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Biomedical subjects

T Masuda

Publications and source records attributed to T Masuda.

At least 775 records · Page 43Linked to original sources
PubMed1980

Increased 17 beta-hydroxysteroid dehydrogenase activity in a masculinizing adrenal adenoma in a patient with isolated testosterone overproduction.

The patient studied had noted the onset of virilization shortly after menopause. Urinary 17-ketosteroid levels were normal, as were fractionated 17-ketosteroid levels by gas liquid chromatography, but for 3 yr, serum testosterone levels had been greater than 490 ng/dl. The ovaries were found to be normal by laparoscopy. Abdominal exploration revealed a 1-cm adenoma in the right adrenal. A part of the adenoma excised from our patient was homogenized and incubated with 5 microCi [14C]androstenedione. Five percent of the 14C was converted by the tumor homogenate to a metabolite with the same mobility as testosterone on LH-20 chromatography. After thin layer chromatography, the radiolabeled material together with 3H-labeled authentic testosterone were crystallized to a constant specific activity. The net rate of testosterone synthesis by the tumor was 26 pmol/mg wet tissue wt.h vs. 0.56 pmol/mg.h by a control adrenal homogenate. Thus, the tumor demonstrated a 50-fold increase in 17 beta-hydroxysteroid dehydrogenase activity compared to normal adrenal tissue. This is the first report to identify altered activity of a specific enzyme system in this syndrome of isolated adrenal testosterone overproduction.

17-Hydroxysteroid Dehydrogenases↗
PubMed1980

Antitumor effect of bactobolin and its influence on mouse immune system and hematopoietic cells.

Bactobolin prolonged survival period of mice bearing leukemia L-1210 in various dose schedules. The administration of bactobolin before or at time of immunization with sheep red blood cells (SRBC) did not affect antibody formation and delayed-type hypersensitivity (DTH) to SRBC. The administration after immunization suppressed antibody formation markedly but not DTH response. Bactobolin showed stronger suppressive action on antibody formation in vitro than mitomycin C. Bactobolin did not reduce establishment of tumor immunity which was mediated by T cells and macrophages. Comparing to other antitumor antibiotics which were effective against L-1210, bactobolin did not affect phagocytosis of mouse peritoneal macrophages. It has an extremely low toxicity to mouse spleen cells treated by concanavalin A (Con A) and lipopolysaccharide (LPS). It did not affect colony formation of mouse bone marrow cells in the presence of LPS-induced colony stimulating factor. The administration of bactobolin did not reduce the number of leucocytes in peripheral blood. From these results, the usefulness of bactobolin in the treatment of cancer was discussed.

Animals↗
PubMed1980

Effect of bestatin on mouse immune system and experimental murine tumors.

Effect of bestatin on the establishment of delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC) and oxazolone was examined in normal and immunity-impaired mice. Administration of a low dose of bestatin (0.1 approximately 100 microgram/mouse) augmented DTH to SRBC and restored their impaired DTH to oxazolone. The effect of bestatin in the mouse was age-dependent. Bestatin retarded the growth of slow growing solid tumors of Gardner lymphosarcoma and IMC carcinoma and the effect was influenced by the time of the administration and the number of cells inoculated. Bestatin enhanced the antitumor action of the antitumor antibiotics, bleomycin and adriamycin. Bestatin also retarded the induction of skin cancer by 20-methylcholanthrene.

Aminopeptidases↗
PubMed1980

Mannan-binding protein in lymphoid tissues of rats.

A binding protein which recognizes mannose and N-acetylglucosamine was isolated from mesenteric lymph nodes of rats by affinity chromatography. The isolated binding protein shares come common properties with liver mannan-binding protein: requirement of Ca2+ for the binding and high affinity for mannan. However, these two proteins were distinguishable by their antigenicity and their binding affinity for mannosamine.

Animals↗
PubMed1980

Immunological properties of Fc receptor on lymphocytes. VIII. The behaviour of FcR+ and FcR- T cells in cell-mediated immune responses.

The roles of splenic FcR+ and FcR- T cells from mice immunized either with allogeneic cells or with LCMV or stimulated either with MMC-treated allogeneic cells or TNP-modified syngeneic cells in vitro were examined for cell-mediated cytolytic responses. Effective lysis was observed in the FcR- cell fraction enriched with nylon wool eluted T cells in all experiments. Killer cells were generated from the FcR- T-cell fraction after exposure to either allo-, virus- or chemically modified antigen. On the other hand, the lytic activity of the FcR+ T-cell fraction, was low but nevertheless still significant. However, this weak cytotoxicity was increased by 24 h of incubation, although the recovery of living cells was found to be significantly lower in the FcR+ than in the FcR- T-cell fraction. This suggested that non-killer cells, which could interfere with the activity of pre-killer cells, were perhaps preferentially eliminated after binding with the immune complexes. Moreover, almost complete inhibition of lytic activity was achieved in allo-activated FcR+ T, but not FcR- T-cell fraction, after they had been treated with immune complexes, implying a functional significance of FcR in the manifestation of lytic activity.

Animals↗
PubMed1980

Ultrastructure of the articular cartilage after systemic administration of hydrocortisone in the rabbit: an electron microscopic study.

The acetabular cartilages from hip joints in adult rabbits receiving daily intramuscular injections of 1 or 5 mg hydrocortisone/kg body weight for periods of four or 12 weeks were studied by electron microscopy for quantitative analysis, nucleus to cell ratio, Golgi apparatus to cell ratio, rough endoplasmic reticulum to cell ratio and number of microvilli of chondrocytes and thickness of territorial matrix surrounding chondrocytes were obtained. Systemic steroid treatments decreased the volume of of rough endoplasmic reticulum and Golgi apparatus in chondrocytes, the number of microvilli, and the thickness of territorial matrix in matrix of the cartilage. These observations suggest that synthesis of proteoglycan and protein by chondrocytes is affected by steroid. These deleterious effects of steroid on cartilage begin with therapeutic dosages and progressively develop with increasing dosages of steroid or with increasing periods of time on steroid therapy.

Animals↗