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.
University of Michigan and University of Mississippi Medical Center | Date: 2015-04-28
Provided herein is technology relating to treatment of sepsis and particularly, but not exclusively, to methods for predicting a response of a sepsis patient to treatment with L-carnitine.
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.
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.
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.
Fox E.R.,University of Mississippi Medical Center
Circulation | Year: 2011
Lower plasma B-type natriuretic peptide (BNP) concentrations in obese individuals ("natriuretic handicap") may play a role in the pathogenesis of obesity-related hypertension. Whether this phenomenon may contribute to hypertension in blacks is unknown. We tested the hypothesis that body mass index is inversely related to BNP concentrations in blacks. We examined the relation of plasma BNP to body mass index in 3742 Jackson Heart Study participants (mean age, 55 ± 13; 62% women) without heart failure using multivariable linear and logistic regression, adjusting for clinical and echocardiographic covariates. The multivariable-adjusted mean BNP was higher for lean participants compared with obese participants in both normotensive (P<0.0001) and hypertensive (P<0.0012) groups. In sex-specific analyses, the adjusted mean BNP was higher in lean hypertensive individuals compared with obese hypertensive individuals for both men (20.5 versus 10.9 pg/mL, respectively; P=0.0009) and women (20.0 versus 13.8 pg/mL; P=0.011). The differences between lean and obese participants were more pronounced in normotensive participants (men, 9.0 versus 4.4 pg/mL; P<0.0001; women, 12.8 versus 8.4 pg/mL; P=0.0005). For both hypertensive and normotensive individuals in the pooled sample, multivariable-adjusted BNP was significantly related to both continuous body mass index (P<0.05 and P<0.0001, respectively) and categorical body mass index (P for trend <0.006 and <0.0001, respectively). Our cross-sectional study of a large community-based sample of blacks demonstrates that higher body mass index is associated with lower circulating BNP concentrations, thereby extending the concept of a natriuretic handicap in obese individuals observed in non-Hispanic whites to this high-risk population.
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.
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.
Agency: NSF | Branch: Standard Grant | Program: | Phase: Accelerating Innovation Rsrch | Award Amount: 199.99K | Year: 2016
This PFI: AIR Technology Translation project, Thermally Targeted Biopolymers for the Delivery of Anticancer Drugs, focuses on translating a thermally responsive biopolymer technology into a new cancer treatment drug delivery system. This system has the potential to improve outcomes and reduce drawbacks now experienced by patients during cancer treatment. Currently, only a small fraction of chemotherapeutic drugs reach tumor sites. The rest of these drugs, systemically administered at dosages strong enough to eradicate cancer cells, are distributed throughout the body, causing extensive damage to normal tissue. The developed drug delivery system attaches a powerful chemo-drug, Doxorubicin, to a thermally responsive, biopolymer, elastin-like polypeptide (ELP). At physiological temperatures (37ºC), this ELP exists in a more liquid state (soluble). However, the ELP can be prompted by an externally applied, clinically available, mild hyperthermia (40-41°C) to undergo a phase transition (into being more solid) and aggregate at the tumor site. To help these aggregated ELPs and their attached Doxorubicin enter the tumor cells at this site, a cell-penetrating peptide (CPP), is also conjugated to the ELP. This drug delivery system thus makes an innovative use of conjugated drug delivery biopolymers, an external, localizing heat, and a peptide able to mediate entry into cancer cells, where it can release the Doxorubicin for a more targeted and efficient tumor cell uptake and action.
The project will yield an externally triggered drug delivery system that can greatly improve the selective delivery of anti-cancer drugs to breast tumors by its unique exploitation of three key features: (1) the passive targeting properties of macromolecular carriers deriving from the enhanced permeability and retention effect, (2) active drug targeting to tumor sites by a clinically available external trigger, and (3) efficient, intracellular tumor drug delivery mediated by a cell penetrating peptide to reduce tumor growth, improve treatment outcomes, and retain better patient quality of life. The developed drug delivery system confers important advantages over competing systems based on drug-polymer conjugates, drug antibody conjugates, liposomes, and nano- and microparticles: (1) this drug delivery system enhances drug half-life and improves drug pharmacokinetic profile; (2) ELP modification by a CPP dramatically (15-20 fold) enhances cellular uptake, yielding more efficient tumor vasculature penetration and greatly enhancing efficacy in both tumor cell entry and the targeting of specific cellular compartments; (3) the water-solubility of lipophilic or water-insoluble drugs can be attained/much improved by their coupling to ELP biopolymers; (4) ELP biopolymers, based on simple genetic code, are simple and inexpensive to manufacture, can be easily modified to add therapeutic peptides for intracellular targeting, and can contain more than one drug, permitting their use in combination therapy. With this targeted drug delivery system, therapeutic drugs can be administered at maximum tolerated dose, but with substantially reduced side effects, resulting in greatly increased cancer treatment efficacy. The system thus addresses current drug delivery technology limitations and yields a competitive advantage over existing approaches for treating localized tumors, one better targeting tumor cells and sparing healthy tissue.
In addition, through a structured program of seminars and workshops, graduate students and post-docs will be guided in recognizing and implementing key steps for advancing the commercial potential of research. They will be introduced to case-based business research and collaboration, as well as regulatory and market research skills, crucial to creating viable business plans that permit the translation of vital research discoveries to the marketplace where their potential benefits can be maximized. The project engages CytRx Inc., a biopharmaceutical research and development company specializing in oncology, to provide guidance on technological aspects of the project and its technology translation from research discovery to commercial reality.
University of Mississippi Medical Center | Date: 2015-01-12
This invention relates to methods for ascertaining at least one of liver fibrosis or cirrhosis in a subject, by processing of one or more medical images of the liver, using a computing machine, to quantify nodularity of the surface of the liver and calculate a liver surface nodularity score.
Soljancic A.,University of Mississippi Medical Center
American journal of physiology. Regulatory, integrative and comparative physiology | Year: 2013
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.