Browsing by Subject "Cardiovascular Diseases"
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Item A Comparison of Medicare Prospective Payment Systems on P.T.C.A. and Stent Outcomes in an Urban Hospital(2001-05-01) Compton, Ben H.; Mains, Doug A.; Hilsenrath, P. E.Compton, Ben H., A Comparison of Medicare Prospective Systems on P.T.C.A. and STENT Outcomes in an Urban Hospital. Master of Public Health (Health Services Administration), May 2001, 57 pp., 10 tables, 1 graph, bibliography, 51 titles. To determine if differences in outcomes exist between Medicare prospective payment systems when doing percutaneous transluminal coronary angioplasty (PTCA) or STENT surgeries. From January 1999 and December 2000, 146 Medicare patients were identified with 35 being outpatient and 111 inpatient. A separate group of 1-day inpatients was used as a comparison for the outpatient group. Results from the comparison reveal that in the three groups, the majority of patients were white, non-Hispanic males who were about 70 years of age. The 1-day inpatient group had the highest profit of all three with about $3,000 while the inpatient group broke even. The outpatient group had no in-hospital deaths or complications while all three had equal amounts of comorbidities. The conclusion is that losses will probably occur if PTCA and STENTs are done outpatient. Possible solutions are moving to an inpatient setting or determining which costs can be reduced in the outpatient setting.Item A Machine Learning Approach to Identify Predictors of Potentially Inappropriate Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Use in Older Adults with Osteoarthritis(MDPI, 2020-12-28) Patel, Jayeshkumar; Ladani, Amit; Sambamoorthi, Nethra; LeMasters, Traci; Dwibedi, Nilanjana; Sambamoorthi, UshaEvidence from some studies suggest that osteoarthritis (OA) patients are often prescribed non-steroidal anti-inflammatory drugs (NSAIDs) that are not in accordance with their cardiovascular (CV) or gastrointestinal (GI) risk profiles. However, no such study has been carried out in the United States. Therefore, we sought to examine the prevalence and predictors of potentially inappropriate NSAIDs use in older adults (age > 65) with OA using machine learning with real-world data from Optum De-identified Clinformatics((R)) Data Mart. We identified a retrospective cohort of eligible individuals using data from 2015 (baseline) and 2016 (follow-up). Potentially inappropriate NSAIDs use was identified using the type (COX-2 selective vs. non-selective) and length of NSAIDs use and an individual's CV and GI risk. Predictors of potentially inappropriate NSAIDs use were identified using eXtreme Gradient Boosting. Our study cohort comprised of 44,990 individuals (mean age 75.9 years). We found that 12.8% individuals had potentially inappropriate NSAIDs use, but the rate was disproportionately higher (44.5%) in individuals at low CV/high GI risk. Longer duration of NSAIDs use during baseline (AOR 1.02; 95% CI:1.02-1.02 for both non-selective and selective NSAIDs) was associated with a higher risk of potentially inappropriate NSAIDs use. Additionally, individuals with low CV/high GI (AOR 1.34; 95% CI:1.20-1.50) and high CV/low GI risk (AOR 1.61; 95% CI:1.34-1.93) were also more likely to have potentially inappropriate NSAIDs use. Heightened surveillance of older adults with OA requiring NSAIDs is warranted.Item Acetoacetate: A Cardioprotective Antioxidant(2002-05-01) Squires, Jeffrey E.; Mallet, Robert T.; Caffrey, James L.; Carroll, JoanSquires, Jeffrey E., Acetoacetate: A Cardioprotective Antioxidant. Master of Science, June 2002, 100 pp., 1 table, 18 illustrations, bibliography, 70 titles. The purpose of this study was to test the effectiveness of acetoacetate and β-hydroxybutyrate as myocardial protectants following peroxide injury and to determine acetoacetate’s ability to potentiate β-adrenergic responsiveness following ischemia-reperfusion injury. This study utilized antegradely perfused isolated working hearts exercised from male guinea pigs and sustained with glucose-fortified Krebs-Henseleit. Hearts were challenged by either 10 min perfusion with 100 μM H2O2 or 45 min of low flow ischemia exacerbated by ι-norepinephrine infusion. H2O2-challenged hearts were treated with 5 mM acetoacetate or β-hydroxybutyrate, whereas hearts injured by ischemia/reperfusion were treated with 5 mM acetoacetate. In the case of the ischemically injured hearts, acetoacetate treatment was combined with 2 nM isoproterenol to delineate acetoacetate’s ability to enhance β-andrenergic responsiveness to submaximal inotropic stimulation. Data were compared to non-injured time control hearts and injured untreated hearts to determine the impact of ketone body treatment. Acetoacetate increased citrate and glucose 6-phosphate content, nearly restored power, and increased the glutathione antioxidant redox potential (GSH/GSSG) by 140% in H2O2-injured myocardium. Although β-hydroxybutyrate increased citrate, an activator of NADPH-generating pathways, and glucose 6-phosphate, the substrate for the hexose monophosphate shunt to the same extent as acetoacetate, β-hydroxybutyrate raised GSH/GSSG by only 60% and did not enhance cardiac power. Therefore, acetoacetate enhances contractile function by augmenting the glutathione redox potential, and does so by additional mechanisms independent of the citrate and hexose monophosphate pathway. In hearts stunned by ischemia/reperfusion, acetoacetate and isoproterenol each increased power and glutathione redox potential three-to-fourfold, but phosphocreatine potential was 70% higher in acetoacetate hearts. Combined, acetoacetate + isoproterenol synergistically increased power and GSH/GSSG 16- and 17- fold respectively, doubled {NADPH/NADP+}, and increased cyclic AMP content 30%. These findings support the conclusion that acetoacetate enhances myocardial sensitivity to β-adrenergic stimulation possibly by enhancing GSH/GSSG.Item Activities of Daily Living and Cardiovascular Risk Factors' Impact on Cardiovascular Disease (CVD) and Cognitive Functioning: A Three Stage Longitudinal Model(2005-05-01) Bozo, Ozlem; Guarnaccia, Charles A.; Hall, James; Kelly, KimberlyBozo, Ozlem, Activities of Daily Living and Cardiovascular Risk Factors’ Impact on Cardiovascular Disease (CVD) and Cognitive Functioning: A Three Stage Longitudinal Model. Doctor of Philosophy (Health Psychology), May, 2005, 122 pp., 23 tables, 4 figures, references, 50 titles. The purpose of this study was to examine the longitudinal relationship of daily living (ADL), cardiovascular risk factors, and cardiovascular diseases to predict the future cognitive functioning of older Americans who are between the ages of 51 and 61 at the time of initial assessment. Three waves of the Health and Retirement Study (HRS) database between the years of 1992 and 2002 were examined with path analysis. The longitudinal hypotheses of the study were that (1) ADLs would positively predict future cognitive functioning, (2) ADLs would negatively predict future cardiovascular risk factors, (3) ADLS would negatively predict future cardiovascular diseases, (5) cardiovascular risk factors would negatively predict future cognitive functioning, (6) cardiovascular disease would negatively predict future cognitive functioning, (7) cardiovascular risk factors would mediate the relationship between ADLS and cardiovascular disease, and (8) cardiovascular disease would mediate the relationship between cardiovascular risk factors and cognitive functioning. The results of the analyses indicate that there was no effect of cardiovascular disease on cognitive functioning; however, there were significant effects of cardiovascular risk factors on cognitive functioning that ranged between B=-/021 and B=-/145. Moreover, it was found that cardiovascular risk factors mediate the relationship between ADLs and cognitive functioning, while cardiovascular disease does not. These results suggest that addressing cardiovascular risk factors may be more important than addressing existing cardiovascular disease to protect future cognitive functioning. This shows the importance of primary/secondary prevention versus tertiary interventions.Item Adult Women and Coronary Heart Disease: Studies on Surgical Procedures and Perception(2010-12-01) Schlorke, Patricia; Bae, Sejong; Biswas, Swati; Chen, OliveSchlorke, Patricia J., Adult Women and Coronary Heart Disease: Studies on Surgical Procedures and Perception. Doctor of Public Health (Biostatistics), December 2010, 124 pp., 12 tables, 3 figures, bibliography, 95 titles. Coronary heart disease (CHD) was the number one cause of death in the United States. The main CHD symptom was a heart attack. The most common form of a heart attack was chest pain and shortness of breath, which occurred in men. However, women did not usually have chest pain, but other symptoms such as abdominal pain or indigestion. This could lead women to perceive or believe that they would not have heart disease or heart attacks. This thought could lead women to not obtaining health care, such as surgical procedures, for CHD. Health professionals knew the signs and symptoms of CHD in men, but they may be uncertain in their diagnosis in women. This could lead to women not asking their health care professional about heart attacks or other symptoms. The purpose of this dissertation analyzed CHD in two areas in all women 18 years and older. These two areas were: (a) comparing hospital length of stay between men and women who had either coronary artery bypass grafting (CABG) or percutaneous transluminal coronary angioplasty (PTCA); and (b) women’s perceptions about CHD. Data for the surgical procedures study came from the 2006 National Hospital Discharge Survey (NHDS) and for the perception study came from the 2007 Behavioral Risk Factor Surveillance System (BRFSS). The results showed for the surgical procedures men and women had increased hospital days of care (DOC) for all surgical procedures. The results for the perception study showed women varied by age, race-ethnicity, education, income, and other factors in heart attack symptom knowledge. These two studies had the following conclusions. The results for increased hospital DOC had implications, such as increased health utilization, for present and future hospitalizations. The results for heart attack symptom knowledge showed a need for more awareness and communication of heart attack symptoms among all women across the United States.Item Alterations in Beta-Adrenergic Receptor Density on Human Lymphocytes in Response to Chronic Exercise(2000-12-01) Brittain, Adam K.; Peter B. Raven; Stephen R. Grant; Michael W. MartinA number of cardiovascular adaptations have been shown to occur in healthy individuals as a result from regular, chronic exercise training. These changes include, but are not limited to, a lower resting heart rate, a lower heart rate at any given submaximal workload, an increase in stroke volume, an increase in maximal cardiac output due primarily to an increase in contractility, a decreased peripheral vascular resistance (increased peripheral vascular conductance), an overall increase in vascularity, an increase in left ventricular mass, and an increase in total body oxygen extraction (Raven, 1994). Some of these adaptations are also known to commonly occur in patients with coronary artery disease enabling them to increase their total work capacity. Therefore, exercise apparently adapts the heart to better cope with the adverse affects of coronary artery disease and helps to prevent the aforementioned disease from developing in healthy individuals. The beta-adrenergic receptor (β-AR) is essential for the activation of many aspects of the cardiovascular system during dynamic exercise (1). The catecholamines epinephrine and norepinephrine are released from the adrenal medulla and postganglionic fibers of the sympathetic nervous system respectively in response to dynamic exercise. Epinephrine and other beta-adrenergic receptor agonists bind and activate the β-AR on the cell membrane thus allowing it to couple with the stimulatory GTP-binding regulatory protein Gs. This step initiate the activation of adenylate cyclase and the synthesis of cyclic adenosine 3’,5’ monophosphate (cyclic AMP), a key intracellular second messenger. Cyclic AMP ultimately activates cyclic AMP-dependent protein kinase (PKA), an enzyme that phosphorylates a number of intracellular proteins that subsequently influence cell metabolism and function. Alterations in the activity of the adrenergic system seen in several clinical and physiological situations, including exercise, are directly associated with changes in lymphocytic β-AR density or function (2). Moreover, it has been suggested that the changes in receptor density on lymphocytes correlate closely with cardiovascular responsiveness to catecholamines in humans (3-6). Additionally, changes in catecholamine concentration within the physiological range have a regulatory effect on β-AR density and function (7). One particular study established an inverse relationship between plasma and urine catecholamine concentrations and lymphocytic β-AR density in man (8). It is the intent of this review to describe some of the cardiovascular adaptations that occur as a result of chronic exercise and how these changes could be caused by alterations in β-AR density and responsiveness. Additionally, the comparisons and contradictions between chronic heart failure and chronic exercise will be made. The role of the beta-adrenergic system in mediating the effects of exercise will be introduced. The structure of the β-AR will be described and how its molecular structure dictates its function. A brief synopsis will be presented on the mechanism in which β-AR operates subsequent to ligand binding. Alterations of the β-AR, particularly its expression in the heart, through transgenics will then be reviewed to show how this receptor could be responsive for some of the aforementioned adaptations to chronic exercise. In this, some of the differences between the β1- and β2-AR will be described as well as some of the therapeutic implications that could result from overexpression of the β-AR. Following this, alterations in the density of the β-AR after both short-term and long-term exposure to catecholamines will be examined. Included in this section with be the detailed description of the mechanism of receptor desensitization that precedes receptor down-regulation. A brief review will then be given on the effects of chronic exercise on β-AR density. The use of human lymphocytes as model cells will then be described. Binding theory will be explained as it will be the basis of methodology used in any subsequent studies. Along with this, [125 Iodo] cyanopindolol (125I-CYP) will be introduced and its advantages and disadvantages as a β-AR ligand probe will be discussed.Item Androgens and Cardiovascular Disease(1998-05-01) Dickerman, Rob D.; Walter J. McConathy; Thomas Yorio; Robert GracyDickerman, Rob D., Androgens and Cardiovascular Disease Doctor of Philosophy (Biomedical Sciences), May 1998; 111 pp; 10 tables, bibliography, 197 titles. Anabolic steroids are commonly used by many muscle and strength dependent athletes due to their ability to enhance the hypertrophic effects of resistance training. The use of anabolic steroids by bodybuilders appears to carry significant health risks, most commonly reported are sudden death, myocardial infarction and cardiomyopathy. To investigate the effects of anabolic steroids on cardiovascular risks, a study was designed to analyze the effects of androgens on lipoprotein levels and structure/function of the heart. For the study on lipid-related risk, twelve competitive bodybuilders were recruited for a comprehensive analysis of serum apolipoprotein A-I, B, total cholesterol, HDL-cholesterol, LDL-cholesterol, and testosterone. Serum total cholesterol, HDL- and LDL-cholesterol, apolipoproteins A-I and Be were significantly lower in androgen-users. Consistent with previous reports, androgens were associated with decreases in HDL-cholesterol and apolipoprotein A-I. However, androgens were also associated with reduced serum total cholesterol, LDL-cholesterol and apolipoprotein B. Despite the significantly higher total cholesterol/HDL-cholesterol ratio, the low levels of serum total cholesterol levels (percentile) in the androgen-users raises questions as to whether there is increased risk for cardiovascular disease and the exact role of androgens in cardiovascular risk. To investigate the effects of anabolic steroids in pathologic concentric left ventricular hypertrophy, the effects of androgens on left ventricular size and function were analyzed. Previous investigations conducted on left ventricular size and function have yielded inconclusive results. Problems existing in each of the previous investigations were small body mass, short length of myocardial exposure time to resistance training (years of training), significantly different body mass between steroid-users and steroid-free subjects and monitoring/reporting of steroid use. These problems may have contributed to the discrepancies between studies. Therefore, we selectively recruited eight competitive heavy weight drug-free bodybuilders and eight matched competitive weight bodybuilders on self-directed regimens of anabolic steroids for examination of left ventricular size and function via echocardiography. Increases in left ventricular posterior wall (LVPW) and ventricular septal thickness (VST) were apparent in the steroid-user group (p [less than] 0.05). Ratio of echocardiographic findings to body mass index (BMI) revealed a significantly smaller left ventricular and diastolic dimension (LVDEd/BMI, p [less than] 0.05) in the steroid-user. The smaller LVDEd in steroid-users is coupled with a significantly disproportionate septal and posterior wall thickness in steroid-users. There was no direct evidence of diastolic dysfunction. Thus it appears from these studies that androgens alter lipoproteins leading to a questionable increased risk for cardiovascular disease and may potentiate concentric left ventricular hypertrophy without affecting cardiac function.Item Arterial Baroreflex Control of Muscle Sympathetic Nerve Activity(2000-07-01) Fadel, Paul Joseph; Peter B. Raven; Michael Smith; Patricia GwirtzFadel, Paul Joseph, Jr., Arterial Baroreflex Control of Muscle Sympathetic Nerve Activity. Doctor of Philosophy (Biomedical Science), July 2000; 100 pp; 3 tables; 10 figures; bibliography. Arterial baroreflex control of sympathetic nerve activity is dependent on afferent nerve activity emanating from both the aortic and carotid baroreceptors. While several investigations have reported that the aortic baroreceptor reflex dominates in the baroreflex control of heart rate in humans, the role of carotid and the aortic baroreceptors in the control of sympathetic nerve activity remains unclear. In addition, the effect of exercise and long term endurance training on baroreflex-sympathetic nerve activity responses requires further definition. Therefore, the purpose of the investigations described within this dissertation was to: i) describe carotid baroreflex (CBR) control of muscle sympathetic nerve activity (MSNA) at rest and during exercise, ii) examine the relative contribution of the carotid and aortic baroreflexes to the overall arterial baroreflex control of MSNA during acute hypotension, and iii) determine the effect of fitness on arterial baroreflex control of MSNA. In the first investigation, we constructed stimulus-response relationships for CBR control of MSNA at rest and during dynamic arm cycling and demonstrated that carotid baroreflex control of MSNA was reset to function at the higher arterial pressures induced by exercise without a change in reflex sensitivity. Thus, we concluded that the carotid baroreflex control of MSNA was preserved during dynamic exercise. In the second investigation, acute hypotension was induced non-pharmacologically by releasing a unilateral arterial thigh cuff (300 Torr) following nine minutes of resting ischemia under two conditions: control (aortic and carotid baroreflex deactivation) and suction (aortic baroreflex deactivation alone). The application of neck suction to negate the CBR during cuff release caused a significant attenuation of the MSNA response and a greater decrease in mean arterial pressure; thereby signifying the importance of the CBR in the control of MSNA and maintenance of arterial blood pressure. However, when the drop in carotid sinus pressure was counteracted with neck suction a significant MSNA response was noted, indicating the dominance of the aortic baroreflex control of MSNA. Furthermore, a comparison between high-fit (HF) and average fit (AF) subjects indicated that despite an augmented baroreflex control of MSNA, HF subjects exhibited a greater decrease in mean arterial pressure compared to AF subjects. Thus, it appeared that although the arterial baroreflex appropriately increased the MSNA response to hypotension, the regulation of blood pressure remained attenuated in the HF subjects. We contend that an impaired control of vasomotion hinders blood pressure regulation in high-fit subjects.Item Assessment of Obesity as a Cardiovascular Disease Risk Factor in a Geriatric Rural Texas Community - A Six Month Follow-Up(1999-12-01) Coustasse, Alberto; Rene, Antonio; Mains, Doug A.; Ramirez, GilbertCoustasse, Alberto, Assessment of Obesity as a Cardiovascular Disease Risk Factor in a Geriatric Rural Texas Community – A Six Month Follow-up. Master of Public Health Track, Public Health Administration, December 1999, 22 pp., 9 tables, 9 illustrations, bibliography, 7 titles. The health fair approach was used as a method to establish individual and population health status baselines and to provide a mechanism to follow-up with an elderly population in a rural Texas community. A controlled trial sample of forty-four seniors was initially screened in a primary care clinic in August 1998. Patients were reevaluated at six months and results demonstrated a 46% increase in BMI [Body Mass Index]; 62% remained obese; 62% maintained elevated cholesterol or increased cholesterol values to abnormal values; 61% maintained or increased their BP [blood pressure] to abnormal values. A significant finding was that a change of one unit in the BMI correlated with a change of 19.88 mmHg [millimeter mercury] of SBP [systolic blood pressure] and 18.59 mmHg of DBP [diastolic blood pressure]. The societal economic impact of mortality and morbidity (without the benefit of target interventions) for the initial forty-four seniors was projected at & 74,949. Keywords: Health fairs; obesity; cardiovascular; cost; case management.Item Comparing Site Management of a NIH versus Industry Sponsored Study: CTSN (Surgical Interventions for Moderate Ischemic Mitral Regurgitation) Trial versus DEEP (Dual Epicardial Endocardial Protocol for Persistent and Longstanding Atrial Fibrillation) Trial(2010-12-01) Ong, Jennifer K.; Patricia GwirtzThe management of a clinical trial requires the coordination of a number of tasks concurrently. Every study has its own individual difficulties and concerns that a research team must work around in order to get a study started and begin subject enrollment. The Baylor Research Institute is participating as a research site for both the CTSN and DEEP studies. Each study is funded by a different type of sponsor, which includes the National Institutes of Health and AtriCure. The two studies were followed from the early stage of site selection up until the point of subject enrollment. The CTSN and DEEP trials provided insight as to how to successfully manage the start-up of both types of studies, demonstrating the delays and difficulties that may arise as a clinical trial agreement approaches execution.Item COPD Handout materials(2008-01-01)Item Detection of Androgen Receptors by Flow Cytometry(2008-05-01) Dutta, Mayurika; McClain, Robert; Singh, Meharvan; Hall, StanDutta, Mayurika, ‘Detection of androgen receptors by Flow Cytometry’. Internship Practicum report, Biotechnology, May 2008, 80 pp., 1 table, 18 figures. The use of androgen therapy is expanding given the documented potential benefits like increasing bone mineral density, muscle mass and strength. Androgen therapy also has potential risks including increasing the likelihood of prostate cancer and cardiovascular disease. So, we need a way to differentiate those who are likely to be benefitted by the therapy and those that are not. Data from Dr. Meharvan Singh’s lab has shown that activation of intracellular androgen receptors triggers cell survival pathways, while activation of the membrane androgen receptor suppresses cytoprotective pathways, and thus promotes cell death. We propose to develop a diagnostic kit that measures the relative ratio of intracellular androgen receptors and membrane androgen receptors, which is predicted to gauge relative risks or benefits associated with androgen therapy.Item Differences in the Rates of Cardiovasular Surgical Procedures in Men and Women with Coronary Heart Disease in the State of Texas(2003-02-01) Moreland, Matthew C.; Marshall, Muriel; Mains, Doug A.Moreland, Mathew, Differences in the rates of cardiovascular surgical procedures between men and women with coronary heart disease in the state of Texas. University of North Texas Health Science Center, School of Public Health, February 2003, 19pp., 3 tables, references, 23 titles. Data for the Texas Health Care Information Council was analyzed to identify the difference in the rates of invasive cardiovascular procedures performed on men and women among 411 Texas hospitals with the diagnosis of coronary heart disease in 1999. In all, 150,361 cases were compared for differences between gender, race, age and type of invasive cardiovascular procedure using chi-square test. Frequencies were tabulated for age, race and gender. Invasive cardiac procedures were differentiated by type: coronary angiography and coronary revascularization. Between the ages of 45 and 79 women were more likely to have angiography performed than men in the same age group. However, young (30-44) and elderly (80+) men were more likely to receive angiographic procedures when presenting with the same symptoms as women. Also, men of all ages and races were more likely to receive revascularization procedures (PTCA, CABG) than women when presenting with coronary heart disease symptomology. Additionally, men between the ages of 35 and 49 received twice the number of revascularization procedures than women. These findings identified patterns of treatment with defined differences between gender which may be attributed to external factors versus a true gender bias.Item Differential Gene Expression Profiling in a Small Animal Model of Progressively Pacing-Induced Heart Failure(2006-06-01) Selby, Donald Evan; Stephen R. Grant; Patricia A. Gwirtz; Dan DimitrijevichDonald Evan Selby, Differential Gene Expression Profiling in a Small Animal Model of Progressively Pacing-Induced Heart Failure. Doctor of Philosophy (Biomedical Sciences), July 2006, 235 pp, 4 tables, 35 illustrations, references, 328 titles. Pacing induced tachycardia (PIT), in mammals, is known to cause a change from normal heart function to early left ventricular dysfunction. Progression to heart failure in experimental animals, such as dogs, pigs, and sheep, takes place in a relatively short period of time compared to the disease development observed in humans. Due to the cost and nature of using such animals, there is a need for a small animal model of PIT, which would delineate the etiology of the disease state by impairing the systolic function. The mode of action of overpacing inducement of cardiomyopathy, as the data suggests, may be through a sarcomere stretch sensor and its length-dependent signaling mechanism. In this study, an internal electrical-overpacing of an isogenic rabbit strain over a 52-day period was used to initiate a pathology consistent with human CHF. The data presented demonstrated that PIT causes alterations in the systolic ability of the heart, observed as reduced fractional shortening of the heart. This is seen in changes of the message pool population for proteins of the contractile architecture. Initially the heart is being paced rapidly and therefore there is insufficient time to get blood into the chamber. Thus, the data suggests that a mechanical stretch sensor is the process by which overpacing the heart leads to changes in gene expression which ultimately cause a compounding cellular condition which exists during heart failure. The data shows that there are gene isoform ratio changes that occur as the disease develops these include changes in differential expression of cardiac titin alternative splicing isoforms. The data suggests that there is also isoform switching occurring with alternative splicing of the gene encoding for SERCA2a, the probe 1587641_at shows a moderate decrease in expression and using BLAST for this probe this sequence is homologous to an alternative splicing variant of SERCA2a of the rabbit accession number J04703. The data shows that ferritin heavy chain also has an alternative splicing variant that are differentially regulated, this dysregulation of the isoform ratio may be linked to ADAMSTS1, a disintegrin and metalloproteinase isoform 1, which is seen to be downregulated in the data, these play a role in negative regulation of cellular proliferation. In addition to these detected isoform changes in the ratios of alternative splice variants changes are seen in genes linked to sarcomere integrity such as dystrophin probe 1582958_at is significantly increased in its expression, also integrin beta-1 probe 1584175)at shows a marginal increase in expression. The protease calpain probe 1604384)at, which uses a substrate the aforementioned integrin, dystrophin, and titin is also significantly upregulated in the data. Interestingly calpastatin, probe 1591603_at the inhibitor of calpain is marginally increased in its expression. Only recently has titin become to be appreciated as the protein that is responsible for the Frank Starling law as it undergoes an isoform ratio change as heart failure develops. These changes are initially caused by changes in ion concentration and stress upon the contractile proteins but as seen in the study, leads to altered gene expression. In this model, these gene alterations lead to diastolic dysfunction and the compounded problems constitute heart failure. This work shows that heart failure induced by over-pacing creates physical demands upon the framework of the heart and these physical stresses are transmitted through mechanical sensors leading to differential expression of the message pools for proteins involved in the way the heart contracts, and fills upon relaxation which ultimately ends in a heart that can do neither, thus leading to death.Item Dobutamine Increases Mechanical Function and Cytosolic Phosphorylation Potential During Moderate Right Ventricular Hypoperfusion(2000-08-01) Yi, Kun Don; H. Fred Downey; Robert Mallet; Eugene E. QuistYi, Kun Don. Dobutamine increases mechanical function and cytosolic phosphorylation potential during moderate right ventricular hypoperfusion Master of Science (Biomedical Sciences), August, 2000, 101 pp, 4 tables, 18 figures, references, 108 titles. This study was conducted to investigate the functional and metabolic effects of regional inotropic stimulation with dobutamine during right ventricular (RV) hypoperfusion. Right coronary perfusion pressure was incrementally lowered to 40 mmHg from 100 mmHg, and two-doses of dobutamine (0.01 and 0.06 μg/kg/min) were continuously infused for 15 min into the right coronary artery in pentobarbital sodium-anesthetized mongrel dogs of either sex. Myocardial energy metabolites, glycolytic intermediates, glycogen, and phosphorylation potential were measured in freeze-clamped RV biopsies. RV hypoperfusion caused a 54% decrease in right coronary blood flow, a decrease in lactate uptake, and an increase in glucose uptake. Systolic segment shortening, isometric force, MVO2, and oxygen utilization efficiency (O2UE: power/MVO2) decreased significantly. Energy reserves were unaffected by the hypoperfusion. Low-dose dobutamine during hypoperfusion improved regional mechanical function without increasing MVO2, and thus, improved O2UE. Remarkably, low-dose dobutamine markedly increased phosphocreatine content and phosphorylation potential. In contrast, high-dose dobutamine produced only transient improvements in function and efficiency and sharp decreases in energy reserves. Analysis of glycolytic intermediates showed a sustained augmentation of glycolysis during low-dose dobutamine, but glycolysis was limited by high-dose dobutamine at the level of glyceraldehyde-3-phosphate dehydrogenase. Dobutamine is capable of improving both contractile function and cellular energetics in underperfused RV myocardium at low but not high dose dobutamine. Therefore, dosage should be carefully selected.Item Duration of unemployment and self-perceived health in Europe(2016-03-01) Brenner, M. HarveyThis study investigates the potential impact of employment loss on self-perceived health according to the duration of national levels of unemployment in EU member states during 2004-2012. The principal findings were that the total unemployment rate, long-term unemployment (LTU) rate and very long-term unemployment (VLTU) rate were all strongly related to increased reports of bad and very bad self-perceived health. In fact, the impact of unemployment (i.e., effects based on the coefficients) increased in a ‘dose-response’ manner with the total unemployment rate showing the smallest coefficient, the LTU rate showing a greater coefficient, and the VLTU rate showing the strongest impact in terms of increasingly bad and very bad self-reported health. The findings complement existing evidence that identified unemployment as an important risk factor for heart disease mortality at the start of the 2008/2009 recession.Item Dysfunctional Control of Coronary Blood Flow in Renovascular Hypertension(1999-06-01) Kline, Geoffrey Philip; Gwirtz, Patricia A.; Shi, Xiangrong; Raven, Peter B.Kline, Geoffrey Philip, Dysfunctional Control of Coronary Blood Flow in Renovascular Hypertension Doctor of Philosophy (Biomedical Sciences), June 1999, 98 pp, 2 tables, 10 figures, references, 142 titles. This study was designed to determine the effects of renovascular hypertension (RVH) on coronary vasoreactivity in conscious, chronically instrumented dogs. Six dogs were instrumented to measure left ventricular pressure, +dP/dtmax, heart rate, mean aortic pressure, circumflex blood flow (CBF), and cardiac output. In order to examine endothelial-dependent and independent coronary vasodilation, intracoronary injections of actylcholine (Ach), bradykinin (BDK), and sodium nitroprusside (SNP) were studied before and after induction of RVH in the presence and absence of nitric oxide (NO) blockade. After RVH, resting CBF was significantly reduced (P [less than] 0.05). In the normotensive state, NO-blockade significantly reduced the coronary vasodilation to Ach and BDK (P [less than] 0.05), but not SNP. After RVH, the coronary vasodilation to Ach, BDK, and SNP were reduced (P[less than] 0.05). After RVH, NO-blockade further reduced the coronary vasodilation to BDK (P [less than] 0.05), but not Ach. Thus, RVH resulted in an impairment of both endothelial-dependent and –independent coronary vasodilation. It also appears that during RVH the endothelium retains the ability to produce/release NO to some, but not all, stimuli. In order to examine the possibility that β-adrenergic mediated coronary vasodilation is impaired after RVH, intracoronary injections of norepinephrine (NE), isoproterenol (ISO), and terbutaline (TRB) were administered. These drugs all caused dose dependent increases in CBF before and after RVH. After RVH, the coronary vasodilatory responses to NE, ISO and TRB were significantly reduced (P [less than] 0.05). β1-blockade with intracoronary atenolol (1 mg) reduced the ISO-induced increases in CBF and had no effect on TRB responses (P [less than] 0.05). β2-blockade with intracoronary ICI-118,551 (1 mg) reduced the ISO-induced coronary vasodilation and abolished TRB responses (p[less than] 0.05). During β2-blockade, ISO-induced increases in CBF were not different after RVH. Therefore, these data indicate that β1-adrenergic mediated coronary vasodilation is preserved after RVH, whereas, β2-mediated is not. We conclude that 1) RVH results in an impairment of both endothelial-dependent and –independent coronary vasodilation; 2) RVH results in an impairment of β2-adrenergic mediated coronary vasodilation.Item Effect of Phosphorylation on Muscle Physiology and Biophysical Characterization of Mutations Responsible for Familial Hypertrophic Cardiomyopathy(2016-08-01) Duggal, Divya; Borejdo, Julian; Gryczynski, Ignacy; Clark, Abbot F.Familial hypertrophic cardiomyopathy (FHC) is the most common cause of sudden cardiac death in young individuals. Molecular mechanisms underlying this disorder are largely unknown; this study aims at revealing how disruptions in actin-myosin interactions can play a role in the pathogenesis of this disorder. Cross-bridge (XB) kinetics and the degree of order were examined in contracting myofibrils from the ex vivo ventricles of transgenic (Tg) mice expressing FHC regulatory light chain (RLC) mutation K104E and Troponin I mutation, R21C. Because the degree of order and the kinetics are best studied when an individual XB makes a significant contribution to the overall signal, the number of observed XBs in an ex vivo ventricle was minimized to 20. Autofluorescence and photobleaching were minimized by using a relatively long-lived red-emitting dye. In case of K104E, mutated XBs were significantly better ordered during steady-state contraction and during rigor, but the mutation had no effect on the degree of order in relaxed myofibrils. The K104E mutation increased the rate of XB binding to thin filaments and the rate of execution of the power stroke. In case of R21C, differences were investigated in the left (LV) and right ventricle (RV) mutant where it was found that the mutation imposed significant difference in the distribution of angles that actin makes with thin filament axis: during contraction, actin angles from LV were more tightly distributed compared to actin angles from RV. Collectively, the data indicates that the mutation-induced changes in the interaction of myosin with actin during the contraction- relaxation cycle may contribute to altered contractility and the development of FHC. Phenotypic differences of the R21C mutation in the left versus right mouse ventricles, even though both ventricles express the same isoform of the cardiac highlights the importance of functional differences between the two ventricles of cardiac disease.Item Examining Coronary Heart Disease Risk Factors and Its Relationship with Physical Activity in a Self-Reported Survey(2004-05-01) Fernandes, Alroy H.; Fridinger, Frederick; Cipher, Daisha; Coggin, ClaudiaFernandes, Alroy H., Examining Coronary Heart Disease Risk Factors and its Relationship with Physical Activity in a Self-Reported Survey. Masters of Public Health (Community Health), May 2004, 49pp., 3 illustrations, references, 38 titles. This study uses ‘Healthstyles,’ a self reported survey of 3,719 respondents above the age of 18, to look at exercise behavior in people at risk for CHD. Married or higher earning individuals were more likely to show sufficient exercise levels. Individuals with high blood pressure, high blood cholesterol, diabetes, obesity or family history of heart disease reported lesser levels of sufficient exercise than those without these conditions. People with CHD risk factor reported lower scores on questions that dealt with attitude and opinions about exercise behavior, and this was significantly correlated with lower levels of sufficient exercise. This supports the ‘positive attributes of the behavior’ aspect of the social cognitive theory of exercise. The attitude questions used, although not specific, could be included in a self-reported survey for the purpose of qualitatively and quantitatively assessing exercise intervention; albeit more studies are required to validate this claim.Item Examining the Theoretical Constructs of Motivational Interviewing: Applying Self-Determination Theory to Physical Activity Among Heart Failure Patients(2008-05-01) Spranger, Catherine Borski; Shawn Jeffries; Sejong Bae; Claudia CogginSpranger, Catherine Borski, Examining the Theoretical Constructs of Motivational Interviewing: Applying Self-Determination Theory to Physical Activity Among Heart Failure Patients. Doctor of Public Health (Social and Behavioral Sciences), May, 2008, 90 pp., 8 tables, reference list, 61 titles. Effective management of heart failure (HF) is one of the major challenges facing health care providers today due to the complexity of a number of inter-related health and self-care behaviors. One health behavior that is important in the management of HF is physical activity. Motivational Interviewing (MI) has been shown to be an effective counseling style engaging individuals to both adopt and maintain physical activity; however, the literature is lacking in this area among HF patients. One underlying theoretical basis of MI that has been proposed is Self-Determination Theory (SDT). The purpose of this pilot study was to explore the relationships between physical activity and the SDT constructs of autonomous motivation, perceived competence, and autonomy support. The sample consisted of 26 HF patients in a heart failure clinic in north central Texas. Participants completed an interviewer-administered questionnaire examining various psychological constructs, as well as, assessing their levels of physical activity during a typical week during the preceding month. The finding of this study lend some support to better understanding the relationships between specific SDT constructs and physical activity. Likewise the findings demonstrated the importance of motivation-related variables to understanding how to motivate HF patients to both initiate physical activity and maintain a regular physical activity regimen.
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