[Experiences in the clinical use of chlormadinone for abortion patients].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Bando.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We previously reported that the extract of seeds from Aeginetia Indica L (AIL), a parasitic plant, induces potent antitumor immunity in tumor-bearing mice and that CD4+ T cells appear to be the main contributors in the induction of antitumor resistance. The present study was set up to investigate the in vitro effects of AIL on various lymphoid cells. Spleen cells from mice pretreated with AIL every 2 days for 1 week produced interleukin 2 (IL-2), interferon gamma (IFN gamma), tumor necrosis factor (TNF) and interleukin 6 (IL-6) when these cells were stimulated in vitro by AIL. Further, we found that CD4+ T cells were main producers of IL-2 and TNF upon the stimulation with ALL in vitro, while both CD4+ and CD8+ T cells secreted IFN. On the other hand, ALL was mitogenic in vitro to T enriched splenic lymphocytes as well as B enriched splenic lymphocytes. Moreover, AIL also proliferated thymocytes and this activity was potently synergistic with a suboptimal dose of concanavalin A (Con A). Lipopolysaccharide (LPS) contamination in AIL preparation was negligible since proliferative activity of AIL to B enriched splenic lymphocytes was not influenced in the presence of an endotoxin antagonist, polymyxin B sulfate (PMB). Further, B cell mitogenic activity of AIL seems to be mediated by different mechanism(s) from that of LPS since ALL could proliferate B enriched lymphocytes of C3H/HeJ mice which do not respond to the stimulation with LPS. A well known biological response modifier (BRM), Krestin (PSK), had no ability in inducing either T or B lymphocyte activation in vitro as shown by AIL.(ABSTRACT TRUNCATED AT 250 WORDS)
Gastric acid outputs were measured and related to plasma oestradiol concentrations in women. An inverse relationship between the acid output and the oestradiol concentrations was detected regardless of the stage of the menstrual cycle. It was also noted that the acid output was reduced in a dose-dependent manner after oral administration of conjugated oestrogen and that the response was partially blocked by atropine sulphate. These findings suggest that oestrogen participates in the control of gastric acid secretion in women and that a cholinergic action is involved in the mode of action.
Cisplatin is a key drug in chemotherapy for lung cancer. It has been reported that intracellular accumulation of cisplatin is an important step as a determinant for resistance to cisplatin, which may be modulated by Na+, K+-ATPase activity. And it has been reported that isoproterenol, a beta-adrenoceptor agonist, enhances sensitivity to cisplatin in non-small cell lung cancer (NSCLC) cell lines. In this study, the effects of the selective beta1, beta2, and beta3-adrenoceptor agonists on membrane Na+, K+-ATPase activity and sensitivity to cisplatin were evaluated using human non-small cell lung cancer cell line. In the NSCLC cell line, sensitivity to cisplatin was improved by treatment with procaterol, a selective beta2-adrenoceptor agonist. Na+, K+-ATPase was activated and intracellular accumulation of cisplatin increased with the treatment. However, beta1 or beta3-adrenoceptor agonist did not modulate sensitivity to cisplatin or Na+, K+-ATPase activity. These results suggest that beta2-adrenoceptor may be one of the determinants for sensitivity to cisplatin in NSCLC. Exogenous beta2-adrenoceptor agonists may improve the antitumor effect of chemotherapy involving cisplatin.
BACKGROUND/AIMS: The efficacy of prophylactic chemolipiodolization following hepatic resection in patients with hepatocellular carcinoma was studied. METHODOLOGY: Forty-four of 67 consecutive patients with hepatocellular carcinoma who underwent hepatectomy between 1980 and 1997 were divided into two groups: group A (n = 21), in which prophylactic chemolipiodolization was performed during postoperative follow-up (2.4 times on average using a 39 mg mean dose of epirubicin or doxorubicin); and group B (n = 23), without prophylactic chemolipiodolization. The clinicopathological background and patient survival were compared retrospectively. RESULTS: There were no differences in the clinicopathological background between the two groups. Multiple intrahepatic recurrence was frequently observed in group B (P < 0.02). The recurrence-free survival rates in group A (54.4% and 31.1% at 3 and 5 years, respectively) were significantly higher than those in group B (15.7% and 7.9%, respectively). The survival rates of group A (95.2% and 80.4% at 3 and 5 years, respectively) were significantly higher than those in group B (40.1% and 22.9%, respectively). CONCLUSIONS: Our data suggest that postoperative prophylactic chemolipiodolization can be an effective treatment in reducing intrahepatic recurrence and may prolong survival for hepatocellular carcinoma patients following hepatic resection.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
There are some active transport systems in the cell membrane, such as potassium pump, calcium pump, and proton pump. Although it has been reported that sodium/potassium and sodium/calcium pumps of cell membrane play roles in the intracellular accumulation of anticancer agents, the significance of the active transport channels in accumulation of mitomycin C (MMC), one of the most active agents for non-small cell lung cancer (NSCLC) has been unclear. In this study, we evaluated the role of the potassium pump, calcium pump, and proton pump as determinants of the sensitivity to MMC in vitro by using the selective inhibitors, ouabain, verapamil or AG-2000 (an active metabolite of Lansoplazole), respectively. PC-9 and PC-9/MC4 cell lines which are sensitive and resistant to MMC were used for these experiments. PC-9/MC4 was 9.4-fold more resistant to MMC than PC-9 cells. Relative resistance was not significantly changed by co-incubation with a non-cytotoxic dosage of these inhibitors. From these results, it was revealed that the active transport systems in cell membrane do not play a role in determining the sensitivity to MMC and the acquisition of resistance to MMC in PC-9 cell lines. Intracellular bioactivation may be an important factor to determine sensitivity to MMC in NSCLC cells under aerobic conditions.
Recently, the importance of the potassium pump in the cellular accumulation of cis-diamminedichloroplatinum(II) (CDDP) has been reported. In this study we evaluated the role of the proton pump as a determinant of the sensitivity to CDDP in non-small cell lung cancer cell lines in vitro by using a selective proton pump inhibitor, AG-2000. PC-9 and PC-9/CDDP cell lines, which are sensitive or resistant to CDDP, were used for these experiments. PC-9/CDDP was 17.4-fold more resistant to CDDP than PC-9 cells. Relative resistance was not altered by co-incubation with a non-cytotoxic dosage of AG-2000. From these studies, it was shown that the proton pump inhibitor AG-2000 did not enhance the sensitivity to CDDP. However, as AG-2000 is not cytotoxic and does not compromise the CDDP-sensitivity in NSCLC cells at the concentration of clinical use for gastroduodenal ulcer, AG-2000 can be used with CDDP in chemotherapy for lung cancer.
Cisplatin is the most active anticancer agent for lung cancer. It has been reported that intracellular accumulation of cisplatin is important in determining resistance to cisplatin, which may be modulated by Na+, K(+)-ATPase activity. On the other hand, it is well-known that sorbitol, a metabolite of glucose mediated by aldose reductase, reduces Na+, K(+)-ATPase in diabetic neuropathy. In this study, the effect of exogenous sorbitol on Na+, K(+)-ATPase activity and sensitivity to cisplatin was evaluated using human non-small-cell lung cancer (NSCLC) cell lines. In the NSCLC cell lines, EBC-1, PC-3, and RERF-LC-MS the cytotoxicities of cisplatin were impaired by exposure to sorbitol in these cell lines. Na+, K(+)-ATPase was inactivated and intracellular accumulation of cisplatin was decreased by the exposure. These results suggest that accumulation of sorbitol may induce resistance to cisplatin in NSCLC cells, and diabetes poorly controlled may be one of the determinants of the antitumor effect of cisplatin in NSCLC.
cis-Diamminedichloroplatinum(II) (CDDP) is a key anticancer agent. It has been reported that intracellular accumulation of CDDP is an important step as a determinant for resistance to CDDP, which may be modulated by Na+, K(+)-ATPase activity. In this study, the significance of membrane Na+, K(+)-ATPase activity and the role of thromboxane (TX) receptors were evaluated using human lung cancer cell lines. In the non-small-cell lung cancer (NSCLC) cell line, EBC-1, sensitivity to CDDP was improved by treatment with two different selective thromboxane receptor antagonists, calcium 5(z)-[1R,2S,3S,4S-7-[3-phenylsulfonylaminobicyclo [2.2.1]hept-2-yl]-5-heptenoate hydrate (S-1452), and (3R)-3-(4-fluorophenyl sulfonamido)-1,2,3,4-tetrahydro-9-carbazolepropanoic acid (BAYu3405). Na+, K(+)-ATPase was activated and intracellular accumulation of CDDP increased with treatment in EBC-1. In the small-cell lung cancer (SCLC) cell lines, SBC-1, sensitivity to CDDP and Na+, K(+)-ATPase activity did not change significantly, and intracellular accumulation of CDDP was not modulated. These results suggest the importance of the TX receptors as determinants of the sensitivity to CDDP in NSCLC cell lines. However, Na+, K(+)-ATPase activity and the role of TX receptors may not be so significant in the resistance mechanisms to CDDP in SCLC cell lines. In EBC-1 cells, the specific binding of S-145 was evident, but not in SBC-1 cells. The difference in TX receptors in NSCLC and SCLC cell lines may be one of the reasons for the variety of the antitumor effects of CDDP in chemotherapy for lung cancer.
cis-Diamminedichloroplatinum(II) (CDDP) is the most active anticancer agent. It has been reported that intracellular accumulation of CDDP is an important step as a determinant for resistance to CDDP, which may be modulated by Na+, K(+)-ATPase activity. In this study, the significance of membrane Na+, K(+)-ATPase activity in the intracellular accumulation of CDDP were evaluated using human lung cancer cell lines. Na+, K(+)-ATPase was active in each cell line, not only non-small-cell lung cancer (NSCLC) but also in small-cell lung cancer (SCLC) cell lines. In NSCLC cell lines, there were significant correlations between Na+, K(+)-ATPase activities and intracellular accumulation of CDDP and the accumulation significantly decreased by ouabain, an inhibitor of Na+, K(+)-ATPase in each cell line. However, the correlation between enzyme activity and intracellular accumulation of CDDP were not significant in SCLC cell lines where sensitivity to CDDP was better than in NSCLC cell lines. These results suggest Na+, K(+)-ATPase are active in both NSCLC and SCLC cells, however, the importance of the enzyme as an active transporter of CDDP may be limited only to NSCLC cells. The mechanisms of intracellular accumulation may not be so important as a determinant of sensitivity to CDDP in SCLC cells.