No abstract

A low rate of apoptosis and high bcl-2 expression were recognized in EBV-positive gastric carcinomas, suggesting that bcl-2 protein is the main inhibitor of apoptosis in EBV-positive carcinomas. In addition, the low apoptotic and proliferative activities may reflect a low biological activity in EBV-positive gastric carcinomas.

We examined apoptosis in 33 gastric carcinomas using the terminal deoxynucleotydil transferase mediated dUTP-digoxigenin nick end labelling technique (TUNEL). Of the tumours, nine were well-differentiated, 13 moderately differentiated and 11 poorly differentiated. In addition, we also analysed MIB-1, a cell proliferation antigen. Morphologically, apoptotic tumour cells were more frequently observed in well-differentiated tumours. In addition, apoptotic signals of the TUNEL method were seen even in the nuclei of tumour cells which did not show apoptosis. The nick end labelling index was 51.0 +/- 26.3 in the well-differentiated and moderately differentiated tumours and 28.0 +/- 18.8 in poorly differentiated tumours. The mean of apoptotic body index and nick end labelling index were both significantly higher in well-differentiated and moderately differentiated tumours than in the poorly differentiated type (P < 0.0001, P = 0.008). The MIB-1 labelling index and higher in poorly differentiated tumours than in the well-differentiated or moderately differentiated tumours, and labelled cells were more numerous in the superficial region than in the middle and deep regions of tumours. No apparent correlation was found between the nick end labelling index and the MIB-1 labelling index. The high number of apoptotic cells (the high Nick end labelling index) and low proliferation potentiality (the low MIB-1 labelling index) in well-differentiated gastric carcinomas may thus be related to their natural tendency to demonstrate slow growth.

The results suggest that OHD is less expensive to use than GD, and the risk of wound infection is not increased compared to GD.

Cell death can now be divided into necrosis and apoptosis, which are different in their morphology, biochemistry and biological significance. The present study was designed to investigate cell death in histiocytic necrotizing lymphadenitis (HNL). The features of cell death in 10 cases of HNL were analyzed using histiomorphology, ultrastructure and in situ apoptosis detection (ApopTag) methods. Two patterns of cell death were discerned. One was apoptosis of individual cells and the other was necrosis. The first pattern could be observed in all cases and the morphological features of the dead cells were consistent with those of apoptosis, which included distinctive cell volume shrinking and chromatin condensation. The apoptotic cells and bodies could frequently be found to be phagocytosed by the histiocytes. ApopTag was positively stained in most of the morphologically apoptotic cells. By double staining, most ApopTag positive cells were found to be T lymphocytes. A previous report showed that the majority of the proliferative cells were T lymphocytes. Based on those results, if was speculated that the main pathological characteristics of HNL therefore consisted of apoptosis and the proliferation of T lymphocytes.