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Oates J.C.,Ralph hnson Va Medical Center | Oates J.C.,Medical University of South Carolina
Autoimmunity | Year: 2010

Systemic lupus erythematosus (SLE) is an autoimmune syndrome marked by autoantibody production. Innate immunity is essential to transform humoral autoimmunity into the clinical lupus phenotype. Nitric oxide (NO) is a membrane- permeable signaling molecule involved in a broad array of biologic processes through its ability to modify proteins, lipids, and DNA and alter their function and immunogenicity. The literature regarding mechanisms through which NO regulates inflammation and cell survival is filled with contradictory findings. However, the effects of NO on cellular processes depend on its concentration and its interaction with reactive oxygen. Understanding this interaction will be essential to determine mechanisms through which reactive intermediates induce cellular autoimmunity and contribute to a sustained innate immune response and organ damage in SLE. © 2010 Informa UK Ltd. Source

George M.S.,Institute of Psychiatry | George M.S.,Medical University of South Carolina | George M.S.,Ralph hnson Va Medical Center | Aston-Jones G.,Medical University of South Carolina
Neuropsychopharmacology | Year: 2010

Although the preceding chapters discuss much of the new knowledge of neurocircuitry of neuropsychiatric diseases, and an invasive approach to treatment, this chapter describes and reviews the noninvasive methods of testing circuit-based theories and treating neuropsychiatric diseases that do not involve implanting electrodes into the brain or on its surface. These techniques are transcranial magnetic stimulation, vagus nerve stimulation, and transcranial direct current stimulation. Two of these approaches have FDA approval as therapies. © 2010 Nature Publishing Group All rights reserved. Source

Lopes-Virella M.F.,Medical University of South Carolina | Baker N.L.,Medical University of South Carolina | Hunt K.J.,Medical University of South Carolina | Cleary P.A.,George Washington University | And 2 more authors.
Diabetes Care | Year: 2013

OBJECTIVE-The current study aimed to determine in the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications cohort whether or not abnormal levels of markers of inflammation and endothelial dysfunction measured in samples collected at DCCT baseline were able to predict the development of macroalbuminuria. RESEARCH DESIGN AND METHODS-Levels of inflammation and endothelial cell dysfunction biomarkers were measured in 1,237 of 1,441 patients enrolled in the DCCT study who were both free of albuminuria and cardiovascular disease at baseline. To test the association of log-transformed biomarkers with albuminuria, generalized logistic regression models were used to quantify the association of increased levels of biomarkers and development of abnormal albuminuria. Normal, micro-, and macroalbuminuria were the outcomes of interest. RESULTS-In the logistic regression models adjusted by DCCT treatment assignment, baseline albumin excretion rate, and use of ACE/angiotensin receptor blocker drugs, one unit increase in the standardized levels of soluble E-selectin (sE-selectin) was associated with an 87% increase in the odds to develop macroalbuminuria and one unit increase in the levels of interleukin-6 (IL-6), plasminogen activator inhibitor 1 (PAI-1; total and active), and soluble tumor necrosis factor receptors (TNFR)-1 and -2 lead to a 30-50% increase in the odds to develop macroalbuminuria. Following adjustment for DCCT baseline retinopathy status, age, sex, HbA1c, and duration of diabetes, significant associations remained for sE-selectin and TNFR-1 and -2 but not for IL-6 or PAI-1. CONCLUSIONS-Our study indicates that high levels of inflammatory markers, mainly E-selectin and sTNRF-1 and -2, are important predictors of macroalbuminuria in patients with type 1 diabetes. © 2013 by the American Diabetes Association. Source

Wangelin B.C.,Ralph hnson Va Medical Center | Tuerk P.W.,Medical University of South Carolina
Journal of Law, Medicine and Ethics | Year: 2014

In this paper, we consider ethical issues related to the treatment of posttraumatic stress disorder (PTSD) in combat zones, via exposure therapy. Exposure-oriented interventions are the most well-researched behavioral treatments for PTSD, and rigorous studies across contexts, populations, and research groups provide robust evidence that exposure therapy for PTSD is effective and can be widely disseminated. Clinical procedures for Prolonged Exposure therapy, a manualized exposure-oriented protocol for PTSD, are reviewed, and we illustrate the potential benefits, as well as the potential difficulties, associated with providing this treatment in combat zones. Several ethical considerations are identified: (1) Assuming successful treatment, is it ethical to send individuals with a known risk of developing PTSD back into combat? (2) If treatment is unsuccessful in theater (perhaps due to the confounding factor of ongoing danger), could that impact treatment effectiveness for soldiers who attempt therapy again post-deployment? (3) If the military finds combat-zone treatment effective and useful in maintaining an efficient work force, will treatment become mandatory for those diagnosed with PTSD? (4) What unintended consequences might be associated with large-scale dissemination of exposure therapy in or near combat, outside of mental health care infrastructures? (5) How would genetic variations known to be associated with PTSD risk influence decisions regarding who receives treatment or returns to combat? We conclude with a review of the personal and societal costs associated with not providing evidence-based PTSD treatments wherever possible. © 2014 American Society of Law, Medicine & Ethics, Inc. Source

Taylor J.J.,Medical University of South Carolina | Borckardt J.J.,Medical University of South Carolina | George M.S.,Medical University of South Carolina | George M.S.,Ralph hnson Va Medical Center
Pain | Year: 2012

The concurrent rise of undertreated pain and opiate abuse poses a unique challenge to physicians and researchers alike. A focal, noninvasive form of brain stimulation called repetitive transcranial magnetic stimulation (rTMS) has been shown to produce acute and chronic analgesic effects when applied to dorsolateral prefrontal cortex (DLPFC), but the anatomical and pharmacological mechanisms by which prefrontal rTMS induces analgesia remain unclear. Data suggest that DLPFC mediates top-down analgesia via gain modulation of the supraspinal opioidergic circuit. This potential pathway might explain how prefrontal rTMS reduces pain. The purpose of this sham-controlled, double-blind, crossover study was to determine whether left DLPFC rTMS-induced analgesia was sensitive to μ-opioid blockade. Twenty-four healthy volunteers were randomized to receive real or sham TMS after either intravenous saline or naloxone pretreatment. Acute hot and cold pain via quantitative sensory testing and hot allodynia via block testing on capsaicin-treated skin were assessed at baseline and at 0, 20, and 40 minutes after TMS treatment. When compared to sham, real rTMS reduced hot pain and hot allodynia. Naloxone pretreatment significantly reduced the analgesic effects of real rTMS. These results demonstrate that left DLPFC rTMS-induced analgesia requires opioid activity and suggest that rTMS drives endogenous opioidergic pain relief in the human brain. Further studies with chronic dosing regimens of drugs that block or augment the actions of opiates are needed to determine whether TMS can augment opiates in chronic or postoperative pain management. © 2011 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. Source

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