Records |
Author |
McGreevy, P.D.; Richardson, J.D.; Nicol, C.J.; Lane, J.G. |
Title |
Radiographic and endoscopic study of horses performing an oral based stereotypy |
Type |
Journal Article |
Year |
1995 |
Publication |
Equine veterinary journal |
Abbreviated Journal |
Equine Vet J |
Volume |
27 |
Issue |
2 |
Pages |
92-95 |
Keywords |
Animals; Endoscopy/*veterinary; Esophagus/physiopathology/radiography; Female; Fluoroscopy/veterinary; Horse Diseases/physiopathology/*psychology/radiography; Horses; Male; Pharynx/physiopathology/radiography; *Stereotyped Behavior; Video Recording |
Abstract |
There is confusion in the veterinary literature concerning the definition of oral based stereotypies in the horse. This study reports the use of fluoroscopy and endoscopy during cribbiting/wind-sucking in afflicted horses. This permitted observations of movements of the pharyngeal and oesophageal tissues and of the air column within during the stereotypic behaviour. The findings reported show that the sequence of events during crib-biting/wind-sucking is not related to deglutition and that air is not swallowed to the stomach. Transient dilation of the upper oesophagus was recorded and the characteristic noise of wind-sucking coincided with the in-rush of air through the cricopharynx. The oesophageal distension was relieved when the air returned to the pharynx although small quantities passed caudally. It is proposed that the role of contraction of the strap muscles of the neck is to create a pressure gradient in the soft tissues surrounding the oesophagus which provokes movement of air from the pharynx into the oesophagus. The findings suggest that the definitions currently used in the sale of horses are in need of revision. |
Address |
Department of Clinical Veterinary Science, University of Bristol, Langford, UK |
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English |
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Edition |
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ISSN |
0425-1644 |
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Conference |
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Notes |
PMID:7607156 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
90 |
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Author |
McGreevy, P.D.; Nicol, C.J. |
Title |
Prevention of crib-biting: a review |
Type |
Journal Article |
Year |
1998 |
Publication |
Equine veterinary journal. Supplement |
Abbreviated Journal |
Equine Vet J Suppl |
Volume |
|
Issue |
27 |
Pages |
35-38 |
Keywords |
Animals; *Behavior, Animal; Horse Diseases/*prevention & control/psychology; Horses; *Stereotyped Behavior |
Abstract |
Crib-biting is a common oral stereotype. Because of perceived deleterious effects on the health and appearance of subjects the prevention of crib-biting is regularly attempted. The resourcefulness of horses in satisfying their motivation to perform this behaviour often frustrates owners' efforts at prevention. This paper reviews the efficacy and observable consequences of attempting to prevent crib-biting by a variety of methods. These include attempts to prevent the grasping of objects, to interfere with air-engulfing and to introduce punishment for grasping and neck-flexion. Other approaches include the use of surgery, acupuncture, pharmaceuticals, operant feeding and environmental enrichment. A remedy that is effective for every crib-biter remains elusive. We conclude that, rather than concentrating on remedial prevention, further research should be directed at establishing why horses crib-bite and how the emergence of crib-biting can be avoided. |
Address |
Department of Clinical Veterinary Science, University of Bristol, UK |
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English |
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Notes |
PMID:10485002 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
87 |
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Author |
McGreevy, P.D.; Nicol, C.J. |
Title |
The effect of short-term prevention on the subsequent rate of crib-biting in thoroughbred horses |
Type |
Journal Article |
Year |
1998 |
Publication |
Equine veterinary journal. Supplement |
Abbreviated Journal |
Equine Vet J Suppl |
Volume |
|
Issue |
27 |
Pages |
30-34 |
Keywords |
Analysis of Variance; Animals; *Behavior, Animal; Horse Diseases/*prevention & control/psychology; Horses; Male; Recurrence; *Stereotyped Behavior; Videotape Recording |
Abstract |
The results of an experimental study of the motivational consequences of short-term prevention of crib-biting are reported here. Eight test horses wore a cribbing collar for 24 h. This was effective in preventing crib-biting in 6 subjects. Using analysis of co-variance that accounted for baseline differences in crib-biting rate, test horses showed significantly more crib-biting than control horses on the first day after prevention (P < 0.05). There was also a highly significant increase in the crib-biting rate of test horses on the first day after prevention in comparison with their baseline rate (P < 0.01). This defines the increase as a post inhibitory rebound. An increase in the novelty of the cribbing bar and an increase in feeding motivation during the period of prevention are rejected as explanations of the rebound in this study. Instead, it is suggested that the rebound reflected a rise in internal motivation to crib-bite during the period of prevention. Behaviours that exhibit this pattern of motivation are generally considered functional; and it has been argued that their prevention may compromise welfare. |
Address |
Department of Clinical Veterinary Science, University of Bristol, UK |
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English |
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Notes |
PMID:10485001 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
88 |
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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. |
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 |
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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 |
0026-0495 |
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:15375783 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
72 |
Permanent link to this record |
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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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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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Conference |
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Notes |
PMID:16303334 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
67 |
Permanent link to this record |
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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 |
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English |
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ISSN |
0022-3565 |
ISBN |
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Conference |
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Notes |
PMID:15356214 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
73 |
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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 |
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English |
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Edition |
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ISSN |
1078-8956 |
ISBN |
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Notes |
PMID:15048110 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
77 |
Permanent link to this record |
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Author |
Gavrilova, O.; Haluzik, M.; Matsusue, K.; Cutson, J.J.; Johnson, L.; Dietz, K.R.; Nicol, C.J.; Vinson, C.; Gonzalez, F.J.; Reitman, M.L. |
Title |
Liver peroxisome proliferator-activated receptor gamma contributes to hepatic steatosis, triglyceride clearance, and regulation of body fat mass |
Type |
Journal Article |
Year |
2003 |
Publication |
The Journal of biological chemistry |
Abbreviated Journal |
J Biol Chem |
Volume |
278 |
Issue |
36 |
Pages |
34268-34276 |
Keywords |
Adipose Tissue/*metabolism; Animals; Blotting, Southern; Blotting, Western; Female; Hypoglycemia/genetics; Insulin Resistance/genetics; Lipid Metabolism; Liver/*metabolism; Liver Diseases/genetics/*metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; RNA/metabolism; Receptors, Cytoplasmic and Nuclear/*genetics/*physiology; Recombination, Genetic; Thiazoles/pharmacology; *Thiazolidinediones; Time Factors; Transcription Factors/*genetics/*physiology; Triglycerides/*metabolism |
Abstract |
Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a nuclear receptor that mediates the antidiabetic effects of thiazolidinediones. PPAR gamma is present in adipose tissue and becomes elevated in fatty livers, but the roles of specific tissues in thiazolidinedione actions are unclear. We studied the function of liver PPAR gamma in both lipoatrophic A-ZIP/F-1 (AZIP) and wild type mice. In AZIP mice, ablation of liver PPAR gamma reduced the hepatic steatosis but worsened the hyperlipidemia, triglyceride clearance, and muscle insulin resistance. Inactivation of AZIP liver PPAR gamma also abolished the hypoglycemic and hypolipidemic effects of rosiglitazone, demonstrating that, in the absence of adipose tissue, the liver is a primary and major site of thiazolidinedione action. In contrast, rosiglitazone remained effective in non-lipoatrophic mice lacking liver PPAR gamma, suggesting that adipose tissue is the major site of thiazolidinedione action in typical mice with adipose tissue. Interestingly, mice without liver PPAR gamma, but with adipose tissue, developed relative fat intolerance, increased adiposity, hyperlipidemia, and insulin resistance. Thus, liver PPAR gamma regulates triglyceride homeostasis, contributing to hepatic steatosis, but protecting other tissues from triglyceride accumulation and insulin resistance. |
Address |
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. oksanag@bdg10.niddk.nih.gov |
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English |
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Series Volume |
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Series Issue |
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Edition |
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ISSN |
0021-9258 |
ISBN |
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Conference |
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Notes |
PMID:12805374 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
81 |
Permanent link to this record |
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Author |
Haslam, S.M.; Brown, S.N.; Wilkins, L.J.; Kestin, S.C.; Warriss, P.D.; Nicol, C.J. |
Title |
Preliminary study to examine the utility of using foot burn or hock burn to assess aspects of housing conditions for broiler chicken |
Type |
Journal Article |
Year |
2006 |
Publication |
British poultry science |
Abbreviated Journal |
Br Poult Sci |
Volume |
47 |
Issue |
1 |
Pages |
13-18 |
Keywords |
Animal Husbandry; *Animal Welfare; Animals; Chickens; Dermatitis, Contact/diagnosis/pathology/*veterinary; Feathers; Female; Foot Diseases/diagnosis/pathology/*veterinary; *Housing, Animal; Male; Poultry Diseases/diagnosis/*pathology; Skin/pathology |
Abstract |
1. Eleven broiler chicken farms, representing 4 production system types, were visited during the last 5 d of the flock cycle: bird and flock details were recorded. Litter friability was assessed at 9 sites within the house, atmospheric ammonia was measured at three sites and bird cleanliness was assessed on a numerical rating scale. 2. For these flocks, hock burn, foot burn and breast burn were measured at the processing plant by standardised assessors. 3. Significant correlations were identified between the percentage of birds with foot burn and average litter score, average house ammonia concentrations and feather score. 4. No correlation was found between the percentage of birds with hock burn or breast burn and average litter scores, average ammonia concentrations or feather score. 5. No correlation was found between stocking density and foot burn, hock burn or breast burn.6. If confirmed, these findings may have implications for the draft EU Broiler Directive, for which it is proposed that permitted stocking density on farm may be determined by the incidence and severity of contact dermatitis measured on plant. |
Address |
Division of Farm Animal Science, School of Veterinary Science, University of Bristol, Bristol, England. sue.haslam@bris.ac.uk |
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English |
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ISSN |
0007-1668 |
ISBN |
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Notes |
PMID:16546791 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
66 |
Permanent link to this record |
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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 |
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English |
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Series Editor |
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Abbreviated Series Title |
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Series Volume |
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Edition |
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ISSN |
0041-008X |
ISBN |
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Conference |
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Notes |
PMID:16081118 |
Approved |
no |
Call Number |
refbase @ user @ |
Serial |
68 |
Permanent link to this record |