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.

The proteolytic effect of bromelain on bullous pemphigoid antigen-2

Abstract: A screen of the histopathologic database identified 142 biopsy-proven cases and 30 cases had both clinical and dermoscopic images of the biopsy site available. All dermoscopic images were captured using a DermLite II Pro polarized light dermatoscope (3Gen LLC). Dermoscopic images were evaluated by two independent dermatologists. Dermoscopic variables were adopted from previous literature describing the dermoscopic features of inflammatory purpuric lesions. Fifteen cases of true vasculitis and 15 cases of vasculopathy were included in this study. Statistical analysis was performed using Fisher’s exact test. Sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) were also obtained for the dermatoscopic diagnosis of vasculitis (Table I). A mottled purpuric pattern was commonly detected in all cases in both groups. Purpuric globules and dots were identified in 40% of the vasculitis group and in 26.7% of the vasculopathy group. An orangebrown backgroundwas found in both groups (40% in the vasculitis group and 53.3% in the vasculopathy group). Blue-gray blotches were exclusively found in the vasculitis group, affecting 73.3%of cases (P\\.001; sensitivity 73.3%, specificity 100%, PPV 100%, NPV 78.9%; Fig 1). These results demonstrated that blue-gray blotch was the most specific dermoscopic feature of true vasculitis, implying vascular injury with severe inflammation. Mottled purpuric pattern, purpuric globules, or dots and orange-brown backgroundwere commonlyobserved inbothgroups, mirroring the peculiar histology of this condition involving perivascular inflammatory cell infiltration, red blood cell extravasation, and hemosiderin deposition, respectively. Based on these findings we recommend searching for a biopsy site that shows dermoscopic findingsof blue-grayblotch for histologic confirmation of true vasculitis. Further prospective studies are needed to confirm the usefulness of the blue-grayblotchpattern for selectionof thebiopsy site.

Differential regulation of TGFβ type-I receptor expressions in TGFβ1-induced myofibroblast differentiation

Abstract: Fibroblast-to-myofibroblast (FibroMF) differentiation is crucial for embryogenesis and organ fibrosis. Although transforming growth factor-β (TGFβ) is the primary mediator of FibroMF differentiatio...

The HMGB1-RAGE axis modulates the growth of autophagy-deficient hepatic tumors

Abstract: Autophagy is an intracellular lysosomal degradative pathway important for tumor surveillance. Autophagy deficiency can lead to tumorigenesis. Autophagy is also known to be important for the aggressive growth of tumors, yet the mechanism that sustains the growth of autophagy-deficient tumors is not unclear. We previously reported that progression of hepatic tumors developed in autophagy-deficient livers required high mobility group box 1 (HMGB1), which was released from autophagy-deficient hepatocytes. In this study we examined the pathological features of the hepatic tumors and the mechanism of HMGB1-mediated tumorigenesis. We found that in liver-specific autophagy-deficient (Atg7ΔHep) mice the tumors cells were still deficient in autophagy and could also release HMGB1. Histological analysis using cell-specific markers suggested that fibroblast and ductular cells were present only outside the tumor whereas macrophages were present both inside and outside the tumor. Genetic deletion of Hmgb1 or one of its receptors, receptor for advanced glycated end product (Rage), retarded liver tumor development. HMGB1 and RAGE enhanced the proliferation capability of the autophagy-deficient hepatocytes and tumors. However, RAGE expression was only found on ductual cells and Kupffer’s cells but not on hepatoctyes, suggesting that HMGB1 might promote hepatic tumor growth through a paracrine mode, which altered the tumor microenvironment. Finally, RNAseq analysis of the tumors indicated that HMGB1 induced a much broad changes in tumors. In particular, genes related to mitochondrial structures or functions were enriched among those differentially expressed in tumors in the presence or absence of HMGB1, revealing a potentially important role of mitochondria in sustaining the growth of autophagy-deficient liver tumors via HMGB1 stimulation.