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Biomedical subjects

M Kitamura

Publications and source records attributed to M Kitamura.

At least 595 records · Page 33Linked to original sources
PubMed1981

An evaluation of mass screening for breast cancer.

In Tokushima Prefecture, Japan, 41,922 women (26,669 in actual number) were subjected to mass screening with physical examination from 1970-1977. In 42 including 10 of so-called "interval cancer", breast cancer was detected. Those with breast cancer detected by mass screening were in the earlier stage of the disease as compared to those diagnosed through regular medical care at our-patient clinic during the same period. Procedures such as inspection and palpation are readily carried out and early occurrences of breast cancer can be detected.

Adult↗
PubMed1981

Heterotransplantation of human esophageal carcinoma to nude mice.

Transplantation to nude mice of 38 tumors originating from 36 human esophageal carcinomas was attempted. Growth of the grafts was obtained in 17 cases and 3 to 11 serial passages were performed in 4 cases. Tumors inoculated into subcutaneous tissue grew locally, but no metastasis nor local invasions were observed. The histological appearances of the grafts were similar to original tumors.

Adenocarcinoma↗
PubMed1981

Effects of hexestrol, medroxyprogesterone acetate and chlormadinone acetate on 7, 12-dimethylbenz [a] anthracene-induced rat mammary cancer in relation to estrogen receptor.

The effects of hexestrol (HXS), medroxyprogesterone acetate (MAP) and chlormadinone acetate (CMA) on 7, 12-dimethylbenz [a] anthracene-induced mammary cancer in rats were evaluated. As a result of successive intramuscular injections of HXS at dosages of 2 or 10 mg/kg or MAP at dosages of 24 or 120 mg/Kg, tumors were markedly reduced in size in all groups on day 7 approximately 14. These effects were the same regardless of the presence or absence of cytoplasmic estrogen receptors (ER) in tumors as determined by the dextran-coated charcoal method. Although such an effect was also seen with CMA, it was much less marked than the effects seen with HXS and MAP. The body weights of HXS-administered groups decreased considerably, whereas those of MAP-administered groups increased. These results may suggest that there is another endocrinological tumor-suppressing mechanism besides the mechanism involving the estrogen-ER system in large-dose administration of HXS and MAP.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1981

Comparative histochemical and biochemical assays of estrogen receptors in breast cancer patients.

Estrogen receptors (ER) in breast cancer tissue were determined in 51 patients by a histochemical method with estradiol-17 beta-bovine serum albumin-fluorescein isothiocyanate conjugate and were compared with those in the adjacent tissue determined by biochemical method, i.e., the sucrose density gradient (SDG) and dextran-coated charcoal (DCC) methods. Excluding one non-evaluable case, 26 specimens were ER(+) and 24 were ER(-) in histochemical assay. The presence of ER(+) cells in histochemical assay was not related to menopause or to the molecular pattern of ER determined by the ASG method, or to the histological type of cancer. The percentage of fluorescent cells to all cancer cells was not related to the number of binding sites of ER determined by the DCC method. As determined by the histochemical assay, breast cancer cells having ER accounted for 20 to 100% of all cancer cells examined and ER(+) cells were in clumps or intermixed with ER(-) cells in cancer tissue. The co-existence of Er(+) and Er(-) cells may be one reason for the fact that surgical ablation of breast cancer rarely results in complete tumor regression.

Adult↗
PubMed1980

Combined treatment by chemotherapy and intravenous hyperalimentation in Japanese patients with advanced breast cancer.

To treat advanced breast cancer that proved refractory to endocrine therapy or other forms of chemotherapy, we administered intravenous administration of adriamycin every 3--4 weeks, in principle, at a dose of 100 mg per 50 kg body weight (total dose, 300--400 mg). At the same time, 50 mg of cyclophosphamide was administered orally every day. In all cases, concomitant hyperalimentation treatment, which is considered an effective method for ameliorating the toxicity of the chemotherapeutic treatment, became necessary. Of 13 cases so treated, 10 showed significant improvement. It was almost impossible in general to administer such a dosage of adriamycin with cyclophosphamide to Japanese patients with advanced breast cancer, since the treatment brought on severe side effects such as depletion of oral intake and suppression of bone marrow function.

Administration, Oral↗
PubMed1980

Structural studies of the sugar chains of human parotid alpha-amylase.

Human parotid amylase can be separated into three families of isoenzymes (A', A, and B) by Sephadex G-75 column chromatography. Isoenzymes in family B were free from carbohydrate, while those in family A were all glycoproteins. The carbohydrate moieties of family A isoenzymes were released from their polypeptide portions by hydrazinolysis and labeled by reduction with NaB[3H]4. The yield of total radioactive oligosaccharides indicated that family A isoenzymes all contain single asparagine-linked sugar chains in one molecule. The radioactive oligosaccharides were fractionated into one acidic and two neutral oligosaccharide fractions by paper electrophoresis and paper chromatography. By sequential exoglycosidase digestion in combination with a methylation study, their structures were determined to be: Gal beta 1 leads to 4 (Fuc alpha 1 leads to 3)GlcNAc beta 1 leads to 2Man alpha 1 leads to 6[Gal beta 1 leads to 4(Fuc alpha 1 leads to 3)GlcNAc beta 1 leads to 2Man alpha 1 leads to 3]Man beta 1 leads to 4GlcNAc beta 1 leads to 4(Fuc alpha 1 leads to 6)GlcNAc Gal beta 1 leads to 4(Fuc alpha 1 leads to 3)GlcNAc beta 1 leads to 2Man alpha 1 leads to 6 and 3[Gal beta 1 leads to 4 GlcNAc beta 1 leads to 2Man alpha 1 leads to 3 and 6]Man beta 1 leads to 4GlcNAc beta 1 leads to 4(Fuc alpha 1 leads to 6)GlcNAc Gal beta 1 leads to 4(Fuc alpha 1 leads to 3) GlcNAc beta 1 leads to 2Man alpha 1 leads to 6 (NeuAc alpha 2 leads to 6Gal beta 1 leads to 4GlcNAc beta 1 leads to 2Man alpha 1 leads to 3)Man beta 1 leads to 4GlcNAc beta 1 leads to 4(Fuc alpha 1 leads to 6)GlcNAc.

Amylases↗
PubMed1980

Interaction between Clostridium botulinum neurotoxin and gangliosides.

The effect of gangliosides on Clostridium botulinum type A neurotoxin was examined in terms of detoxification. The molar concentrations of gangliosides necessary to detoxify 50% of 1 M Cl. botulinum neurotoxin were as follows: GM1, 2073; GM2, 2439; GM3, 6098; GD1a, 610; GD1b, 488; GT1a, 829; GT1b, 6 and GQ1b, 27. Inhibition by gangliosides of the neurotoxin binding to synaptosomes showed that GT1b was highly effective, but the others were not. Low-temperature treatment inhibited the detoxification of neurotoxin by GT1b and the binding of 125I-labelled neurotoxin to the synaptosome fraction. 125I-labelled neurotoxin was mixed with GM1 or GT1b and their molecular size was estimated by sucrose-density-gradient centrifugation. When 125I-labelled neurotoxin was incubated with GM1, a single radioactive peak having a sedimentation coefficient of 7.3 S appeared. When incubated with GT1b, however, 125I-labelled neurotoxin gave three peaks having sedimentation coefficients 14, 10 and 7.3 S, respectively. The present results indicated that the location and the number of sialic acids in ganglioside molecules are of significance in the detoxification and the binding of Cl. botulinum neurotoxin with ganglioside molecules.

Animals↗
PubMed1980

Clinical basis of chemotherapy for gastric cancer with uracil and 1-(2'-tetrahydrofuryl)-5-fluorouracil.

Studies were performed on the clinical basis of chemotherapy for human cancer with uracil and 1-(2'-tetrahydrofuryl)-5-fluorouracil (FT). In 62 operated patients with stomach, breast, and uterine cancers, the concentration of 5FU and FT were compared in serum, tumor and normal tissues 1, 2, 4, 6, 8, and 12 hours following the administration of 300 mg of UFT (300 mg of FT plus 672 mg uracil, a uracil/FT molar ratio of 4), or FT alone. It was found that the level of 5-FU in tumor tissue remained above 0.05 mcg/g over 12 hours. This value for 5-FU corresponds to a minimum inhibitory concentration in the Vitro experiment with L1210 cells. BLood levels of 5-FU increased up to 0.1 mcg/ml 1 hour after UFT administration and then decreased below 0.05 mcg/ml. The drug concentration in normal tissues was lower than that of the tumor tissues. On the basis of the above findings and phase I study, a protocol of UFT-therapy was made and applied for the treatment of gastric cancer. Our patients were given an oral dose of 300 mg of UFT twice a day per 50 kg body weight (12 mg/kg BW). Therapeutic effects were detectable in 7 of 20 cases. In addition, a combination of mitomycin C (6 mg i.v. weekly) with UFT seemed to improve the response rate (5/7). Diarrhea (15%) and skin pigmentation (10%) were major side effects of UFT.

Female↗
PubMed1980

Occurrence of persistent elevated levels of serum glutamic oxaloacetic transiminase as a result of enzyme-immunoglobulin complex formation --with a report of two cases--.

Two cases of macro-molecular GOT (glutamic oxaloacetic transaminase) were encountered recently. Both were middle-aged women, showing no abnormality in laboratory test results including those for GPT (glutamic pyruvic transaminase), except that abnormality high values (ca. 200 Karmen unit) were obtained for GOT. Clinical examinations and tests on the liver, heart, skeletal muscle and other organs were negative. By column chromatography, immunoelectrophoresis and other procedures, this macro-molecular GOT was shown to be an anzyme immunoglobulin complex with a molecular weight of about 250,000 formed by the binding of the GOT of the cytoplasmic fraction to Ig-G-Kappa.

Alanine Transaminase↗