Browsing by Subject "Other Veterinary Medicine"
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Item An Analytical Study of the Perceptions, Prevention Strategies, Treatment and Economic Impact of Equine West Nile Virus(2004-06-01) Galvan, Robert; Lurie, Sue; Singh, Karan; Gonzalez, AdelaGalvan, Robert, M.P.H., M.S. An Analytical Study of the Perceptions, Prevention Strategies, Treatment and Economic Impact of Equine West Nile Virus. Doctor of Public Health, Social and Behavioral Sciences, June 2004, 109 pp., 16 Tables, 15 Figures, 47 Titles. Since the introduction of the West Nile Virus (WNV) in the United State in 1999, WNV has been the cause of disease and deaths in humans, wild birds, zoo birds, and horses. In 2002, more than 15,000 equines in 40 states were diagnosed with illness associated with WNV. Approximately one third of those horses died or were euthanized (Campbell et al, 2002). Horses are infected with the WNV more often than humans or any other mammal. It is becoming on e of the fastest growing health threats to horses nationwide. Texas responded to the discovery of WNV by expanding their surveillance systems in the eastern counties of the state (Texas Department of Health, 2003). Positive reports for WNV were announced in 2002, which prompted an increase in public education and equine vaccination recommendations. Although much has been reported on the economic impact WNV has on human health and hospital care facilities, documentation is lacking on these issues in the equine population. Understanding the biology, epidemiology, economic impact, and how WNV affects the equine industry are important aspects to public health programs and prevention activities. The objectives of this study are to: (1) examine WNV cases in the equine population in Texas in order to better understand the distribution of clinical disease, signs, treatments and outcomes; (2) to provide information regarding the perceptions, knowledge, concerns, and treatment of the WNV by Texas veterinarians; and (3) to determine the economic impact of the WNV on the equine population in the state. A 14 question survey was mailed to licensed veterinarians in Texas in an effort to gather information about their perceptions and beliefs of the WNV, recommended treatment preferences, and the estimated cost of treatment. Outcomes included case fatality rate, descriptive data, veterinarians’ knowledge of WNV, veterinarians’ beliefs/perceptions of WNV, and the economic impact of WNV. Descriptive analyses were performed by using SPSS version 11. The methods used for analysis of WNV data were primarily simple descriptive statistics including summations and frequencies. A cross-tabulation was performed between the results of Questions 1, 2, and 3 and a variable created to approximate the number of veterinarians that actually treated cases of WNV (treat). A cross-tabulation and Chi-square analysis was performed between the treatment variables (treat) and derived variables of Questions 1, 2, and 3 to examine differing beliefs and knowledge between veterinarians who had treated WNV and those who had not. Seven hundred of 4,177 surveys returned yielded a response rate of 16.8 percent. Among the veterinarians, 73.4% (514/691) believed that they are receiving or received enough training and/or education concerning WNV. The vaccination regimen is believed to be effective and reliable by 56.1% (393/691) of the respondents. There were 1,256 cases of equine WNV reported confirmed via laboratory testing. There were also 766 cases reported that were not confirmed via laboratory testing. Among the 2,022 diagnosed cases, 257 were vaccinated against WNV prior to illness; and, 159 cases were vaccinated after signs of illness. A total of 441 horses died as either a direct cause of the disease or by owner or veterinarian elected euthanasia. The most common criteria used to decide euthanasia in these horses was prolonged recumbency as reported by 44.2% (87/197) or the veterinarians. Fifty-two percent (233/488) of the veterinarians did not recommend prevention strategies to equine owners. The cost of vaccination regimen was reported by 63% (269/434) of the veterinarians to be $25 or less. The results of the survey suggest that there could be a need for WVN education among veterinarians in areas of prevention, control, and treatment. Future studies should be conducted to examine owner perceptions, knowledge and beliefs of WNV vaccinations and prevention strategies. Values for lost horses were not solicited in the survey, thus, a total economic impact could not be completely estimated. However, a formula to approximate the aggregate economic impact of the WNV on the Texas equine industry was employed.Item Mechanistic Studies of the Sheep Liver 6-Phosphogluconate Dehydrogenase and cDNA Cloning(1996-07-01) Price, Nancy E.; Neeraj Agarwal; Robert Easom; Stephen R. GrantPrice, Nancy E., Mechanistic Studies of the Sheep Liver 6-Phosphogluconate Dehydrogenase and cDNA Cloning. Doctor of Philosophy (Biomedical Sciences), July, 1996, 124 pp., 5 tables, 28 Figures, 2 appendices, bibliography, 45 titles. A kinetic characterization of sheep liver 6-phosphogluconate dehydrogenase including product and dead-end inhibition patterns, primary deuterium isotope effects, and the pH dependence of kinetic parameters has been completed in order to determine the kinetic mechanism, and chemical mechanism of the enzyme. A rapid equilibrium random kinetic mechanism has been proposed, with product and dead-end inhibition patterns both being symmetric. Primary deuterium isotope effects were equal on V and V/K, confirming a rapid equilibrium mechanism, and indicate that hydride transfer is at least partially rate limiting in the overall reaction. The maximum velocity is pH dependent, decreasing at low and high pH with slopes of 1 and -1, respectively. The V/KNADP and V/K6PG also decrease at low and high pH with slopes of 1 and -1. The pH rate profiles are consistent with a general acid/general base mechanism where the catalytic residues are involved in binding. Reverse protonation states between the general acid and the general base is proposed where an unprotonated general base accepts a proton from the C-3 hydroxyl of 6PG concomitant with hydride transfer followed by decarboxylation of the resulting 3-keto intermediate to give an enediol which is protonated by the general acid to form ribulose-5-phosphate. The pH dependence of the pKi profile of the inhibitory analog 5-phosphoribonate decreases at low and high pH with slopes of 1, and -1 respectively, and suggests that intrinsic pKs are observed in the V/K profiles. The pKs of both the general base and general acid in the E:6PG complex appears to be perturbed such that the general base pK decreases slightly, and the pK of the general acid increases slightly, as a result of direct interaction with 6PG. Additionally, in preparation for site-directed mutagenesis, cDNA clones for sheep liver 6PHDH were obtained by RT-PCR.Item The Effects of Pyruvate on Oxidative Stress and Myocardial Energetics During Cardioplegic Arrest and Reperfusion(2005-10-01) Knott, E. Marty; Robert T. Mallet; James Caffrey; Jerry SimeckaKnott, E. Marty, The Effects of Pyruvate on Oxidative Stress and Myocardial Energetics During Cardioplegic Arrest and Reperfusion Doctor of Philosophy (Integrative Physiology), October 2005, 118 pp, 1 tables, 17 figures, references, 130 titles. Cardioplegic arrest for bypass surgery imposes global ischemia on the myocardium generating oxyradicals which contribute to post surgical cardiac dysfunction. Early clinical trials have demonstrated that pyruvate-fortified cardioplegia reduces myocardial energy and improves mechanical recovery in patients undergoing elective cardiopulmonary bypass for coronary artery bypass grafting. This study was designed to determine the effects of the natural carbohydrate, pyruvate, on oxidative stress, myocardial energy state, and activities of myocardial metabolic enzymes during and immediately following cardiopulmonary bypass. In the first set of experiments, in situ swine hearts were arrested for 60 min with a 4:1 mixture of blood and crystalloid cardioplegia solution containing 188 mM glucose alone (control) or with additional 23.8 mM lactate or 23.8 mM pyruvate, then reperfused for 3 min with cardioplegia-free blood. Glutathione redox state (GSH/GSSG) and phosphocreatine phosphorylation potential were determine from measurements of myocardial metabolites in left ventricular heart tissue snap frozen at 45 min arrest and 3 min reperfusion. Coronary sinus 8-isoprostane indexed oxidative stress. Pyruvate-fortified cardioplegia decreased oxidative stress, lowering 8-isoporstane content accumulate during arrest and reperfusion. Phosphorylation potential was maintained in all groups during arrest but fell upon reperfusion in the control and lactate and cardioplegia groups. Use of pyruvate cardioplegia during arrest prevented the decline in phosphorylation potential during reperfusion. Pyruvate cardioplegia doubled GSH/GSSG during arrest as compared to lactate, but GSH/GSSG fell during reperfusion all 3 groups. Pyruvate proved to be an effective antioxidant and energy yielding fuel in the setting of carioplegic arrest and reperfusion. From these data, we hypothesized that pyruvate would protect oxidant-sensitive enzymes from inactivation. To test this hypothesis, in situ swine hearts were arrested for 60 min with control cardioplegia and reperfused for 3 min with cardioplegia-free blood alone or with co-infusion c. 12 mM pyruvate. Activities of oxidant-sensitive enzymes, 8-isoprostane content, and energy and antioxidant metabolites were measured in left ventricular myocardium snap-frozen at 45 min arrest and 3 min reperfusion. At 3 min reperfusion, glutathione redox state fell by 70% while 8-isoprostane content increased 75%. Pyruvate administration during reperfusion suppressed oxidative stress, maintained glutathione redox state, and enhanced phosphocreatine phosphorylation potential. Aconitase and glucose 6-phosphate dehydrogenase activities fell during arrest; creatine kinase and phosphofructokinase were inactivated upon reperfusion. Pyruvate protected creatine kinase and reactivated aconitase, which are at least partially mitochondrial enzymes, but did not modify the cytosolic enzymes glucose 6-phosphofructokinase. We conclude that 1) pyruvate-fortified cardioplegia and administration of pyruvate during early perfusion increase the antioxidant state of the heart and reduce oxidative stress occurring as a result of cardioplegic arrest and reperfusion; 2) pyruvate bolsters the myocardial energy state during early reperfusion when administered during cardioplegic arrest or during reperfusion; 3) Cardioplegic arrest and reperfusion inactivated several key metabolic enzymes. Pyruvate administration during reperfusion, the period of most intense oxidative stress, increases the activity of two mitochondrial enzymes during early reperfusion when compared to control. These investigations provide likely mechanisms for the ability of pyruvate-fortified cardioplegia to reduce myocardial injury and improve post-surgical cardiac performance in patients undergoing CPB. More research must be done to solidify pyruvate’s role as a cardioprotective intervention during CPB.