We examined whether apoptosis occurs in cardiomyocytes by hypoxia in vitro. Neonatal rat cardiomyocytes and nonmyocytes were cultured in 95% N2-5% CO2 atmosphere to produce hypoxic conditions. DNA fragmentation into ultraviolet exposure,2,6 anticancer drugs,8-10 viral infection, 11-3 and hyperthermia,14 in a variety of tissues. Ischemia of the heart, which is usually caused by reduction of coronary flow, induces the death of cardiomyocytes and replacement by fibrosis. Although this cardiomyocyte death is classically believed to be induced via necrosis, which is the mechanism of accidental cell death, its precise mechanism remains unclear. It has been recently reported that ischemia induces apoptotic death in the liver15 and in the brain16 in vivo. Thus, in addition to necrotic death, the mechanism of cardiomyocyte death may be involved in the apoptotic process. © 1994 American Heart Association, Inc.myocytes and nonmyocytes as revealed by Northern blotting and in situ hybridization. In hypoxic conditions, Fas messenger RNA levels in cardiomyocytes were upregulated by twofold over controls, whereas those of nonmyocytes were downregulated. These results indicate that cardiomyocyte death by hypoxia can occur via apoptosis and that Fas antigen may be associated with the mechanism of this apoptotic process. (Circ Res. 1994;75:426-433.)

Dendritic cells (DCs) take up tumour-specific antigen and migrate to regional lymph nodes to generate anti-tumour immunity. Although DC infiltration within human tumour tissue has been reported, the subset distribution has not been fully investigated. This study used immunohistochemistry to investigate DC subset distribution in colorectal adenocarcinoma. DCs expressing CD83, which are considered to be mature DCs, were present mainly in the invasive margin of cancer stroma. CD83(+) DCs in the invasive margin formed clusters with lymphocytes, the majority of which were CD45RO(+) T cells. The number of CD4(+) T cells was greater than that of CD8(+) T cells in these DC-lymphocyte clusters. The elongated cytoplasmic processes of CD83(+) DCs engulfed CD4(+) T cells. DCs that express CD1a were located throughout tumour tissue. Although the number of CD1a(+) DCs was almost the same as that of CD83(+) DCs in the invasive margin of cancer stroma, CD1a(+) DCs were mostly scattered and rarely formed clusters with lymphocytes. DCs that expressed both CD1a and CD83 were rare. Moreover, about 20% of lymphocytes in DC-lymphocyte clusters were positive for Ki-67, and CD83(+) DCs were attached to Ki-67(+) cells. CD83(+) DCs were also present in T-cell areas that had a distinctive structure involving the presence of B-cell lymphoid follicles. These results suggest that in the invasive margin of the colorectal cancer stroma, mature CD83(+) DCs form clusters with T cells to promote T-cell activation for the generation of tumour-specific immunity.

A case of transfusion-associated graft-versus-host disease (TA-GVHD) in a patient with non-Hodgkin's lymphoma is reported. The patient, a 67-year-old woman, was diagnosed as having diffuse, mixed type non-Hodgkin's lymphoma, at clinical stage IIIA. She was treated with combination chemotherapy and received multiple blood transfusions for anemia and thrombocytopenia. Although white cells (WBCs) were reduced in the transfused components by WBC-reduction filters, the patient developed TA-GVHD that was confirmed by skin biopsy. It is suggested that the WBC reduction attained with these filters does not prevent TA-GVHD in immunocompromised patients. It is recommended that all blood components should be irradiated before transfusion to such patients.

Excess amounts of NO produced by iNOS appear to contribute to the progression of myocardial damage in myocarditis. AG may prove to be useful in the treatment of myocarditis.