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.

A Review of Epidemiologic Studies of the Health of Gulf War Women Veterans.

Abstract: Introduction In the 25 years since the 1990-1991 Gulf War (GW), studies have evaluated Gulf War Illness (GWI), sometimes referred to as medically unexplained multi symptom illness, and other medical and neurological conditions in women GW veterans. Materials and methods In this article, we review epidemiologic studies of the health of women who served in the 1990-1991 GW based upon bibliographic searches in PubMed and CINAHL with relevant search terms through September 2015. Results A total of 56 articles were identified in the bibliographic searches. By screening abstracts or full-text articles, a total of 21 relevant studies were identified. Results from some studies, but not all, suggest that GWI is more common in women GW veterans than their male counterparts. Few studies of GW veterans focused on women's health. A small number of studies suggested excess rates of woman's health problems, e.g., breast cysts, abnormal Papanicolaou (Pap) smears, yeast infections, and bladder infections. Several studies have identified significantly elevated rates of birth defects and adverse reproductive outcomes among GW veterans. However, findings have varied with different study designs and sample sizes, with some studies showing elevated risks of stillbirths, miscarriages, and/or birth defects and others have not. In some studies, participants reported increased risks of ectopic pregnancies and spontaneous abortions. Conclusion Further research is needed to provide a comprehensive picture of the health of women GW veterans and to examine a broad range of women's health issues including adverse reproductive outcomes. Some deployment-related health problems only become apparent decades later and other conditions may worsen or improve over time. Assessments are needed of current health status, changes in health symptoms and conditions over time, and possible differences in health outcomes associated with specific experiences and exposures during the war. Future studies would be strengthened by assessing GWI symptom patterns that may be specific to women veterans, examine diagnosed medical conditions among women veterans, and evaluate changes in women's health over time, including changes potentially associated with menopause and age.

Deletion of TXNIP mitigates high-fat diet-impaired angiogenesis and prevents inflammation in a mouse model of critical limb ischemia

Abstract: Background: Previous work demonstrated that high-fat diet (HFD) triggered thioredoxin-interacting protein (TXNIP) and that silencing TXNIP prevents diabetes-impaired vascular recovery. Here, we examine the impact of genetic deletion of TXNIP on HFD-impaired vascular recovery using hind limb ischemia model. Methods: Wild type mice (WT, C57Bl/6) and TXNIP knockout mice (TKO) were fed either normal chow diet (WT-ND and TKO-ND) or 60% high-fat diet (WT-HFD and TKO-HFD). After four weeks of HFD, unilateral hind limb ischemia was performed and blood flow was measured using Laser doppler scanner at baseline and then weekly for an additional three weeks. Vascular density, nitrative stress, infiltration of CD68+ macrophages, and expression of inflammasome, vascular endothelial growth factor (VEGF), VEGF receptor-2 were examined by slot blot, Western blot and immunohistochemistry. Results: By week 8, HFD caused similar increases in weight, cholesterol and triglycerides in both WT and TKO. At week 4 and week 8, HFD significantly impaired glucose tolerance in WT and to a lesser extent in TKO. HFD significantly impaired blood flow and vascular density (CD31 labeled) in skeletal muscle of WT mice compared to ND but not in TKO. HFD and ischemia significantly induced tyrosine nitration, and systemic IL-1β and infiltration of CD68+ cells in skeletal muscle from WT but not from TKO. HFD significantly increased cleaved-caspase-1 and IL-1 β compared to ND. Under both ND, ischemia tended to increase VEGF expression and increased VEGFR2 activation in WT only but not TKO. Conclusion: Similar to prior observation in diabetes, HFD-induced obesity can compromise vascular recovery in response to ischemic insult. The mechanism involves increased TXNIP-NLRP3 (nucleotide-binding oligomerization domain-like receptor protein 3) inflammasome activation, nitrative stress and impaired VEGFR2 activation. Deletion of TXNIP restored blood flow, reduced nitrative stress and blunted inflammasome-mediated inflammation; however, it did not impact VEGF/VEGFR2 in HFD. Targeting TXNIP-NLRP3 inflammasome can provide potential therapeutic target in obesity-induced vascular complication.