Đang chuẩn bị nút TẢI XUỐNG, xin hãy chờ
Tải xuống
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Morphological characterization of intra-articular HMGB1 expression during the course of collagen-induced arthritis. | Available online http arthritis-research.eom content 9 2 R35 Research article Morphological characterization of intra-articular HMGB1 expression during the course of collagen-induced arthritis Karin Palmblad1 2 Erik Sundberg1 2 Margarita Diez3 Riikka Soderling2 Ann-Charlotte Aveberger2 Ulf Andersson1 2 and Helena Erlandsson Harris2 Open Access Department of Woman and Child Health Karolinska Institutet Astrid Lindgren Children s Hospital SE-171 76 Stockholm Sweden department of Medicine Rheumatology Research Unit Center of Molecular Medicine L8 04 Karolinska Institutet SE-171 76 Stockholm Sweden department of Clinical Neuroscience Neuroimmunology Unit Center of Molecular Medicine L8 04 Karolinska Institutet SE-171 76 Stockholm Sweden Corresponding author Karin Palmblad Karin.Palmblad@ki.se Received 18 Nov 2006 Revisions requested 21 Dec 2006 Revisions received 9 Feb 2007 Accepted 30 Mar 2007 Published 30 Mar 2007 Arthritis Research Therapy 2007 9 R35 doi 10.1186 ar2155 This article is online at http arthritis-research.com content 9 2 R35 2007 Palmblad et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract High-mobility group chromosomal box protein 1 HMGB1 is a structural nuclear protein that promotes inflammation when present extracellularly. Aberrant extracellular HMGB1 expression has been demonstrated in human and experimental synovitis. The aim of the present study was to elucidate the temporal and spatial expression of HMGB1 compared to that of the central mediators tumor necrosis factor TNF and interleukin-1-beta IL-1P during the course of collagen-induced arthritis. Thus Dark Agouti rats were immunized with homologous type II collagen and synovial tissue specimens were obtained at various time points prior to
