Charlie Norwood VA Medical Center

About: Charlie Norwood VA Medical Center is a healthcare organization based out in Augusta, Georgia, United States. It is known for research contribution in the topics: Autophagy & Kidney. The organization has 349 authors who have published 490 publications receiving 16360 citations. The organization is also known as: Augusta VA Medical Center.

Pet Ownership and the Risk of Dying from Cardiovascular Disease Among Adults Without Major Chronic Medical Conditions

Abstract: In a recent statement, the American Heart Association stated “There are scant data on pet ownership and survival in people without established cardiovascular disease (CVD)”. This study sought to fill this gap. We analyzed nationally representative data of 3964 adults aged ≥50 who were free from major physical illnesses. Pet ownership was assessed at baseline between 1988 and 1994. Vital status was followed through December 31st 2006. With dogs being most popular pets owned by 22.0 (standard error 0.34) % of the participants, 34.6 % of the study population owned a pet. Pet ownership was associated with low rates of CVD deaths [hazard ratio (HR) = 0.69 (95 % CI 0.45–1.07)] and stroke [0.54 (0.28–1.01)] at borderline significant levels among women. These associations were adjusted for physical activity and largely attributed to having a cat rather than a dog. Among cat owners, the HR of all CVD deaths was 0.62 (0.36–1.05) and the HR of dying from stroke was 0.22 (0.07–0.68) compared with non-cat owners. The corresponding HRs among dog owners were 0.82 (0.51–1.34) and 0.76 (0.34–1.71) respectively. No similar associations were observed among men. The hazard of dying from hypertension was not associated with pet ownership for both men and women. Owning a cat rather than a dog was significantly associated with a reduced hazard of dying from CVD events, in particular, stroke. The protection pets confer may not be from physical activities, but possibly due to personality of the pet owners or stress-relieving effects of animal companionship.

Niacin Ameliorates Neuro-Inflammation in Parkinson's Disease via GPR109A.

Abstract: In this study, we used macrophage RAW264.7 cells to elucidate the molecular mechanism underlying the anti-inflammatory actions of niacin. Anti-inflammatory actions of niacin and a possible role of its receptor GPR109A have been studied previously. However, the precise molecular mechanism of niacin’s action in reducing inflammation through GPR109A is unknown. Here we observed that niacin reduced the translocation of phosphorylated nuclear kappa B (p-NF-κB) induced by lipopolysaccharide (LPS) in the nucleus of RAW264.7 cells. The reduction in the nuclear translocation in turn decreased the expression of pro-inflammatory cytokines IL-1β, IL-6 in RAW264.7 cells. We observed a decrease in the nuclear translocation of p-NF-κB and the expression of inflammatory cytokines after knockdown of GPR109A in RAW264.7 cells. Our results suggest that these molecular actions of niacin are mediated via its receptor GPR109A (also known as HCAR2) by controlling the translocation of p-NF-κB to the nucleus. Overall, our findings suggest that niacin treatment may have potential in reducing inflammation by targeting GPR109A.

Anti-inflammatory IL-10 is upregulated in both hemispheres after experimental ischemic stroke: Hypertension blunts the response.

Abstract: Background Exogenous administration of the anti-inflammatory cytokine, interleukin 10 (IL-10), is known to promote neuroprotection and mitigate neuroinflammation after ischemia. However, endogenous expression and localization of IL-10 and its receptor (IL-10R) in the post-ischemic brain are still to be elucidated. In this investigation we aimed at determining the temporospatial expression of IL-10 in the rat brain relative to its systemic levels after ischemic stroke.

Recommendations for Preclinical Research in Hemorrhagic Transformation

Abstract: Hemorrhagic transformation (HT) is an important complication of ischemic stroke and is responsible for most of the mortality associated with acute reperfusion therapy. Although many important publications address the preclinical models of ischemic stroke, there are no current recommendations on the conduct of research aimed at understanding the mechanisms and consequences of HT. The purpose of this review is to present the various models used in HT research, the clinical correlates, and the experimental variables known to influence the quantitation of HT in preclinical investigation. Lastly, recommendations for the conduct of preclinical research in HT are provided.

Arginase 2 Deficiency Prevents Oxidative Stress and Limits Hyperoxia-Induced Retinal Vascular Degeneration

Abstract: Background: Hyperoxia exposure of premature infants causes obliteration of the immature retinal microvessels, leading to a condition of proliferative vitreoretinal neovascularization termed retinopathy of prematurity (ROP). Previous work has demonstrated that the hyperoxia-induced vascular injury is mediated by dysfunction of endothelial nitric oxide synthase resulting in peroxynitrite formation. This study was undertaken to determine the involvement of the ureahydrolase enzyme arginase in this pathology. Methods and Findings: Studies were performed using hyperoxia-treated bovine retinal endothelial cells (BRE) and mice with oxygen-induced retinopathy (OIR) as experimental models of ROP. Treatment with the specific arginase inhibitor 2(S)amino-6-boronohexanoic acid (ABH) prevented hyperoxia-induced apoptosis of BRE cells and reduced vaso-obliteration in the OIR model. Furthermore, deletion of the arginase 2 gene protected against hyperoxia-induced vaso-obliteration, enhanced physiological vascular repair, and reduced retinal neovascularization in the OIR model. Additional deletion of one copy of arginase 1 did not improve the vascular pathology. Analyses of peroxynitrite by quantitation of its biomarker nitrotyrosine, superoxide by dihydroethidium imaging and NO formation by diaminofluoroscein imaging showed that the protective actions of arginase 2 deletion were associated with blockade of superoxide and peroxynitrite formation and normalization of NOS activity. Conclusions: Our data demonstrate the involvement of arginase activity and arginase 2 expression in hyperoxia-induced vascular injury. Arginase 2 deletion prevents hyperoxia-induced retinal vascular injury by preventing NOS uncoupling resulting in decreased reactive oxygen species formation and increased nitric oxide bioavailability.