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J Miyakoshi

Publications and source records attributed to J Miyakoshi.

70 records · Page 4Linked to original sources
PubMed1986

Effects of step-up and step-down heating on a transplantable murine tumor.

The effects of step-up (42----44 degrees sequence) and step-down (44----42 degrees sequence) heating were studied on a transplantable mammary adenocarcinoma of C3H/He mouse. Tumor-bearing legs were immersed in a water bath and the response to hyperthermia was evaluated in terms of the delay in tumor growth. Tumor growth was delayed greatly with increase in the duration of treatment with 44 degrees hyperthermia, whereas with 42 degrees hyperthermia of up to 180 min, tumor growth was delayed only slightly. The effects of step-up heating were similar to those of 44 degrees hyperthermia alone and the response was enhanced by a factor of 0.9-1.1 with the 60-min treatment at 42 degrees followed by treatment at 44 degrees. Thermal resistance developed when the preheating time at 42 degrees was longer than 30 min. On the other hand, the tumor response was markedly enhanced by step-down heating by a factor of 1.8-2.4 with the treatment at 44 degrees followed by 60-min treatment at 42 degrees. Since the enhancement factor for skin damage found previously was similar to that for the tumor, therapeutic gain cannot be expected by the use of these combined heat treatments.

Animals↗
PubMed1985

Changes in microsomal Na+, K+-, Mg2+- and Ca2+-ATPase activities during proliferation of Chinese hamster V-79 and human HeLaS-3 cells.

Changes in microsomal Na+, K+-, Mg2+- and Ca2+-ATPase activities during cell proliferation were examined in Chinese hamster V-79 (V-79) cells (normal cells) and human HeLaS-3 (HeLaS-3) cells (malignant cells). For V-79 cells, the Mg2+-ATPase activity per cell (pmol Pi/h/cell) in the confluent phase was higher than that in the logarithmically growing (log) phase. The amount of microsomal protein per cell was also high in the confluent phase. Specific activities (mumol Pi/h/mg protein) of Na+, K+-, Mg2+- and Ca2+-ATPase were significantly lower in the confluent phase than in the log phase. For HeLaS-3 cells, an increase in Ca2+-ATPase activity per cell was observed. The amount of microsomal protein per cell did not change between the log and confluent phase. The specific activity of Ca2+-ATPase in the confluent phase was also markedly higher than in the log phase. The relation between changes in ATPase activities and cell proliferation is discussed.

Adenosine Triphosphatases↗
PubMed1985

Effects of m-aminobenzamide on the response of Chinese hamster cells to hyperthermia and/or radiation.

The modifying effects of m-aminobenzamide (m-ABA), an inhibitor of poly(ADP-ribose) synthesis, on 42 degrees C hyperthermia- and/or radiation-induced cell killing were examined in Chinese hamster V-79 cells. When cells were exposed to 42 degrees C hyperthermia in combination with m-ABA (10 mM), cell survival decreased compared with that for 42 degrees C hyperthermia alone. Thermosensitizing effects of m-ABA changed with treatments in a decreasing order of during and after heating greater than during heating greater than after heating. Treatments with m-ABA during and/or after X irradiation enhanced radiation-induced cell killing. When cells were exposed to combined treatment with X irradiation, 42 degrees C hyperthermia (60 min), and m-ABA (24 hr), cell survival decreased markedly compared with that for X irradiation alone. However, with both X----42 degrees C and X----42 degrees C----m-ABA, the enhancement ratios (ER), designated as D0 ratio, were similar. These results suggest that the mechanisms of radiosensitization by m-ABA may be similar to those of 42 degrees C hyperthermia.

Animals↗
PubMed1984

Effects of methylglyoxal bis(guanylhydrazone) on tumour and skin responses to hyperthermia in mice.

Effects of methylglyoxal bis(guanylhydrazone) (MGBG) on tumour and skin responses to hyperthermia (42 degrees C) were examined in C3H mice. MGBG (50 mg/kg) was administered intraperitoneally to mice 4 hours before hyperthermic treatment. The tumour (FM3A) growth time was elongated by an amount dependent on the exposure time of treatment at 42 degrees C (60, 90 and 120 min). Pre-treatment of mice with MGBG (50 mg/kg, i.p.) apparently further lengthened the tumour growth time after treatment at 42 degrees C. No significant damage of foot skin was caused by 42 degrees C hyperthermia. Pre-treatment with MGBG did not make the foot skin susceptible to the heating. From these findings, it can be considered that MGBG or related less-toxic compounds may have a clinical advantage for the mild (42 degrees C) hyperthermic treatment in cancer therapy.

Animals↗
PubMed1983

Skin responses to step-up and step-down heating in C3H mice.

The effects of step-up (42 leads to 44 degrees C sequence) and step-down (44 leads to 42 degrees C sequence) heating were studied on the skin of C3H/He mouse feet. Skin damage in mouse feet exposed to 44 degrees C alone became proportionally more severe with increasing exposure time, while it was slight or not observed at 42 degrees C for up to 2 hr. Preheating to 42 degrees C for 60 or 120 min (step-up) had little effect on the damage from 30-60 min exposure at 44 degrees C, but increased the damage seen with 90 min at 44 degrees C. However, skin damage was markedly enhanced by exposure to step-down heating. On the other hand, thermal resistance was induced in the mouse skin by 44 degrees C fractionated treatments. The induced thermal resistance reached a maximum with a 1 day interval, and then disappeared after a 3 day interval. In another fractionation schedule of step-down heating, the enhanced skin damage which was observed when here was no interval, recovered rapidly and attained an additive response within a 1 day interval. No thermal resistance was observed.

Animals↗
PubMed1983

Thermosensitization by methylglyoxal bis(guanylhydrazone) in Chinese hamster cells.

The modification of methylglyoxal bis(guanylhydrazone) (MGBG) by 42 degrees C hyperthermia-and/or radiation-induced cell killing was examined in Chinese hamster V-79 cells. At concentrations of more than 10 microM, cell survival decreased exponentially with increased MGBG exposure times. Cell lethality of MGBG (10 microM) was not specific for cell-cycle phases tested from G1/S through G2. When cells were treated with MGBG (10 microM) for 6 hr and then exposed to 42 degrees C hyperthermia with or without a 24-hr interval, cell survival decreased markedly compared with that for 42 degrees C alone. Cells became thermosensitive after MGBG treatment. Cells exposed to MGBG (10 microM) for 6 hr before or after X irradiation were slightly radiosensitive. When X irradiation was combined with MGBG and 42 degrees C hyperthermia, cells became more radiosensitive. From these results, it is suggested that MGBG may change the intracellular state to sensitize cells to the cytotoxic action(s) of hyperthermia.

Animals↗
PubMed1983

Enhancement of thermal cell killing by methylglyoxal bis(guanylhydrazone) in Chinese hamster V-79 cells.

Using the method of colony formation, the modifying effect of methylglyoxal bis(guanylhydrazone) (MGBG) was examined on 44 degrees hyperthermia- and/or radiation-induced cell killing and on thermotolerance development after 44 degrees exposure in Chinese hamster V-79 cells. After exposure to MGBG (10 microM) for more than 6 hr, cells became more sensitive to 44 degrees hyperthermia. When an interval at 37 degrees (up to 24 hr) was interposed between MGBG and hyperthermic treatments, cell survival was not significantly increased, as compared with that for MGBG immediately followed by 44 degrees. Cells treated with MGBG remained more thermosensitive, even after a 24 hr interval. On the other hand, when cells were exposed to split dose 44 degrees hyperthermia in the presence of MGBG during an interval of 6 hr at 37 degrees, the development of thermotolerance was not inhibited. After the combined treatments of MGBG followed by X-ray irradiation and hyperthermia, cell survival was markedly decreased, as compared with that in the case of X-ray irradiation alone or in combination with hyperthermia.

Animals↗
PubMed1982

Cytotoxicity of methylmercuric chloride attenuated by serum proteins and it's release from the treated cells in vitro.

Knowledges on the characteristics in toxicity of methylmercuric chloride (MMC), obtained in the present series of experiments in vitro, would be summarized as follows: (1) No appreciable cell-phase-specific age-response to MMC through the cell cycle of JTC-11 line of cells in vitro was shown. Cytolethal sensitivity of the mitotic cells to MMC was equal to that of the exponentially growing cells. (2) Culture media were prepared in graded concentrations of serum proteins and the various albumin/globulin ratios. Cytolethal toxicity of MMC in the graded treatment periods and concentrations was assayed in the prepared media. The apparent MMC toxicity was decreased both by albumin and by globulin. The both serum proteins appeared to be cytoprotective from MMC toxicity. In culture medium containing albumin, or inactivated bovine whole serum, the cytolethal toxicity of MMC was not observed in the MMC treatment concentrations below 0.5 micrograms/ml, but it was observed for any MMC treatment periods in the any concentrations above 0.5 micrograms/ml. Increases in the concentrations of either albumin or globulin, or the both, correlated with the decrease of MMC toxicity. (3) MMC uptake to the given number of cells was measured and decreased MMC uptake of cells in the medium containing serum protein, compared with that in the serum-protein-free medium, was obtained. Rapid transfer of MMC from the cells to the MMC free medium was observed during the first 30 min after the MMC treatment, which was followed by a slower exponential regression of MMC content of the cells during the successive incubation in the MMC free growth medium.

Blood Proteins↗
PubMed1976

Modifying effects of inactivated bovine serum on the acute toxicity of methylmercuric chloride in cells cultured in vitro.

Dynamics of the killing of Ehrlich's murine ascites tumor cells by methylmercuric chloride, MMC, were investigated. Thresholds in the killing action of MMC were observed in the MMC treatment concentration, but not in the MMC treatment time. Inactivated bovine serum protected the E-cells from killing by MMC in vitro. The apparent MMC toxicity was reduced as the serum concentration increased, but remaining partially at high concentrations. Thus the serum increases the threshold for MMC toxicity. It was confirmed that the mode of action, observed as the kinetics of the acute lethality by suspicious substances, could be examined promptly on the mammalian cell level by the present experimental system.

Animals↗