The Experts below are selected from a list of 7602 Experts worldwide ranked by ideXlab platform
Hirofumi Makino - One of the best experts on this subject based on the ideXlab platform.
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interCellular adhesion molecule 1 mediates Mononuclear Cell Infiltration into rat glomeruli after renal ablation
Nephron, 1998Co-Authors: Nobuyuki Miyatake, Masayuki Miyasaka, Hikaru Sugimoto, Kenichi Shikata, Masahiko Kushiro, Yasushi Shikata, Saeko Ogawa, Yoshiko Hayashi, Hirofumi MakinoAbstract:Mononuclear Cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. InterCellular adhesion molecule 1 (ICAM-1)
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Increased expression of interCellular adhesion molecule-1 (ICAM-1) in diabetic rat glomeruli : glomerular hyperfiltration is a potential mechanism of ICAM-1 upregulation
Diabetes, 1997Co-Authors: Hikaru Sugimoto, Masayuki Miyasaka, Kenichi Shikata, Kyoji Hirata, Kenji Akiyama, Mitsuhiro Matsuda, Masahiko Kushiro, Yasushi Shikata, Nobuyuki Miyatake, Hirofumi MakinoAbstract:Mononuclear Cells, including monocytes/macrophages and T-Cells, are considered to be involved in the progression of diabetic nephropathy, although the mechanism of their recruitment into diabetic glomeruli is unclear. The interCellular adhesion molecule-1 (ICAM-1) promotes the Infiltration of leukocytes into atherosclerotic lesions as well as inflammatory tissues. In the present study, we investigated the expression of ICAM-1 in the glomeruli of streptozotocin-induced diabetic rats. The expression of ICAM-1 was increased significantly during the early stage of diabetes. The number of Mononuclear Cells, primarily monocytes/macrophages and lymphocytes, was significantly increased in diabetic glomeruli. Mononuclear Cell Infiltration into diabetic glomeruli was prevented by anti-ICAM-1 monoclonal antibody. Insulin treatment decreased ICAM-1 expression and Mononuclear Cell Infiltration. The ICAM-1 expression on cultured human umbilical vein endothelial Cells was not induced under high glucose culture conditions. Glomerular hyperfiltration is a characteristic change in the early stage of diabetic nephropathy. Treatment with aldose reductase inhibitor, which prevented glomerular hyperfiltration without changes in blood glucose levels, decreased ICAM-1 expression and Mononuclear Cell Infiltration. Moreover, we examined the ICAM-1 expression in the glomeruli of the 5/6 nephrectomized rat, which is a model for glomerular hyperfiltration without hyperglycemia. The ICAM-1 expression and Infiltration of Mononuclear Cells was significantly increased in the glomeruli of 5/6 nephrectomized rats. We conclude that ICAM-1 is upregulated and promotes the recruitment of Mononuclear Cells in diabetic glomeruli. Moreover, glomerular hyperfiltration that occurs in the early stage of diabetic glomeruli may be one of the potential mechanisms of ICAM-1 upregulation in diabetic nephropathy.
William J Karpus - One of the best experts on this subject based on the ideXlab platform.
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cc chemokine receptor 2 is critical for induction of experimental autoimmune encephalomyelitis
Journal of Experimental Medicine, 2000Co-Authors: Brian T Fife, Gary B Huffnagle, William A Kuziel, William J KarpusAbstract:Experimental autoimmune encephalomyelitis (EAE) is a CD4+ T lymphocyte–mediated disease of the central nervous system (CNS) characterized by Mononuclear Cell Infiltration, demyelination, and paralysis. We previously demonstrated a role for chemokines in acute and relapsing EAE pathogenesis. Presently, we investigated the role of CC chemokine receptor 2 (CCR2) in acute EAE. CCR2−/− mice did not develop clinical EAE or CNS histopathology, and showed a significant reduction in T Cell– and CNS-infiltrating CD45highF4/80+ monocyte subpopulations. Peripheral lymphocytes from CCR2−/− mice produced comparable levels of interferon-gamma (IFN-γ) and interleukin (IL)-2 in response to antigen-specific restimulation when compared with control mice. Adoptively transferred myelin oligodendrocyte glycoprotein 35-55–specific T Cells lacking expression of CCR2 were able to induce EAE, whereas CCR2−/− recipients of wild-type T Cells failed to develop disease. These results suggest that CCR2 expression on host-derived Mononuclear Cells is critical for disease induction.
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acute and relapsing experimental autoimmune encephalomyelitis are regulated by differential expression of the cc chemokines macrophage inflammatory protein 1α and monocyte chemotactic protein 1
Journal of Neuroimmunology, 1998Co-Authors: Kevin J Kennedy, Robert M Strieter, Steven L Kunkel, Nicholas W Lukacs, William J KarpusAbstract:Abstract Experimental autoimmune encephalomyelitis (EAE) is a T lymphocyte-mediated disease of the central nervous system (CNS), characterized by Mononuclear Cell Infiltration and demyelination resulting in paralysis. We examined CC chemokine expression in the CNS throughout the entire course of the disease and found that the production of macrophage inflammatory protein (MIP)-1α correlated with increasing acute disease severity and remained elevated throughout chronic, relapsing disease. In contrast, a substantial level of monocyte chemotactic protein (MCP)-1 expression was not observed until late in acute disease and continued to be evident in the relapsing phase of the disease. MCP-1 expression correlated with increasing severity of clinical relapses. Lower levels of RANTES in the CNS were noted throughout the disease course, but showed little correlation with either acute or relapsing disease. Although RANTES expression was observed during the entire course of disease, anti-RANTES treatment had no effect on clinical disease progression. Anti-MCP-1, but not anti-MIP-1α, treatment during relapsing EAE decreased clinical severity of relapsing disease. Furthermore, anti-MCP-1 treatment reduced CNS macrophage accumulation during relapsing EAE. These results suggest that MIP-1α controls Mononuclear Cell accumulation during acute EAE, while MCP-1 controls Mononuclear Cell Infiltration during relapsing EAE.
Takashi Sawai - One of the best experts on this subject based on the ideXlab platform.
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vascular lesion in a patient of chronic active epstein barr virus infection with hypersensitivity to mosquito bites vasculitis induced by mosquito bite with the Infiltration of nonneoplastic epstein barr virus positive Cells and subsequent developmen
Human Pathology, 2005Co-Authors: Fumihiko Maeda, Hanae Onodera, Shoichi Chida, Mikiya Endo, Hiroyuki Kanno, Toshihide Akasaka, Takashi SawaiAbstract:This report describes a vasculitis and subsequently developing angiodestructive lymphoma in an 11-year-old Japanese-Filipino girl exhibiting mosquito allergy with the background of chronic active Epstein-Barr virus (EBV) infection. She developed necrotic skin ulcer at the site of mosquito bite, and histopathological examination revealed EBV-positive Mononuclear Cell Infiltration throughout the wall of small-sized muscular artery. These EBV-positive lymphoid Cells were oligoclonal in Southern blot analysis for EBV terminal repeats. Effectiveness of steroid therapy also supports the nonneoplastic nature. Approximately 1 year later, she developed progressive large skin ulcer without mosquito bites. Microscopically, the angiocentric or angiodestructive pattern of EBV-positive atypical Cells supported the diagnosis of extranodal natural killer/T-Cell lymphoma. Southern blot analysis revealed the monoclonal neoplastic nature of EBV-positive Cells. In contrast to the primary mosquito bite lesion, natural killer/T-Cell lymphoma Cells exhibited the higher expression of EBV latent membrane protein 1 mRNA and the apparent protein expression detected by immunohistochemistry.
Mehmet Haberal - One of the best experts on this subject based on the ideXlab platform.
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relationship of hla dr expression to rejection and Mononuclear Cell Infiltration in renal allograft biopsies
Renal Failure, 2004Co-Authors: Handan B Ozdemir, Pinar Kaynak Aksoy, Nihan A Haberal, Beyhan Demirhan, Mehmet HaberalAbstract:Research on renal biopsies has shown that HLA class I antigens are distributed throughout the renal parenchyma, but that the distribution of HLA-DR varies greatly. We investigated HLA-DR expression in biopsies of 90 renal transplants, and also semiquantitatively assessed the proportions of CD68-, CD3-, and HLA-DR-positive infiltrating Cells by immunohistochemistry. The relationships between tubular DR expression and interstitial lymphocyte and macrophage Infiltration were examined. Forty of the biopsies showed acute rejection (AR), 33 showed chronic rejection (CR), 10 showed suspected rejection (SR), and 7 showed no evidence of rejection (NR). HLA-DR expression was noted in 35/40 (87.5%) of the AR cases, 22/33 (66.6%) of the CR cases, and 6/10 (60%) of the SR cases. Only 1 (14.3%) of the NR cases exhibited HLA-DR antigen expression in the renal tubules. The proportions of lymphocyte and macrophage Infiltration observed in the interstitium were significantly correlated with tubular DR expression in all cases (p<0.01). At 6 months after biopsy was done, 24/35 (68.6%) of the AR patients with tubular DR expression had showed second episode of rejection or showed deteriorated renal function. The remaining 11 AR cases with tubular DR expression had stable renal function at this stage. The cases that had no significant tubular DR expression had no problems with rejection or functional deterioration. These findings are consistent with the theory that expression of HLA-DR antigens on renal tubular Cells may be a marker of rejection and poor graft outcome.
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relationship of hla dr expression with rejection and Mononuclear Cell Infiltration in renal allograft biopsies
Tissue Antigens, 2002Co-Authors: Handan B Ozdemir, Nihan A Haberal, Beyhan Demirhan, Kaynak P Aksoy, Mehmet HaberalAbstract:Research on renal biopsies has shown that HLA class I antigens are distributed throughout the renal parenchyma, but that the distribution of HLA-DR varies greatly. We investigated HLA-DR expression in the biopsies of 90 renal transplants, and also semiquantitatively assessed the proportions of CD68-, CD3-, and HLA-DR-positive infiltrating Cells by immunohistochemistry. The relationships between tubular DR expression and interstitial lymphocyte and macrophage Infiltration were examined. Forty of the biopsies showed acute rejection (AR), 33 showed chronic rejection (CR), 10 showed suspected rejection (SR), and seven showed no evidence of rejection (NR). HLA-DR expression was noted in 35/40 (87.5%) of the AR cases, 22/33 (66.6%) of the CR cases, and 6/10 (60%) of the SR cases. Only one (14.3%) of the NR cases exhibited HLA-DR antigen expression in the renal tubules. The proportions of lymphocyte and macrophage Infiltration observed in the interstitium were significantly correlated with the tubular DR expression in all cases (P<0.01). Six months after the biopsies were carried out, 24/35 (68.6%) of the AR patients with tubular DR expression showed second-episode rejection or deteriorated renal function. The remaining 11 AR cases with tubular DR expression had stable renal function at this stage. The cases that had no significant tubular DR expression had no problems with rejection or functional deterioration. These findings are consistent with the theory that expression of HLA-DR antigens on renal tubular Cells may be a marker of rejection and poor graft outcome.
Hikaru Sugimoto - One of the best experts on this subject based on the ideXlab platform.
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interCellular adhesion molecule 1 mediates Mononuclear Cell Infiltration into rat glomeruli after renal ablation
Nephron, 1998Co-Authors: Nobuyuki Miyatake, Masayuki Miyasaka, Hikaru Sugimoto, Kenichi Shikata, Masahiko Kushiro, Yasushi Shikata, Saeko Ogawa, Yoshiko Hayashi, Hirofumi MakinoAbstract:Mononuclear Cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. InterCellular adhesion molecule 1 (ICAM-1)
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Increased expression of interCellular adhesion molecule-1 (ICAM-1) in diabetic rat glomeruli : glomerular hyperfiltration is a potential mechanism of ICAM-1 upregulation
Diabetes, 1997Co-Authors: Hikaru Sugimoto, Masayuki Miyasaka, Kenichi Shikata, Kyoji Hirata, Kenji Akiyama, Mitsuhiro Matsuda, Masahiko Kushiro, Yasushi Shikata, Nobuyuki Miyatake, Hirofumi MakinoAbstract:Mononuclear Cells, including monocytes/macrophages and T-Cells, are considered to be involved in the progression of diabetic nephropathy, although the mechanism of their recruitment into diabetic glomeruli is unclear. The interCellular adhesion molecule-1 (ICAM-1) promotes the Infiltration of leukocytes into atherosclerotic lesions as well as inflammatory tissues. In the present study, we investigated the expression of ICAM-1 in the glomeruli of streptozotocin-induced diabetic rats. The expression of ICAM-1 was increased significantly during the early stage of diabetes. The number of Mononuclear Cells, primarily monocytes/macrophages and lymphocytes, was significantly increased in diabetic glomeruli. Mononuclear Cell Infiltration into diabetic glomeruli was prevented by anti-ICAM-1 monoclonal antibody. Insulin treatment decreased ICAM-1 expression and Mononuclear Cell Infiltration. The ICAM-1 expression on cultured human umbilical vein endothelial Cells was not induced under high glucose culture conditions. Glomerular hyperfiltration is a characteristic change in the early stage of diabetic nephropathy. Treatment with aldose reductase inhibitor, which prevented glomerular hyperfiltration without changes in blood glucose levels, decreased ICAM-1 expression and Mononuclear Cell Infiltration. Moreover, we examined the ICAM-1 expression in the glomeruli of the 5/6 nephrectomized rat, which is a model for glomerular hyperfiltration without hyperglycemia. The ICAM-1 expression and Infiltration of Mononuclear Cells was significantly increased in the glomeruli of 5/6 nephrectomized rats. We conclude that ICAM-1 is upregulated and promotes the recruitment of Mononuclear Cells in diabetic glomeruli. Moreover, glomerular hyperfiltration that occurs in the early stage of diabetic glomeruli may be one of the potential mechanisms of ICAM-1 upregulation in diabetic nephropathy.