Search PubMed⌕ Search

Biomedical subjects

M Miyauchi

Publications and source records attributed to M Miyauchi.

At least 199 records · Page 11Linked to original sources
PubMed1987

Establishment of a human ovarian cancer cell line capable of forming ascites in nude mice and effects of tranexamic acid on cell proliferation and ascites formation.

The present study was designed to obtain an experimental tumor model as similar as possible to human ovarian cancer which often had a large amount of ascites and to assess the therapeutic value of tranexamic acid. Human tumor cell lines which form ascites in nude mice were established from ascites of patient with serous cystadenocarcinoma of the ovary. Two cloned cell lines designated HRA and HR-1 were obtained from the parent cell line designated HR. All of these cultured cell lines had about 2.5-3.5 times higher lactate dehydrogenase activities than the original tumor. The original tumor and the tumor grown in nude mice had all 5 bands of lactate dehydrogenase isoenzymes, while all cultured cell lines had only a marked lactate dehydrogenase-3 in addition to a faint lactate dehydrogenase-2. Modal chromosome numbers of HR cells ranged from 50-76, while that of HRA cells ranged widely from 40-140. The DNA histograms of HR and HRA cells were similar to each other, showing predominant G1 and S phases. Although these cell lines had ability to produce ascites in the nude mice when the cells were inoculated i.p., the HRA cell inoculation made ascites most rapidly and brought about the shortest median survival (39 days). The proliferations of all three cell lines were dose-dependently inhibited by tranexamic acid. However, the concentration of this drug required for 50% inhibition of the proliferation of HRA cells was about one-half of that of HR and HR-1 cells. In addition, i.p. injections of tranexamic acid to nude mice treated with cisplatin resulted in a significant inhibition of the ascites formation and prolongation of 50% survival.

Animals↗
PubMed1987

[Three cases of thoracic or thoracoabdominal aortic aneurysm successfully treated with cell saver].

During a three-month period from January to March 1986, reconstructive surgery was performed on three patients with thoracic or thoracoabdominal aortic aneurysm using a temporary bypass procedure. To reduce the amount of blood transfusion required during operation, an autologous blood recovery system, Cell Saver, was used in these three cases. The amount of blood loss, including the blood passing through the Cell Saver, was 7,020g in Case 1, 6,600g in Case 2 and 16,700g in Case 3. The amount of blood transfusion given to these three cases was 1,400g, 4,400g and 6,800g, respectively. The results indicated that the ratio of transfused blood amount to blood loss during operation was successfully reduced to a level of 20-67% of two other cases with thoracoabdominal aortic aneurysm, operated upon without using Cell Saver. Cell Saver was especially effective in Case 3 in which the blood for transfusion was restricted, for it was difficult to collect enough donors to complete operation because of rare blood type of Rh(-) in this case. That is, Cell Saver withdrew 15,000ml of blood through the sucker from the patient and returned it as concentrated and washed RBC during operation.

Aorta, Abdominal↗
PubMed1987

[Inhibition of human ovarian cancer cell growth by prostaglandin D2].

The effects of prostaglandin D2 (PGD2) on human ovarian tumor growth were examined in vitro and in vivo by using a cell line, designated HR, derived from patients with serous cystadenocarcinoma of the ovary. The cell proliferation was dose-dependently inhibited by PGD2 between concentrations of 0.1 and 4.0 micrograms/ml after 24 hrs, 48 hrs and 72 hrs of contact time. Concentrations of PGD2 required for 50% inhibition of the cell proliferation were 2.0, 1.1 and 0.55 micrograms/ml with 24, 48 and 72 hrs of contact time, respectively. From the results of 51Cr-release assay, the inhibition of cell proliferation by PGD2 was considered to result from the direct cytotoxic effects. The incorporations of 3H-thymidine, 3H-uridine and 3H-valine were inhibited in a dose-dependent fashion with more than 1.0 micrograms/ml of PGD2. Tumor growth in nude mice treated with 0.3 mg/mouse PGD2 was significantly inhibited, compared to that of untreated nude mice. In untreated nude mice the tumor growth curve was parallel to the changes in the plasma alpha-hydroxybutyrate dehydrogenase (HBD). In both PGD2-treated groups with 0.1 mg/mouse and 0.3 mg/mouse, the HBD activity markedly decreased on the 14th and the 21st day after inoculation. The 50% survival time in untreated mouse, 0.1 mg/mouse and 0.3 mg/mouse PGD2-treated groups was 52 days, 55 days and 67 days, each respectively.

Adenocarcinoma, Mucinous↗
PubMed1987

Effects of naloxone on human ovarian cancer cell growth in vitro and in vivo.

The effects of naloxone on human ovarian cancer cell growth in vitro and in vivo were examined by using an established cell line, designated KF, derived from human ovarian carcinoma. When the KF cells were incubated in the presence of various concentrations of naloxone for 72 hr, the cell proliferation was inhibited in a dose-dependent manner in the concentration range of 30 to 120 microM naloxone. The growth-inhibitory effect of naloxone could not be detected by 51Cr-release assay or colony-forming assay. The inhibition of cell proliferation by naloxone resulted from the inhibitory effect on protein synthesis in the KF cells, as confirmed by a marked decrease of incorporation of [3H]valine. In order to determine the effect of naloxone on tumor growth in vivo, ip injections 3 times a week of 2.5 or 5.0 mg/kg naloxone were initiated either one week prior to tumor inoculation (pretreated groups) or one week after tumor inoculation (post-treated groups). Nude mice in the pretreated groups had significantly smaller tumor volumes than those in the untreated group as long as naloxone was administered. On the other hand, in the post-treated groups a significant growth retardation was observed 2 weeks after initiation of treatment with 2.5 mg/kg naloxone. In comparison to a median survival time of 38 days for untreated controls, the naloxone pre- and post-treated groups showed increases of 26-71% in median survival.

Animals↗
PubMed1987

[Effects of cimetidine and PSK on interleukin-2 production by PBL in patients with advanced ovarian carcinoma during the course of chemotherapy].

The present study was designed to elucidate the effect of cimetidine and PSK on T-cell subsets, interleukin-2 (IL-2) production and its receptor in peripheral blood lymphocytes (PBL) from patients with advanced ovarian carcinoma during the course of chemotherapy. Preoperative levels of OKT 4/8 cell ratio and IL-2 production in PBL from patients with advanced ovarian carcinoma were significantly lower than those with benign ovarian tumor. When a combination chemotherapy which consisted of cisplatin, adriamycin and cyclophosphamide was given to these ovarian cancer patients, the OKT 4/8 cell ratio was significantly increased while the IL-2 production was markedly inhibited. When PSK and cimetidine were combined with the combination chemotherapy, the inhibition of IL-2 production was reduced. When treatment with PSK or cimetidine was initiated after completion of the combination chemotherapy, the OKT 4/8 cell ratio was significantly elevated on 30 days and 60 days, compared to 7 days after the completion of chemotherapy. The depressed IL-2 production after completion of the combination chemotherapy was increased to about 8 times by cimetidine and about 2.5 times by PSK on 60 days after completion of chemotherapy. On the other hand, the IL-2 receptor remained unchanged even if PSK or cimetidine was administered.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Monitoring by alpha-hydroxybutyrate dehydrogenase of human ovarian carcinoma grown in nude mice.

In order to establish that the tumor burden in nude mice bearing a xenografted human ovarian tumor can be assessed by measuring plasma levels of alpha-hydroxybutyrate dehydrogenase (HBD) (E.C. 1.1.1.30), the plasma HBD and the tumor volume were measured every week after inoculation of a human ovarian carcinoma cell line designated HR. About 3 weeks after tumor inoculation, all nude mice had a palpable tumor while elevated levels of HBD were observed in a half of the mice at that time. Thereafter the HBD levels rose with increasing tumor volume. There was a quantitative linear relationship between the tumor weight and HBD activity per mouse. When 40 micrograms of cisplatin (about 2 mg/kg) was administered i.p. every week for 5 weeks 2 weeks after inoculation, plasma levels of HBD were significantly decreased on day 27 compared to those in untreated nude mice. Decreases in the HBD levels during treatment with cisplatin occurred 7 days prior to changes in tumor volumes. Further, removal of local tumor mass resulted in a marked decrease in HBD levels on day 1 after surgery and the HBD levels in nude mice which had no recurrent tumor fell into the normal range 8 days after surgery.

Animals↗
PubMed1986

Inhibition of human ovarian cancer cell growth in vitro and in nude mice by prostaglandin D2.

In vitro and in vivo effects of prostaglandin D2 on human ovarian tumor growth were examined by using a cell line, designated HR, derived from ascites of a patient with serous cystadenocarcinoma of the ovary. The HR cell proliferation in vitro was dose dependently inhibited between concentrations of 0.1 and 4.0 micrograms of prostaglandin D2 per ml. From results of 51Cr release assays and trypan blue dye exclusion tests the inhibitory effect seemed to result from a direct cytotoxic effect by prostaglandin D2. All DNA, RNA, and protein syntheses by the HR cells were also inhibited in a dose-dependent manner with exposure time of 48 h to prostaglandin D2. When 5 X 10(5) HR cells were inoculated to nude mice, the 50% survival time of them in untreated groups was 52 days after inoculation. Although 4 mg of prostaglandin D2 per kg caused inhibition of the tumor growth, a significant prolongation of the survival time was not observed. On the other hand, the 50% survival time of nude mice treated with 12 mg of prostaglandin D2 per kg was significantly (P less than 0.05) prolonged to 67 days, in addition to a significant inhibition of the tumor growth.

Animals↗
PubMed1986

Establishment of a cisplatin-resistant human ovarian cancer cell line.

A cisplatin-resistant cell line was established by use of KF-1 cells derived from human serous cystadenocarcinoma of the ovary. This resistant cell line, designated "KFr," was capable of proliferating in the presence of 1.0 micrograms cisplatin/ml. It had doubling times of 24.8 and 27.2 hours in the presence of 0.5 and 1.0 micrograms cisplatin/ml, respectively. The KFr cells had lactate dehydrogenase (LDH) activities about fourfold higher than those of the parent KF-1 cells. Analysis of the isozymes of the KFr cells revealed that they had a faint LDH-3 band in addition to LDH-4, the only stained band in the parent KF-1 cells. The morphologic characteristics of the KFr cells were an enlarged nucleus and prominent nucleoli, unlike the nucleus and nucleoli of the parent KF-1 cells. The degree of resistance to cisplatin of the KFr cells was about twenty-fold higher than that of the KF-1 cells, with regard to the concentrations of cisplatin required for 50% inhibition of cell proliferation. However, when 5 microM calmodulin antagonists [N-(6-aminohexyl)-1-naphthalenesulfonamide or N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide] were added in the presence of concentrations of cisplatin that hardly inhibited cell proliferation, the KFr cell proliferation was markedly inhibited. These results suggest that cisplatin resistance can be overcome by calmodulin antagonists.

Calmodulin↗
PubMed1985

Comparison of substrates for measuring serum choline esterase activity in hepato-biliary disease.

The efficacy of various substrates for measuring serum choline esterase for the evaluation of hepatic function was studied using o-toluoyl- and succinyl-choline, and acetyl, butyryl- and propionyl-thiocholine. In hepatic disease, the serum choline esterase activity with these substrates was decreased at a similar rate, showing no significant difference. In 78 - 84% of cases with hepatic cirrhosis the enzyme activity with these substrates was less than 50% of the average level of normal individuals, but in acute and chronic hepatitis only 4-9 and 12-14% of patients showed these lower values, respectively. The present study indicates the usefulness of sequential monitoring of serum choline esterase activity with any of these substrates for assessing hepatic disease, particularly cirrhosis, and for monitoring the course of hepatic disease.

Acute Disease↗
PubMed1984

Mutagenic activity of possible metabolites of 4-nitrobiphenyl ether.

A series of possible metabolites--4-nitrosobiphenyl ether (4-NO), 4-hydroxylaminobiphenyl ether (4-NHOH), 4-aminobiphenyl ether (4-NH2), 4-hydroxyacetylaminobiphenyl ether (4-N(OH)Ac), 4-acetoxyacetylaminobiphenyl ether (4-N(OAc)Ac)involved in the toxic effects of 4-nitrobiphenyl ether (4-NO2) was synthesized and tested for mutagenic activity toward Salmonella typhimurium TA100 strain in the presence and the absence of liver homogenates of guinea pig treated with Kaneclor-500. 4-NO2, 4-NO and 4-NHOH showed direct-acting mutagenicity. 4-NO and 4-NHOH showed high mutagenic activity, while the mutagenic activity of 4-NO2 was very weak compared to 4-NO and 4-NHOH. 4-NO showed antimicrobial action at high concentrations. The other three compounds tested induced no mutation. Upon addition of NAD(P)H, the mutagenic activities of 4-NO and 4-NHOH were slightly enhanced, but no enhancement was observed by addition of NAD(P)+. Metabolic activation with guinea pig liver homogenates enhanced the mutagenic activities of 4-NO2 and 4-NO, and converted 4-NH2, 4-N(OH)Ac and 4-N(OAc)Ac to the product(s) responsible for the mutagenic activity. Addition of bis(p-nitrophenyl)phosphate, a deacetylase inhibitor, inhibited the mutagenic activities of 4-N(OH)Ac and 4-N(OAc)Ac by about 70% in the presence of NADPH and about 77% in the absence of NADPH. High performance liquid chromatography (HPLC) analysis of non-enzymatic conversion-products of 4-NHOH and 4-BO with and without NADPH indicated that 4-NHOH disappeared after 30 min of incubation and was converted completely to 4-NO without NADPH, while with NADPH, 4-NHOH disappeared very slowly and was detected even after 4 h of incubation. In the case of 4-NO, no decrease of 4-NO was observed without NADPH, while with NADPH 4-NO decreased quickly and a significant amount of 4-NHOH appeared. The mechanism of the NAD(P)H-dependent increase in mutagenicity is also discussed.

Animals↗
PubMed1984

Conversion of procarcinogens to mutagens by the S-9 fraction from the liver of rainbow trout (Salmo gairdneri): inducibility with PCB, 3-methylcholanthrene and phenobarbital and inhibition by metyrapone and alpha-naphthoflavone.

S-9 fractions from the liver of rainbow trout were found to convert 2-aminoanthracene and 2-acetylaminofluorene to mutagenic intermediates in the Salmonella/microsome test. The S-9 fractions from the liver of rainbow trout treated with either PCB or 3-methylcholanthrene enhanced the mutagenicity of 2-aminoanthracene and 2-acetylaminofluorene, and converted benzo(a)pyrene to mutagenic intermediates. Treatment of rainbow trout with phenobarbital failed to enhance the mutagenicity of these carcinogens. alpha-Naphthoflavone strongly inhibited the mutagenicity of procarcinogens with the S-9 fractions from the liver of untreated or treated rainbow trout with PCB, 3-methylcholanthrene or phenobarbital, however metyrapone had little effect in vitro. These results demonstrate that rainbow trout have the capacity to convert procarcinogens to mutagenic intermediates and that the major part of this capacity is derived from a cytochrome P-450 system resembling the mammalian cytochrome P-448 system.

2-Acetylaminofluorene↗
PubMed1984

Frequency of criteria-defined borderline patients among the first-visit patients at a psychiatric clinic.

Five trained psychiatrists evaluated 330 first-visit patients aged from 12 to 30 at a psychiatric outpatient facility using the DSM-III criteria (Axis-I and Axis-II). Seven cases were diagnosed as definite Borderline Personality Disorder and six cases as definite Schizotypal Personality Disorder. Hence, we had a total of 13 criteria-defined borderline patients (3.9%). Discussions were held on some methodological problems involved in collecting information and making diagnostic judgments.

Adolescent↗