Fereshteh Fani; Eskandar kamali-Sarvestani; Razieh Yazdanparast; Ahmad Monabati; Shahnaz Rafiei
Volume 3, Issue 4 , December 2006, , Pages 169-175
Abstract
Background: Autoimmune type 1 diabetes mellitus is caused by T-cell mediated immune destruction of the insulin-producing β-cell in pancreatic islets of Langerhans. Specificity of the auto-antibodies and of the auto-reactive T-cells has been investigated, in which several auto-antigens were proposed. ...
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Background: Autoimmune type 1 diabetes mellitus is caused by T-cell mediated immune destruction of the insulin-producing β-cell in pancreatic islets of Langerhans. Specificity of the auto-antibodies and of the auto-reactive T-cells has been investigated, in which several auto-antigens were proposed. Objective: To determine whether glutamic acid decarboxylase (GAD) feeding would induce oral tolerance of either T-cell or B-cell compartment in streptozotocin (STZ) diabetic rats. Methods: Rats in the experimental group were fed 2 mg/kg of GAD (extracted from Escherichia coli ) 14 days before intra-peritoneal injections of streptozotocin (30 mg/kg body weight for 5 consecutive days). Two control groups were considered: diabetic control group, which underwent STZ injections without receiving GAD, and normal control group. Systemic response was compared between the three groups. T-cells response was assessed by a proliferation assay of spleen cells and those of the B-cells by enzyme-linked immunosorbent assay (ELISA) for anti-GAD specific antibodies in serum. Results: Compared with the diabetic control group, a significant reduction was observed only in the proliferative response of spleen cells, but not in the level of anti-GAD antibody. Conclusion: GAD feeding induces systemic T-cell tolerance in STZ-induced diabetes.
Nasser Gholijani; Ahmad Monabati; Zahra Amirghofran
Volume 1, Issue 1 , June 2004, , Pages 34-40
Abstract
Background: Prostate cancer is one of the most commonly diagnosed cancers in males. Tumor suppressor gene p53 plays an important role in causing cell cycle arrest and allowing apoptosis to proceed. Objective: To investigate the expression of p53 protein and its relation to apoptosis and prostate cancer ...
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Background: Prostate cancer is one of the most commonly diagnosed cancers in males. Tumor suppressor gene p53 plays an important role in causing cell cycle arrest and allowing apoptosis to proceed. Objective: To investigate the expression of p53 protein and its relation to apoptosis and prostate cancer traditional prognostic indicators. Methods: In this study expression of p53 was examined in paraffin-embedded tissues from 50 cases of prostate carcinoma by immunohistochemistry and evaluated using an index of staining. Correlation between p53 expression and apoptosis was detected by TUNEL method. Pathological grade, Gleason score and stage of carcinoma were also determined. Results: P53 expression was observed in 48 of 50 cases (26-100% of tumor cells) with mean staining index of 141±65. A significant association between p53 expression and pathologic grade (r=0.37, p=0.004) and Gleason score (r= 0.4, p=0.009) of patients was observed. Apoptosis was detected in only 6 patients. p53 expression showed no correlation with apoptotic index. No correlation between p53 expression and stage or apoptosis and clinicopathological characteristics of patients was found. Conclusion: p53 expression showed a significant correlation with differentiation status of the prostate carcinoma and can be helpful as a prognostic marker. Decreased level of apoptosis observed in our cases was not correlated with p53 expression indicating the possible role of other regulatory molecules involved in the apoptosis.
