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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. |
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Title |
Molecular and biochemical mechanisms in teratogenesis involving reactive oxygen species |
Type |
Journal Article |
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Year |
2005 |
Publication |
Toxicology and applied pharmacology |
Abbreviated Journal |
Toxicol Appl Pharmacol |
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Volume |
207 |
Issue |
2 Suppl |
Pages |
354-366 |
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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. |
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Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada; Department of Pharmacology, University of Toronto, Toronto, Ontario, Canada |
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0041-008X |
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PMID:16081118 |
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no |
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Call Number |
refbase @ user @ |
Serial |
68 |
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Author |
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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Abstract |
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 |
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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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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. |
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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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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. |
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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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no |
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refbase @ user @ |
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73 |
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Author |
McGreevy, P.D.; Richardson, J.D.; Nicol, C.J.; Lane, J.G. |
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Title |
Radiographic and endoscopic study of horses performing an oral based stereotypy |
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Journal Article |
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Year |
1995 |
Publication |
Equine veterinary journal |
Abbreviated Journal |
Equine Vet J |
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Volume |
27 |
Issue |
2 |
Pages |
92-95 |
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Keywords |
Animals; Endoscopy/*veterinary; Esophagus/physiopathology/radiography; Female; Fluoroscopy/veterinary; Horse Diseases/physiopathology/*psychology/radiography; Horses; Male; Pharynx/physiopathology/radiography; *Stereotyped Behavior; Video Recording |
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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. |
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Department of Clinical Veterinary Science, University of Bristol, Langford, UK |
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0425-1644 |
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PMID:7607156 |
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no |
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Call Number |
refbase @ user @ |
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90 |
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Author |
Carroll, G.L.; Matthews, N.S.; Hartsfield, S.M.; Slater, M.R.; Champney, T.H.; Erickson, S.W. |
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Title |
The effect of detomidine and its antagonism with tolazoline on stress-related hormones, metabolites, physiologic responses, and behavior in awake ponies |
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Journal Article |
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Year |
1997 |
Publication |
Veterinary surgery : VS : the official journal of the American College of Veterinary Surgeons |
Abbreviated Journal |
Vet Surg |
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Volume |
26 |
Issue |
1 |
Pages |
69-77 |
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Adrenergic alpha-Antagonists/administration & dosage/*pharmacology; Animals; Behavior, Animal/drug effects/physiology; Blood Glucose/metabolism; Blood Pressure/drug effects/physiology; Consciousness/physiology; Dose-Response Relationship, Drug; Drug Interactions; Epinephrine/blood; Fatty Acids, Nonesterified/blood; Female; Heart Rate/drug effects/physiology; Horse Diseases/metabolism/physiopathology/psychology; Horses/blood/metabolism/*physiology; Hydrocortisone/blood; Hypnotics and Sedatives/administration & dosage/*pharmacology; Imidazoles/administration & dosage/*pharmacology; Injections, Intravenous; Male; Norepinephrine/blood; Receptors, Adrenergic, alpha/drug effects/*physiology; Stress/metabolism/physiopathology/veterinary; Time Factors; Tolazoline/administration & dosage/*pharmacology |
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Six ponies were used to investigate the effect of tolazoline antagonism of detomidine on physiological responses, behavior, epinephrine, norepinephrine, cortisol, glucose, and free fatty acids in awake ponies. Each pony had a catheter inserted into a jugular vein 1 hour before beginning the study. Awake ponies were administered detomidine (0.04 mg/kg intravenously [i.v.]) followed 20 minutes later by either tolazoline (4.0 mg/kg i.v.) or saline. Blood samples were drawn from the catheter 5 minutes before detomidine administration (baseline), 5 minutes after detomidine administration, 20 minutes before detomidine administration which was immediately before the administration of tolazoline or saline (time [T] = 0), and at 5, 30, and 60 minutes after injections of tolazoline or saline (T = 5, 30, and 60 minutes, respectively). Compared with heart rate at T = 0, tolazoline antagonism increased heart rate 45% at 5 minutes. There was no difference in heart rate between treatments at 30 minutes. Blood pressure remained stable after tolazoline, while it decreased over time after saline. Compared with concentrations at T = 0, tolazoline antagonism of detomidine in awake ponies resulted in a 55% increase in cortisol at 30 minutes and a 52% increase in glucose at 5 minutes. The change in free fatty acids was different for tolazoline and saline over time. Free fatty acids decreased after detomidine administration. Free fatty acids did not change after saline administration. After tolazoline administration, free fatty acids increased transiently. Tolazoline tended to decrease sedation and analgesia at 15 and 60 minutes postantagonism. Antagonism of detomidine-induced physiological and behavioral effects with tolazoline in awake ponies that were not experiencing pain appears to precipitate a stress response as measured by cortisol, glucose, and free fatty acids. If antagonism of an alpha-agonist is contemplated, the potential effect on hormones and metabolites should be considered. |
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Department of Small Animal Medicine and Surgery, Texas A&M University, College Station, USA |
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ISSN |
0161-3499 |
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Notes |
PMID:9123816 |
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no |
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Call Number |
refbase @ user @ |
Serial |
96 |
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Author |
Grubb, T.L.; Foreman, J.H.; Benson, G.J.; Thurmon, J.C.; Tranquilli, W.J.; Constable, P.D.; Olson, W.O.; Davis, L.E. |
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Title |
Hemodynamic effects of calcium gluconate administered to conscious horses |
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Journal Article |
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Year |
1996 |
Publication |
Journal of veterinary internal medicine / American College of Veterinary Internal Medicine |
Abbreviated Journal |
J Vet Intern Med |
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Volume |
10 |
Issue |
6 |
Pages |
401-404 |
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Keywords |
Animals; Blood Pressure/drug effects/physiology; Calcium/blood; Calcium Gluconate/administration & dosage/*pharmacology; Cardiac Output/drug effects/physiology; Consciousness/*physiology; Dose-Response Relationship, Drug; Female; Heart Rate/drug effects/physiology; Hemodynamic Processes/*drug effects/physiology; Horses/blood/*physiology; Infusions, Intravenous; Male; Myocardial Contraction/drug effects/physiology; Respiration/drug effects/physiology; Stroke Volume/drug effects/physiology; Time Factors |
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Calcium gluconate was administered to conscious horses at 3 different rates (0.1, 0.2, and 0.4 mg/kg/min for 15 minutes each). Serum calcium concentrations and parameters of cardiovascular function were evaluated. All 3 calcium administration rates caused marked increases in both ionized and total calcium concentrations, cardiac index, stroke index, and cardiac contractility (dP/dtmax). Mean arterial pressure and right atrial pressure were unchanged; heart rate decreased markedly during calcium administration. Ionized calcium concentration remained between 54% and 57% of total calcium concentration throughout the study. We conclude that calcium gluconate can safely be administered to conscious horses at 0.1 to 0.4 mg/kg/min and that administration will result in improved cardiac function. |
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Department of Veterinary Clinical Medicine, University of Illinois at Urbana-Champaign, USA |
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ISSN |
0891-6640 |
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PMID:8947873 |
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no |
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Call Number |
refbase @ user @ |
Serial |
97 |
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Author |
Forster, H.V.; Pan, L.G.; Bisgard, G.E.; Flynn, C.; Hoffer, R.E. |
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Title |
Changes in breathing when switching from nares to tracheostomy breathing in awake ponies |
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Journal Article |
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Year |
1985 |
Publication |
Journal of applied physiology (Bethesda, Md. : 1985) |
Abbreviated Journal |
J Appl Physiol |
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Volume |
59 |
Issue |
4 |
Pages |
1214-1221 |
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Airway Resistance; Animals; Chemoreceptors/physiology; Consciousness; Exertion; Horses/*physiology; Lung Compliance; Pulmonary Gas Exchange; Pulmonary Stretch Receptors/physiology; *Respiration; Respiratory Dead Space; *Tracheotomy |
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Abstract |
We assessed the consequences of respiratory unloading associated with tracheostomy breathing (TBr). Three normal and three carotid body-denervated (CBD) ponies were prepared with chronic tracheostomies that at rest reduced physiological dead space (VD) from 483 +/- 60 to 255 +/- 30 ml and lung resistance from 1.5 +/- 0.14 to 0.5 +/- 0.07 cmH2O . l-1 . s. At rest and during steady-state mild-to-heavy exercise arterial PCO2 (PaCO2) was approximately 1 Torr higher during nares breathing (NBr) than during TBr. Pulmonary ventilation and tidal volume (VT) were greater and alveolar ventilation was less during NBr than TBr. Breathing frequency (f) did not differ between NBr and TBr at rest, but f during exercise was greater during TBr than during NBr. These responses did not differ between normal and CBD ponies. We also assessed the consequences of increasing external VD (300 ml) and resistance (R, 0.3 cmH2O . l-1 . s) by breathing through a tube. At rest and during mild exercise tube breathing caused PaCO2 to transiently increase 2-3 Torr, but 3-5 min later PaCO2 usually was within 1 Torr of control. Tube breathing did not cause f to change. When external R was increased 1 cmH2O . l-1 . s by breathing through a conventional air collection system, f did not change at rest, but during exercise f was lower than during unencumbered breathing. These responses did not differ between normal, CBD, and hilar nerve-denervated ponies, and they did not differ when external VD or R were added at either the nares or tracheostomy.(ABSTRACT TRUNCATED AT 250 WORDS) |
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ISSN |
8750-7587 |
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PMID:4055600 |
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no |
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Call Number |
refbase @ user @ |
Serial |
100 |
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Permanent link to this record |
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Author |
Kraus-Hansen, A.E.; Fackelman, G.E.; Becker, C.; Williams, R.M.; Pipers, F.S. |
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Title |
Preliminary studies on the vascular anatomy of the equine superficial digital flexor tendon |
Type |
Journal Article |
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Year |
1992 |
Publication |
Equine veterinary journal |
Abbreviated Journal |
Equine Vet J |
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Volume |
24 |
Issue |
1 |
Pages |
46-51 |
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Keywords |
Angiography/veterinary; Animals; Exercise Test/veterinary; Forelimb; Horses/*anatomy & histology/surgery; Microcirculation; Microscopy, Electron, Scanning; Tendons/*blood supply/surgery/ultrastructure |
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Abstract |
The vascular and microvascular anatomy of normal equine superficial digital flexor tendons was studied by dissection of vinyl-perfused specimens and by microangiography on high detail film. The presence of an extensive intratendinous vascular latticework was confirmed, and a 'nutrient artery' described closely associated with the accessory ligament of the superficial digital flexor tendon (proximal check ligament). Circumferential stripping of the paratenon from the tendon to eliminate afferent vessels was performed bilaterally in three horses and unilaterally in a fourth, followed by a treadmill training regimen. No resulting intratendinous lesions could be documented on gross post mortem and histological examination at three, 10, or 35 days post operatively. There was mild paratendinous proliferation in all instances. In one horse, four intratendinous ligatures were placed within the medial and lateral borders of the contralateral tendon to isolate further from its blood supply a 10 cm segment. Gross lesions at 35 days post operatively included a marked paratendinous response involving the entire 10 cm segment, and a darkened, soft focus within the core of the tendon. Histopathology and electron microscopy demonstrated focal degeneration. It was concluded that the blood supply of the normal equine superficial digital flexor tendon is primarily intratendinous, rather than paratendinous as previously thought. The lesions in one horse similar to those in naturally occurring tendinitis supported a vascular aetiology of the disease, and set the groundwork for studies aimed at the development of a clinically relevant tendinitis model. |
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Address |
Department of Surgery, Tufts University School of Veterinary Medicine, North Grafton, Massachusetts 01536 |
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0425-1644 |
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PMID:1555540 |
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refbase @ user @ |
Serial |
151 |
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Author |
de Waal, F.B.; Aureli, F.; Judge, P.G. |
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Title |
Coping with crowding |
Type |
Journal Article |
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Year |
2000 |
Publication |
Scientific American |
Abbreviated Journal |
Sci Am |
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Volume |
282 |
Issue |
5 |
Pages |
76-81 |
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Keywords |
*Adaptation, Psychological; Animals; Behavior, Animal; Emotions; Female; Grooming; Homicide; Humans; Macaca mulatta; Male; Pan troglodytes; *Population Density; Primates; Rodentia; Rural Population; Territoriality; Urban Population; Violence |
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Living Links Center, Yerkes Regional Primate Research Center, Atlanta, USA |
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English |
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ISSN |
0036-8733 |
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Notes |
PMID:11056991 |
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no |
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Call Number |
refbase @ user @ |
Serial |
184 |
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