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Jackson, MS, United States

University of Mississippi Medical Center is the health science campus of the University of Mississippi and is located in Jackson, Mississippi, United States. UMMC is the only academic health science center in the state.UMMC houses the University of Mississippi School of Medicine, University of Mississippi Medical Center School of Dentistry, Nursing, Health Related Professions, Graduate Studies in the Health science and part of the School of Pharmacy.UMMC is also home to the University Hospital and Clinics, a 722-bed tertiary care facility providing about 27,000 inpatient visits and 418,000 outpatient and emergency visits each year. On the Medical Center campus, the University Hospitals and Health System includes the University Hospital, Winfred L. Wiser Hospital for Women & Infants, Blair E. Batson Hospital for Children and, for faculty practice, the University Medical Pavilion.The university is the only hospital in the state designated as a level 1 trauma center. Specialized hospital services include: an interventional MRI; the only level 3 neonatal intensive care unit in the state; separate medical, surgical, cardiac, neuroscience and pediatric ICUs; a heart station for diagnosis and treatment of heart disease; a heart failure clinic; heart, kidney, cornea and bone marrow transplant programs; a comprehensive stroke unit; state-of-the-art radiological imaging systems; a sleep disorders laboratory; an in vitro fertilization program; and special pharmaceutical services.The parcel of land on which the university hospital sits was once the site of the Mississippi Insane Asylum, which moved its operations in 1935 and became Mississippi State Hospital. Wikipedia.

Background-Using data from 4 community-based cohorts of African Americans, we tested the association between genomewide markers (single-nucleotide polymorphisms) and cardiac phenotypes in the Candidate-gene Association Resource study. Methods and Results-Among 6765 African Americans, we related age, sex, height, and weight-adjusted residuals for 9 cardiac phenotypes (assessed by echocardiogram or magnetic resonance imaging) to 2.5 million single-nucleotide polymorphisms genotyped using Genome-wide Affymetrix Human SNP Array 6.0 (Affy6.0) and the remainder imputed. Within the cohort, genomewide association analysis was conducted, followed by meta-analysis across cohorts using inverse variance weights (genome-wide significance threshold=4.0 ×10-7). Supplementary pathway analysis was performed. We attempted replication in 3 smaller cohorts of African ancestry and tested lookups in 1 consortium of European ancestry (EchoGEN). Across the 9 phenotypes, variants in 4 genetic loci reached genome-wide significance: rs4552931 in UBE2V2 (P=1.43×10-7) for left ventricular mass, rs7213314 in WIPI1 (P=1.68×10-7) for left ventricular internal diastolic diameter, rs1571099 in PPAPDC1A (P=2.57×10-8) for interventricular septal wall thickness, and rs9530176 in KLF5 (P=4.02×10-7) for ejection fraction. Associated variants were enriched in 3 signaling pathways involved in cardiac remodeling. None of the 4 loci replicated in cohorts of African ancestry was confirmed in lookups in EchoGEN. Conclusions-In the largest genome-wide association study of cardiac structure and function to date in African Americans, we identified 4 genetic loci related to left ventricular mass, interventricular septal wall thickness, left ventricular internal diastolic diameter, and ejection fraction, which reached genome-wide significance. Replication results suggest that these loci may be unique to individuals of African ancestry. Additional large-scale studies are warranted for these complex phenotypes. © 2013 American Heart Association, Inc. Source

Maric-Bilkan C.,University of Mississippi Medical Center
Medical Clinics of North America

Obesity and diabetes are major health concerns worldwide. Along with other elements of the metabolic syndrome, including hypertension, they contribute to the development and progression of renal disease, which, if not treated, may lead to end-stage renal disease (ESRD). Although early intervention and management of body weight, hyperglycemia, and hypertension are imperative, novel therapeutic approaches are also necessary to reduce the high morbidity and mortality associated with renal disease. This review provides perspectives regarding the mechanisms by which obesity may lead to ESRD and discusses prevention strategies and treatment of obesity-related renal disease. © 2013 Elsevier Inc. Source

Booz G.W.,University of Mississippi Medical Center
Free Radical Biology and Medicine

Oxidative stress with reactive oxygen species generation is a key weapon in the arsenal of the immune system for fighting invading pathogens and initiating tissue repair. If excessive or unresolved, however, immune-related oxidative stress can initiate further increasing levels of oxidative stress that cause organ damage and dysfunction. Targeting oxidative stress in various diseases therapeutically has proven more problematic than first anticipated given the complexities and perversity of both the underlying disease and the immune response. However, growing evidence suggests that the endocannabinoid system, which includes the CB 1 and CB 2 G-protein-coupled receptors and their endogenous lipid ligands, may be an area that is ripe for therapeutic exploitation. In this context, the related nonpsychotropic cannabinoid cannabidiol, which may interact with the endocannabinoid system but has actions that are distinct, offers promise as a prototype for anti-inflammatory drug development. This review discusses recent studies suggesting that cannabidiol may have utility in treating a number of human diseases and disorders now known to involve activation of the immune system and associated oxidative stress, as a contributor to their etiology and progression. These include rheumatoid arthritis, types 1 and 2 diabetes, atherosclerosis, Alzheimer disease, hypertension, the metabolic syndrome, ischemia-reperfusion injury, depression, and neuropathic pain. © 2010 Elsevier Inc. All rights reserved. Source

Gomez-Sanchez E.P.,University of Mississippi Medical Center
Trends in Endocrinology and Metabolism

A small proportion of brain mineralocorticoid receptors (MR) mediate control of blood pressure, water and electrolyte balance, sodium appetite, and sympathetic drive to the periphery. Circulating inflammatory cytokines modulate MR-mediated changes in sympathoexcitation. Aldosterone binding to MR in the brain occurs, despite concentrations that are 2-3 orders of magnitude less than those of cortisol and corticosterone, which have similar affinity for the MR. The possible mechanisms for selective MR activation by aldosterone, the cellular mechanisms of MR action and the effects of brain MR on hemodynamic homeostasis are considered in this review. MR antagonists are valuable adjuncts to the treatment of chronic cardiovascular and renal disease; the crucial need to discover targets for development of selective therapy for specific MR functions is also discussed. © 2011. Source

Soljancic A.,University of Mississippi Medical Center
American journal of physiology. Regulatory, integrative and comparative physiology

Men are at greater risk for renal injury and dysfunction after acute ischemia-reperfusion (I/R) than are women. Studies in animals suggest that the reason for the sex difference in renal injury and dysfunction after I/R is the protective effect of estrogens in females. However, a reduction in testosterone in men is thought to play an important role in mediating cardiovascular and renal disease, in general. In the present study, we tested the hypothesis that I/R of the kidney reduces serum testosterone, and that contributes to renal dysfunction and injury. Male rats that were subjected to renal ischemia of 40 min followed by reperfusion had a 90% reduction in serum testosterone by 3 h after reperfusion that remained at 24 h. Acute infusion of testosterone 3 h after reperfusion attenuated the increase in plasma creatinine and urinary kidney injury molecule-1 (KIM-1) at 24 h, prevented the reduction in outer medullary blood flow, and attenuated the increase in intrarenal TNF-α and the decrease in intrarenal VEGF at 48 h. Castration of males caused greater increases in plasma creatinine and KIM-1 at 24 h than in intact males with renal I/R, and treatment with anastrozole, an aromatase inhibitor, plus testosterone almost normalized plasma creatinine and KIM-1 in rats with renal I/R. These data show that renal I/R is associated with sustained reductions in testosterone, that testosterone repletion protects the kidney, whereas castration promotes renal dysfunction and injury, and that the testosterone-mediated protection is not conferred by conversion to estradiol. Source

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