[Physiological and biochemical aspects of fruit-body formation in Basidiomycetes].
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Biomedical subjects
Publications and source records attributed to Y Kitamoto.
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It has been demonstrated that hyperthermia can enhance the cytotoxicity of several anticancer drugs. Pirarubicin (THP-adriamycin) is a less cardiotoxic derivative of adriamycin. The thermal enhancement of cytotoxicity of pirarubicin was studied at various elevated temperatures in vitro by using a Chinese hamster cell line, V79. Cell survival curves were obtained at elevated temperatures for V79 cells treated with heat given alone or in combination with pirarubicin, and D0, the treatment time to reduce cell survival from S to S/e, was obtained for each cell survival curve. The relationship between the logarithm of the D0 and the treatment temperature for cells treated with heat alone was biphasic with a breaking point at 43 degrees C, although that for cells treated with a combination of heat and pirarubicin was exponential with no breaking point. The slope of this relationship for heat alone > 43 degrees C was -0.72 +/- 0.094 h/degree C which was not significantly different from the slope for combined heat and pirarubicin, -0.64 +/- 0.032 h/degree C. The results indicated that the cytotoxicity of pirarubicin was thermally enhanced specifically by mild hyperthermia. Pirarubicin uptake into the V79 cells during hyperthermia was independent of the treatment temperature (37, 42, and 44 degrees C), suggesting that the thermal enhancement of pirarubicin was not due to the increased drug-uptake at elevated temperatures. Based on these results, it is predictable that hyperthermia combined with pirarubicin is more effective below 43 degrees C which is easily achievable clinically.
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Effect of blood-air contact in the venous line air-trap chamber on blood clotting was studied. Fourteen chronic hemodialysis patients (six men, eight women; mean age, 49 years) with elevation of thrombin-antithrombin III were studied. To prevent blood-air contact, triglyceride (NOF-005) was floated over the blood in the chamber. Control hemodialysis was performed for 4 weeks and hemodialysis using NOF-005 followed for the next 4 weeks. Clot formation in the circuit was examined after each hemodialysis and clotting factors including thrombin-antithrombin III, FXII Antigen, vWF Antigen, PF4 and beta-thromboglobulin were measured before and after the last hemodialysis of each control and NOF-005 hemodialysis. Clotting in the chamber was improved when NOF-005 was used. Thrombin-antithrombin III increase during hemodialysis was suppressed to about 30% of control values by using NOF-005. blood-air contact seems to promote thrombin generation and accelerate clot formation.
A case of embryonal rhabdomyosarcoma (RMS) arising from adult lower proximal extremity is described. Rhabdomyosarcoma (RMS) is most common among children, but adult embryonal RMS is rare. The patient was a 44-year-old man with a large tumor of the left extremity invading to the pelvis. The histological diagnosis was embryonal RMS. Radiation therapy was delivered a total dose of 50 Gy to the tumor. Although adult RMS, usually pleomorphic type, is considered to be radioresistant, the tumor showed marked response to radiotherapy and local control was achieved easily in this case.
PURPOSE: The aim of this study was to investigate the cell killing induced by low dose-rate irradiation (LDRI) simultaneously combined with long duration mild hyperthermia in LK87 human lung cancer cells. Cell cycle alteration due to this combined treatment was also observed. MATERIALS AND METHODS: Human lung adenocarcinoma cells, LK87, were treated with concurrent LDRI (50 cGy/hr) and mild hyperthermia (38 to 42 degrees C). Cell survival was estimated by clonogenic assay. Flow cytometry was performed with FACScan. The treatments were simultaneously performed for up to 48 hr (24 Gy). RESULTS: Survival curves of mild hyperthermia alone revealed development of chronic thermotolerance up to 48 hr, whereas LDRI plus hyperthermia caused an exponential decrease in survival. The LDRI cytotoxicities were enhanced by mild hyperthermia over a non-lethal temperature range. The Do values calculated from dose response curves at 37, 38, 39, 40, 41 41.5 and 42 degrees C were 6.55, 5.25, 4.24, 3.99, 3.46, 1.83 and 0.70 Gy, respectively. Cell cycle analysis demonstrated a remarkable G2 and a mild G1 block for LDRI alone, but only a G1 block was observed for LDRI combined with 41 degrees C hyperthermia. CONCLUSION: The LDRI cytotoxicity was enhanced by long duration mild temperature hyperthermia. The suppression of chronic thermotolerance was considered to be a mechanism involved in this sensitization.