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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.

Jones A.E.,University of Mississippi Medical Center
Academic Emergency Medicine | Year: 2013

Severe sepsis remains a major public health problem both with a high hospital mortality rate and with staggering associated health care expenditures. The past decade has seen new insights into the early resuscitation of severe sepsis and this is an important, controversial, and constantly changing topic to emergency physicians. In this article, the recent support for lactate clearance as a measure of early sepsis resuscitation effectiveness is summarized, lactate-derived to oxygen-derived resuscitation variables are compared, and the shortcomings of lactate-derived variables are described. As summarized in this article, the best available experimental evidence suggests that lactate clearance of at least 10% at a minimum of 2 hours after resuscitation initiation is a valid way to assess initial response to resuscitation in severe sepsis. Associative data suggest that lactate normalization during resuscitation is a more powerful indicator of resuscitative adequacy; however, further research on the optimal lactate clearance parameters to use during resuscitation is needed, and many other important questions have yet to be answered. © 2013 by the Society for Academic Emergency Medicine. Source

Fox E.R.,University of Mississippi Medical Center
Circulation: Cardiovascular Genetics | Year: 2013

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 | Year: 2013

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 | Year: 2011

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 | Year: 2011

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

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