ABSTRACT
In this study, we analyzed high expression of protein phosphatase (PP) 2A in Alzheimer's disease brain compared to that of the control brain, which result from hyperphosphorylation of histone H1. PP1alpha and PP1gamma1 were slightly expressed in all cases, but there was no relation to the levels of the phosphate in histone H1.
Subject(s)
Alzheimer Disease/metabolism , Histones/metabolism , Phosphoprotein Phosphatases/metabolism , Phosphotransferases/metabolism , Alzheimer Disease/enzymology , Case-Control Studies , Humans , Phosphorylation , Protein Phosphatase 2ABSTRACT
Few autopsy cases of sudden death in renal transplant recipients have been reported in the literature. The present case was a 50-year-old female recipient of a living-related renal transplant, who died suddenly after a good post-transplant course of 14 years. The patient was admitted in December 2000 for detailed investigation for ascites, and died unexpectedly 1 month later. She complained of mild dyspnoea approximately 3 h before death. Detailed clinical and laboratory investigations after admission showed no malignant findings in the abdominal cavity. Postmortem pathological examination also showed no tumour in the abdominal cavity. Both lungs were pneumatized. Histopathological examinations revealed metastatic calcification. Calcification was observed in the heart, lungs, kidney graft and pancreas. Calcification in the heart was found in the central fibrous body surrounding the atrioventricular node and bundle of His, as well as in the origin of bifurcating bundle. In the myocardial fibres, fibre rupture and waviness were observed. Although these findings may indicate agonal changes, they might also be a consequence of sudden cardiac death. This patient was in a state of renal failure, which presumably caused metastatic calcification involving also the cardiac conduction system. This calcification might partially account for the sudden death.
Subject(s)
Calcinosis/pathology , Death, Sudden/pathology , Kidney Transplantation , Death, Sudden, Cardiac/pathology , Female , Humans , Middle Aged , Myocardium/pathologyABSTRACT
BACKGROUND: Investigation of transcription regulators in carcinoma can contribute greatly to clarifying the biological character of the carcinoma. In this study, we examined the expression of ets-1 and ets-2, prominent transcription regulators belonging to the ets family, in various colonic tissues. MATERIALS AND METHODS: We investigated the expression of ets-1 and ets-2 in normal colon, hyperplastic polyps, adenomas, carcinoma-in-adenoma and colonic adenocarcinomas by means of immunohistochemistry. RESULTS: Expression of ets-1 and ets-2 was not observed in normal colon and hyperplastic polyp. The ets-1 labeling index significantly increased with the successive events of colonic carcinogenesis. A similar tendency was observed for ets-2 expression in colonic neoplasms. In adenocarcinoma, ets-1 and ets-2 expression was directly linked to lymph node metastasis. CONCLUSION: These results suggest that ets-1 and ets-2 may act as transcription regulators of the genes related to colonic carcinogenesis and the progression of colonic adenocarcinoma.
Subject(s)
Adenocarcinoma/metabolism , Colonic Neoplasms/metabolism , DNA-Binding Proteins , Proto-Oncogene Proteins/biosynthesis , Repressor Proteins , Trans-Activators/biosynthesis , Transcription Factors/biosynthesis , Adenocarcinoma/pathology , Adenoma/metabolism , Adenoma/pathology , Cell Transformation, Neoplastic/metabolism , Colon/metabolism , Colon/pathology , Colonic Neoplasms/pathology , Colonic Polyps/metabolism , Colonic Polyps/pathology , Epithelium/metabolism , Humans , Hyperplasia , Immunohistochemistry , Proto-Oncogene Protein c-ets-1 , Proto-Oncogene Protein c-ets-2 , Proto-Oncogene Proteins c-etsABSTRACT
BACKGROUND: Cell-proliferating activity is one of the prominent parameters for evaluating the biological aggressiveness of carcinomas. Pancreatic adenocarcinoma has been studied to identify modulators of the G1-S boundary. In the present study we investigated the modulators of another important checkpoint, the G2-M checkpoint. METHODS: We immunohistochemically studied three representative G2-M modulators, cdc2, cyclin A and cyclin B1 in 62 pancreatic adenocarcinomas and 7 cystadenomas. RESULTS: Overexpression of cdc2, cyclin A and cyclin B1, was observed in 54.8, 54.9 and 56.4%, respectively, of the pancreatic adenocarcinomas. cdc2 overexpression was directly related to lymph node metastasis, Ki-67 labeling index (LI), and cyclin A overexpression which was significantly linked to the stage, carcinoma differentiation, tumor size, and lymphatic invasion. On the other hand, cyclin B1 was not linked to clinicopathological parameters including Ki-67 LI and cdc2 overexpression, except for tumor size. CONCLUSION: The findings suggest that cdc2 and cyclin A play a role in the progression of pancreatic adenocarcinoma, while the clinical significance of cyclin B1 remains to be clarified because of its more random expression.
