[Activity of some enzymes in peripheral blood erythrocytes in sportsmen].

It is determined that physical exercises in sportsmen-runners at medium distances cause changes of glucose-6-phosphate dehydrogenase, lactate dehydrogenase and its fractions activity in peripheral blood erythrocytes. The maximal changes are observed after competitions.

Retinoic acid dramatically enhances the arsenic trioxide-induced cell cycle arrest and apoptosis in retinoic acid receptor alpha-positive human T-cell lymphotropic virus type-I-transformed cells.

INTRODUCTION: Adult T-cell leukemia/lymphoma, caused by the human T-cell lymphotropic virus type I, is an aggressive neoplasm of mature activated T cells that is generally resistant to conventional therapy. While arsenic trioxide (As) inhibits the growth and induces apoptosis in HTLV-I-infected T cells, synergistically, when combined with interferon-alpha, variable effects on growth with all trans retinoic acid treatment have been reported in ATL-derived cell lines and fresh ATL cells. In this study, we investigate the effects of ATRA alone or in combination with As in HTLV-I-transformed cells. MATERIALS AND METHODS: Four HTLV-I-transformed cell lines (HuT-102, MT2, C8166 and C91PL) were treated with different doses of ATRA alone or in combination with As for one to three days. Cell growth was assessed by cell count with 3H-thymidine incorporation. Cell cycle distribution was assessed by propidium iodine-labeled DNA content by flow cytometry. Apoptosis was evaluated by Hoechst nuclear staining and annexin-V binding assays. Expression of retinoid receptors, the viral transactivator Tax, and the proteins bcl-2 and IkappaB-alpha proteins, was analysed by Western blot. RESULTS: Only C8166 cells were sensitive to the ATRA-induced growth inhibitory effect while HuT-102, MT2, and C91PL were resistant to ATRA treatment (up to 10(-5) M). The retinoid X receptor alpha and the retinoic acid receptor gamma (RARgamma) proteins were expressed in all four cell lines, while RARalpha protein was only detected in the HuT-102 and C8166 cells. The combination ATRA/As showed a highly synergistic effect on HuT-102 cells, and, to a lesser extent, on C8166 cells and resulted in a dramatic inhibition of cell proliferation and induction of massive apoptosis in HuT-102 cells, associated with caspase activation. While ATRA alone had no effect on Tax and IkappaB-alpha protein levels, ATRA increased the As-induced Tax degradation and the up-regulation of IkappaB-alpha protein. In contrast, the expression of bcl-2 protein was not significantly affected by any of the treatments. CONCLUSION: Our data provide a rationale for combined ATRA and As-therapies in ATL patients refractory to conventional therapy and expressing RARalpha in their leukemic cells.

Survival after antilymphocyte globulin therapy for aplastic anemia depends on disease severity.

Sixty-four patients with aplastic anemia were treated with antilymphocyte globulin (ALG Merieux) between 1980 and 1985. The actuarial survival for all patients was 53% at 6 years, with 79% survival for nonsevere aplastic anemia (NSAA) and 36% for severe aplastic anemia (SAA). The neutrophil and platelet counts before treatment with ALG were highly predictive of survival, whereas sex, age, and etiology were not. Duration of disease prior to ALG treatment was inversely related to survival, although this was not statistically significant. Survival was closely associated with response to ALG, especially for patients with SAA. The response to one course of ALG was 33%. Eighteen patients who did not respond to an initial course of ALG received a second course; of these, four (22%) responded. The overall response to one or two courses of ALG was 40%. The mean RBC volume (MCV) measured after ALG treatment was a useful early indicator of response. Both the minimum lymphocyte count during ALG therapy and the mean lymphocyte count after therapy, however, were not significantly different between responders and nonresponders. The disappointing survival of patients with SAA in this study may reflect the poor clinical condition of severely affected patients referred to us and/or the presence of longstanding aplasia. The importance of studying a large series of patients with long-term follow-up to assess ALG in the treatment of aplastic anemia is shown by this investigation.

Antibody titres to a rough-mutant strain of Escherichia coli in patients undergoing allogeneic bone-marrow transplantation. Evidence of a protective effect against graft-versus-host disease.

Much clinical and experimental evidence suggests that infection and graft-versus-host disease (GvHD) are commonly associated as complications of bone-marrow transplantation (BMT). A likely basis for this association is the gram-negative faecal flora,the origin of many septicaemias and a source of bacterial endotoxin, which has potent immunostimulatory effects. A rough-mutant strain, Escherichia coli J5, has only core determinants in its endotoxin,and antibodies to E coli J5 protect animals and human beings from the consequences of septic shock. Naturally occurring antibodies to E coli J5 ("anti-endotoxin") were assayed in serum from patients undergoing BMT, healthy controls, and patients with obstructive jaundice. BMT recipients had significantly lower titres than the other two groups. Furthermore, the titre of IgM class anti-J5 antibody was significantly associated with protection from GvHD.