of reactive oxygen species (ROS), which oxidatively damage cellular macromolecules and/or alter signal transduction. This minireview focuses upon several model drugs (phenytoin, thalidomide, methamphetamine), environmental chemicals (benzo[a]pyrene) and gamma irradiation to examine this hypothesis in vivo and in embryo culture using mouse, rat and rabbit models. Embryonic prostaglandin H synthases (PHSs) and lipoxygenases bioactivate xenobiotics to free radical intermediates that initiate ROS formation, resulting in oxidation of proteins, lipids and DNA. Oxidative DNA damage and embryopathies are reduced in PHS knockout mice, and in mice treated with PHS inhibitors, antioxidative enzymes, antioxidants and free radical trapping agents. Thalidomide causes embryonic DNA oxidation in susceptible (rabbit) but not resistant (mouse) species. Embryopathies are increased in mutant mice deficient in the antioxidative enzyme glucose-6-phosphate dehydrogenase (G6PD), or by glutathione (GSH) depletion, or inhibition of GSH peroxidase or GSH reductase. Inducible nitric oxide synthase knockout mice are partially protected. Inhibition of Ras or NF-kB pathways reduces embryopathies, implicating ROS-mediated signal transduction. Atm and p53 knockout mice deficient in DNA damage response/repair are more susceptible to xenobiotic or radiation embryopathies, suggesting a teratological role for DNA damage, consistent with enhanced susceptibility to methamphetamine in ogg1 knockout mice with deficient repair of oxidative DNA damage. Even endogenous embryonic oxidative stress carries a risk, since untreated G6PD- or ATM-deficient mice have increased embryopathies. Thus, embryonic processes regulating the balance of ROS formation, oxidative DNA damage and repair, and ROS-mediated signal transduction may be important determinants of teratological risk. |
|
| |
Address |
Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada; Department of Pharmacology, University of Toronto, Toronto, Ontario, Canada |
|
| |
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 |
0041-008X |
ISBN |
|
Medium |
|
|
| |
Area |
|
Expedition |
|
Conference |
|
|
| |
Notes |
PMID:16081118 |
Approved |
no |
|
| |
Call Number |
refbase @ user @ |
Serial |
68 |
|
| Permanent link to this record |
| |
|
| |
|
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 |
|
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 |
|
| Permanent link to this record |
| |
|
| |
|
Author |
Crosby, M.B.; Svenson, J.L.; Zhang, J.; Nicol, C.J.; Gonzalez, F.J.; Gilkeson, G.S. |
|
| |
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 |
| |
Year |
2005 |
Publication |
The Journal of pharmacology and experimental therapeutics |
Abbreviated Journal |
J Pharmacol Exp Ther |
|
| |
Volume |
312 |
Issue |
1 |
Pages |
69-76 |
|
| |
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 |
|
| |
Abstract |
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. |
|
| |
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 |
0022-3565 |
ISBN |
|
Medium |
|
|
| |
Area |
|
Expedition |
|
Conference |
|
|
| |
Notes |
PMID:15356214 |
Approved |
no |
|
| |
Call Number |
refbase @ user @ |
Serial |
73 |
|
| Permanent link to this record |
| |
|
| |
|
Author |
Abeyesinghe, S.M.; Nicol, C.J.; Hartnell, S.J.; Wathes, C.M. |
|
| |
Title |
Can domestic fowl, Gallus gallus domesticus, show self-control? |
Type |
Journal Article |
| |
Year |
2005 |
Publication |
Animal Behaviour. |
Abbreviated Journal |
Anim. Behav. |
|
| |
Volume |
70 |
Issue |
1 |
Pages |
1-11 |
|
| |
Keywords |
|
|
| |
Abstract |
An important aspect of cognition is whether animals live exclusively in the present or can anticipate the future. Defined as self-control, the ability to choose a large, remote reinforcer over a small, proximate reinforcer available at the same frequency has been examined in a number of species, often proving difficult to demonstrate. We investigated self-control for food in domestic fowl using a standard two-key operant task and an equivalent two-choice return maze (TCRM) task. When hens chose between a 2-s delay to a 3-s feed access (impulsive) and a 6-s delay to a 7-s feed access (self-control), they appeared unable to discriminate in the TCRM but were impulsive in the operant task. We explored reasons for not choosing self-control in the operant task, first by examining the relation between feed access time and actual feed intake. A second operant experiment examined whether failure to show self-control could be attributed to an inability to combine the delay and access (quantity) reward information associated with choices to reach overall predictions of value. New hens chose between a 2-s delay to a 3-s feed access (impulsive) and either a 22-s delay to a 22-s feed access (standard self-control) or a 6-s delay to a 22-s feed access (jackpot self-control). While hens were impulsive in the standard condition, they showed significant and pronounced self-control in the jackpot condition, eliminating the possibility of an absolute cognitive constraint. Impulsive behaviour can instead be explained by temporal discounting: perceived depreciation of reward value as a function of the uncertainty associated with delay. Implications for welfare are discussed. |
|
| |
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 |
2897 |
|
| Permanent link to this record |
| |
|
| |
|
Author |
Nicol, C.J.; Badnell-Waters, A.J. |
|
| |
Title |
Suckling behaviour in domestic foals and the development of abnormal oral behaviour |
Type |
Journal Article |
| |
Year |
2005 |
Publication |
Animal Behaviour. |
Abbreviated Journal |
Anim. Behav. |
|
| |
Volume |
70 |
Issue |
1 |
Pages |
21-29 |
|
| |
Keywords |
|
|
| |
Abstract |
We investigated how the behaviour of domestic foals, Equus caballus, living at pasture with their dams was associated with foal gender, mare rank and the development of abnormal oral behaviour, both during the preweaning period, and over a period of up to 4 years postweaning. A population of 186 foals belonging to private owners and commercial studs was studied. The behaviour of male and female foals hardly differed, but mare rank affected patterns of foal social interaction and suckling behaviour, with foals of subordinate mares involved in more affiliative interactions. These foals also spent more time in perisuckling activities such as teat nuzzling than foals of other mares. During the study, 18 foals developed abnormal oral behaviour before weaning and 42 foals developed abnormal oral behaviour after weaning. The development of abnormal oral behaviour was associated with suckling behaviour in a variety of ways. Foals that had already developed abnormal oral behaviour at the time of the preweaning observations were involved in more suckling terminations within bouts than normal foals or foals that developed future abnormal behaviour, and pushing the udder with the muzzle was most frequent in these foals. Foals that had no current abnormal oral behaviour, but that would develop this in the future, spent more time suckling and twice as much time teat nuzzling as other foals. The results add to the growing evidence of associations between digestive function and abnormal oral behaviour in horses. |
|
| |
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 |
3631 |
|
| Permanent link to this record |
