The Experts below are selected from a list of 11940 Experts worldwide ranked by ideXlab platform
Stephen J Dumler - One of the best experts on this subject based on the ideXlab platform.
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lymph node hemophagocytosis in rickettsial diseases a pathogenetic role for cd8 t lymphocytes in human monocytic ehrlichiosis hme
BMC Infectious Diseases, 2006Co-Authors: Kerry L. Dierberg, Stephen J DumlerAbstract:Human monocytic ehrlichiosis (HME) and Rocky Mountain spotted fever (RMSF) are caused by Ehrlichia chaffeensis and Rickettsia rickettsii, respectively. The pathogenesis of RMSF relates to rickettsia-Mediated vascular Injury, but it is unclear in HME. To study histopathologic responses in the lymphatic system for correlates of Immune Injury, lymph nodes from patients with HME (n = 6) and RMSF (n = 5) were examined. H&E-stained lymph node tissues were examined for five histopathologic features, including hemophagocytosis, cellularity, necrosis, and vascular congestion and edema. The relative proportions of CD68 macrophages, CD8 and CD4 T lymphocytes, and CD20 B lymphocytes were evaluated by immunohistochemical staining. Hemophagocytosis was similar in HME and RMSF, and was greater than in control cases (p = .015). Cellularity in HME was not different from controls, whereas RMSF lymph nodes were markedly less cellular (p < 0.002). E. chaffeensis-infected mononuclear phagocytes were infrequent compared to R. rickettsii-infected endothelial cells. More CD8 cells in lymph nodes were observed with HME (p < .001), but no quantitative differences in CD4 lymphocytes, macrophages, or B lymphocytes were identified. Hemophagocytosis, CD8 T cell expansion, and the paucity of infected cells in HME, suggest that E. chaffeensis infection leads to macrophage activation and Immune-Mediated Injury.
Jeffrey B Halter - One of the best experts on this subject based on the ideXlab platform.
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islet autoimmunity identifies a unique pattern of impaired pancreatic beta cell function markedly reduced pancreatic beta cell mass and insulin resistance in clinically diagnosed type 2 diabetes
PLOS ONE, 2014Co-Authors: Angela Subauste, Roberto Gianani, Annette M Chang, Cynthia Plunkett, Susan L Pietropaolo, Ying Jian Zhang, Emma Barinasmitchell, Lewis H Kuller, Andrzej T Galecki, Jeffrey B HalterAbstract:There is a paucity of literature describing metabolic and histological data in adult-onset autoImmune diabetes. This subgroup of diabetes mellitus affects at least 5% of clinically diagnosed type 2 diabetic patients (T2DM) and it is termed Latent AutoImmune Diabetes in Adults (LADA). We evaluated indexes of insulin secretion, metabolic assessment, and pancreatic pathology in clinically diagnosed T2DM patients with and without the presence of humoral islet autoimmunity (Ab). A total of 18 patients with at least 5-year duration of clinically diagnosed T2DM were evaluated in this study. In those subjects we assessed acute insulin responses to arginine, a glucose clamp study, whole-body fat mass and fat-free mass. We have also analyzed the pancreatic pathology of 15 T2DM and 43 control cadaveric donors, using pancreatic tissue obtained from all the T2DM organ donors available from the nPOD network through December 31, 2013. The presence of islet Ab correlated with severely impaired β-cell function as demonstrated by remarkably low acute insulin response to arginine (AIR) when compared to that of the Ab negative group. Glucose clamp studies indicated that both Ab positive and Ab negative patients exhibited peripheral insulin resistance in a similar fashion. Pathology data from T2DM donors with Ab or the autoImmune diabetes associated DR3/DR4 allelic class II combination showed reduction in beta cell mass as well as presence of autoImmune-associated pattern A pathology in subjects with either islet autoantibodies or the DR3/DR4 genotype. In conclusion, we provide compelling evidence indicating that islet Ab positive long-term T2DM patients exhibit profound impairment of insulin secretion as well as reduced beta cell mass seemingly determined by an Immune-Mediated Injury of pancreatic β-cells. Deciphering the mechanisms underlying beta cell destruction in this subset of diabetic patients may lead to the development of novel immunologic therapies aimed at halting the disease progression in its early stage.
Jai Radhakrishnan - One of the best experts on this subject based on the ideXlab platform.
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drug induced glomerular disease Immune Mediated Injury
Clinical Journal of The American Society of Nephrology, 2015Co-Authors: Jonathan J Hogan, Glen S Markowitz, Jai RadhakrishnanAbstract:Drug-induced autoImmune disease was initially described decades ago, with reports of vasculitis and a lupus-like syndrome in patients taking hydralazine, procainamide, and sulfadiazine. Over the years, multiple other agents have been linked to Immune-Mediated glomerular disease, often with associated autoantibody formation. Certain clinical and laboratory features may distinguish these entities from their idiopathic counterparts, and making this distinction is important in the diagnosis and management of these patients. Here, drug-induced, ANCA-associated vasculitis, drug-induced lupus, and drug-associated membranous nephropathy are reviewed.
Kerry L. Dierberg - One of the best experts on this subject based on the ideXlab platform.
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lymph node hemophagocytosis in rickettsial diseases a pathogenetic role for cd8 t lymphocytes in human monocytic ehrlichiosis hme
BMC Infectious Diseases, 2006Co-Authors: Kerry L. Dierberg, Stephen J DumlerAbstract:Human monocytic ehrlichiosis (HME) and Rocky Mountain spotted fever (RMSF) are caused by Ehrlichia chaffeensis and Rickettsia rickettsii, respectively. The pathogenesis of RMSF relates to rickettsia-Mediated vascular Injury, but it is unclear in HME. To study histopathologic responses in the lymphatic system for correlates of Immune Injury, lymph nodes from patients with HME (n = 6) and RMSF (n = 5) were examined. H&E-stained lymph node tissues were examined for five histopathologic features, including hemophagocytosis, cellularity, necrosis, and vascular congestion and edema. The relative proportions of CD68 macrophages, CD8 and CD4 T lymphocytes, and CD20 B lymphocytes were evaluated by immunohistochemical staining. Hemophagocytosis was similar in HME and RMSF, and was greater than in control cases (p = .015). Cellularity in HME was not different from controls, whereas RMSF lymph nodes were markedly less cellular (p < 0.002). E. chaffeensis-infected mononuclear phagocytes were infrequent compared to R. rickettsii-infected endothelial cells. More CD8 cells in lymph nodes were observed with HME (p < .001), but no quantitative differences in CD4 lymphocytes, macrophages, or B lymphocytes were identified. Hemophagocytosis, CD8 T cell expansion, and the paucity of infected cells in HME, suggest that E. chaffeensis infection leads to macrophage activation and Immune-Mediated Injury.
Robert J. Porte - One of the best experts on this subject based on the ideXlab platform.
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protection of bile ducts in liver transplantation looking beyond ischemia
Transplantation, 2011Co-Authors: Sanna Op Den Dries, Ton Lisman, Michael E Sutton, Robert J. PorteAbstract:Biliary complications, especially nonanastomotic biliary strictures (NAS), are a major cause of morbidity after orthotopic liver transplantation. Of all donor and recipient characteristics known to increase the risk of developing NAS, the role of prolonged ischemia times is most extensively described in the literature. However, there is increasing evidence that several other, non-ischemia-related factors play a critical role in the pathogenesis of NAS as well. The clinical presentation of NAS may vary considerably among liver transplant recipients, including large variations in time of occurrence, and in location and severity of the strictures. Additional underlying causes such as bile salt toxicity and Immune-Mediated Injury are believed to explain the wide spectrum of biliary strictures after orthotopic liver transplantation. Current and emerging insight in the pathogenesis of NAS and potential targets to reduce biliary Injury and preserve bile ducts are discussed in this overview.
