Objective: To investigate the time course of serum S-100 concentrations of patients with acute cerebral infarction,and their relation with the clinical data and the prognosis. Methods: Serum S-100 levels were serially...Objective: To investigate the time course of serum S-100 concentrations of patients with acute cerebral infarction,and their relation with the clinical data and the prognosis. Methods: Serum S-100 levels were serially determined in 36 patients with acute cerebral infarction within 12 h, at 24 h and day 2, 3, 4, 5, 7 and 10 after acute cerebral infarction and in 20 age- and sex-matched control subjects. An S-100 content assay was performed using a two-site radioimmunoassay technique. The clinical status was assessed using NIH Stroke Scale. The functional deficit at 4 weeks after acute cerebral infarction was scored using the modified Rankin scale. A cranial computed tomography was performed initially. Results: Elevated concentrations of S-100 (>0.2 μg/L) were observed in 29 of 36 patients with acute cerebral infarction,but none of the control subjects. The S-100 peak levels were at day 2 and 3 after acute cerebral infarction and were significantly high in those patients with severe neurological deficit at admission, with extensive infarction or with space-occupying effect of ischemic edema as compared with the rest of the populations. Conclusion: Serum S-100 level assay can be used as a peripheral marker of ischemic brain damage, and may be helpful for evaluation of therapeutic effects in acute ischemic stroke.展开更多
To investigate the expression and distribution of S-100 protein and CD83 in the thyroid tissues of autoimmune thyroid diseases (ATDs), and to study the role of the dendritic cells in the pathogenesis of ATDs,immunohis...To investigate the expression and distribution of S-100 protein and CD83 in the thyroid tissues of autoimmune thyroid diseases (ATDs), and to study the role of the dendritic cells in the pathogenesis of ATDs,immunohistochemical staining was used on pathological tissues of 20 patients with Hashimoto's thyroiditis (HT)and 20 patients with Graves' disease (GD) to check the expression and distribution of S-100 protein and CD83.Compared with control group (20 cases of thyroid follicular adenoma, TFA), the higher expressions of S-100 in HT (139.38±5.92 vs 59.47±11.69) and GD (119.42±14.48 vs 59.47±11.69) were observed respectively (p＜0.001). The increased positive expressions of CD83 which is known as a marker of mature and activated DCs in HT (22.58±13.96 vs 5.19±8.08) and GD (29.92±14.43 vs 5.19±8.08) were also found respectively (p＜0.001).Serum TPO antibody (TPO-Ab, 67.3 ± 11.6%) and Tg antibody (Tg-Ab, 59.8±10.1%) in HT were higher than that in GD (28.4±5.7%, 23.1±4.9%) and that in TFA (6.1±3.4%, 7.2±4.6%)(p＜0.01). Serum TR-Ab in GD(16.3±5.6 U/L) was higher than that in HT (4.8±2.3 U/L) and that in TFA (2.5±1.2 U/L) (p＜0.01). Our findings suggest that the high expression of DCs' markers may be related to the pathogenesis of HT and GD.The upregulation of both number and matured functions of DCs, may lead to present more antigens and to produce more auto-antibodies (such as TgAb and TPOAb in HT, TRAb in GD), which may be involved in pathogenesis of the autoimmune thyroid diseases. Cellular & Molecular Immunology. 2004; 1(5):378-382.展开更多
文摘Objective: To investigate the time course of serum S-100 concentrations of patients with acute cerebral infarction,and their relation with the clinical data and the prognosis. Methods: Serum S-100 levels were serially determined in 36 patients with acute cerebral infarction within 12 h, at 24 h and day 2, 3, 4, 5, 7 and 10 after acute cerebral infarction and in 20 age- and sex-matched control subjects. An S-100 content assay was performed using a two-site radioimmunoassay technique. The clinical status was assessed using NIH Stroke Scale. The functional deficit at 4 weeks after acute cerebral infarction was scored using the modified Rankin scale. A cranial computed tomography was performed initially. Results: Elevated concentrations of S-100 (>0.2 μg/L) were observed in 29 of 36 patients with acute cerebral infarction,but none of the control subjects. The S-100 peak levels were at day 2 and 3 after acute cerebral infarction and were significantly high in those patients with severe neurological deficit at admission, with extensive infarction or with space-occupying effect of ischemic edema as compared with the rest of the populations. Conclusion: Serum S-100 level assay can be used as a peripheral marker of ischemic brain damage, and may be helpful for evaluation of therapeutic effects in acute ischemic stroke.
文摘To investigate the expression and distribution of S-100 protein and CD83 in the thyroid tissues of autoimmune thyroid diseases (ATDs), and to study the role of the dendritic cells in the pathogenesis of ATDs,immunohistochemical staining was used on pathological tissues of 20 patients with Hashimoto's thyroiditis (HT)and 20 patients with Graves' disease (GD) to check the expression and distribution of S-100 protein and CD83.Compared with control group (20 cases of thyroid follicular adenoma, TFA), the higher expressions of S-100 in HT (139.38±5.92 vs 59.47±11.69) and GD (119.42±14.48 vs 59.47±11.69) were observed respectively (p＜0.001). The increased positive expressions of CD83 which is known as a marker of mature and activated DCs in HT (22.58±13.96 vs 5.19±8.08) and GD (29.92±14.43 vs 5.19±8.08) were also found respectively (p＜0.001).Serum TPO antibody (TPO-Ab, 67.3 ± 11.6%) and Tg antibody (Tg-Ab, 59.8±10.1%) in HT were higher than that in GD (28.4±5.7%, 23.1±4.9%) and that in TFA (6.1±3.4%, 7.2±4.6%)(p＜0.01). Serum TR-Ab in GD(16.3±5.6 U/L) was higher than that in HT (4.8±2.3 U/L) and that in TFA (2.5±1.2 U/L) (p＜0.01). Our findings suggest that the high expression of DCs' markers may be related to the pathogenesis of HT and GD.The upregulation of both number and matured functions of DCs, may lead to present more antigens and to produce more auto-antibodies (such as TgAb and TPOAb in HT, TRAb in GD), which may be involved in pathogenesis of the autoimmune thyroid diseases. Cellular & Molecular Immunology. 2004; 1(5):378-382.
