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Y Kitamura

Publications and source records attributed to Y Kitamura.

At least 739 records · Page 41Linked to original sources

Production of androgens and estrogens by tubular adenomas which developed in ovaries of mutant mice of Sl/Slt genotype.

Bilateral tubular adenomas develop spontaneously in ovaries of WB X C57BL/6 F1-Sl/Slt mice after exponential loss of oocytes. We investigated the ability of this tumor to produce sex steroids. Incubation of tubular adenoma tissue with [3H] progesterone resulted in production of [3H]androstenedione and [3H]-testosterone. The amount of androgens produced by the tumor tissue was much greater than that produced by the normal ovarian tissue. The concentration of testosterone in the serum of the Sl/Slt mice bearing tubular adenomas, measured by radioimmunoassay, was about five times as high as the value in the serum of the congenic +/+ mice. Although incubation of the tumor tissue with [3H]androstenedione resulted in production of 3H-estrogens, the aromatase activity of the tumor tissue was about one-fifth of that of the normal ovarian tissue. Therefore, the major sex steroid secreted by tubular adenomas seemed to be testosterone. These endocrinological features of tubular adenomas were consistent with the following pathological features of the Sl/Slt mice with the tumors: (a) although the weight of uterus of the Sl/Slt mice was about one-half of the value observed in the +/+ mice, it decreased markedly after oophorectomy; and (b) submandibular glands of the Sl/Slt mice were significantly heavier than those of the +/+ mice.

Adenoma↗

Mode of degradation of myofibrillar proteins by rabbit muscle cathepsin D.

The mode of degradation of myofibrillar proteins by the action of highly purified rabbit muscle cathepsin D (EC 3.4.23.5) was studied using SDS-polyacrylamide gel electrophoresis. Cathepsin D optimally degraded myosin heavy chain, alpha-actinin, tropomyosin, troponin T and troponin I at around pH 3. It did not degrade actin or troponin C. Degradation of myosin heavy chain produced four major fragments of 155000, 130000, 110000 and 90000 daltons. Troponin T was hydrolyzed to 33000-, and 20000- and 11000-dalton fragments. Troponin I was degraded into fragments of 13000 and 11000 daltons. Degradation of alpha-actinin and tropomyosin was not as rapid as that of myosin and troponins T and I. Tropomyosin gave a fragment of 30000 daltons, but alpha-actinin showed no distinct band of this fragment on gels.

Actins↗

Presence of mast cell precursors in the yolk sac of mice.

Concentration of mast-cell precursors in hematopoietic tissues of mouse embryos was evaluated by a limiting dilution method. Cells from yolk sacs, livers, and bodies of (WB x C57BL/6)F1 (hereafter called WBB6F1)- +/+ embryos were injected directly into the skin of adult WBB6F1-W/Wv mice which were genetically depleted of tissue mast cells. Concentration of mast-cell precursors was calculated from the proportion of injection sites at which mast cells did not appear. Since the concentration of mast-cell precursors in the yolk sac was about 30 times as great as that of embryonic body at Day 9.5 of the pregnancy, the mast-cell precursors seemed to be generated within the yolk sac. The concentration in the yolk sac reached the maximum level at Day 11, and then dropped markedly at Day 13. In contrast, mast-cell precursors increased from Day 11 to Day 15 in the fetal liver. As a result, the concentration of 11-day yolk sacs was comparable to that of 15-day fetal liver. Although intravenous injection of 15-day fetal liver cells (2 x 10(6)) rescued the general mast-cell depletion of WBB6F1-W/Wv mice, the intravenous injection of the same number of 11-day yolk sac cells did not rescue it. In contrast with fetal livers, yolk sacs scarcely contained hematopoietic stem cells which were measured by spleen colony formation. Therefore, the mast-cell precursors of the yolk sac may not originate from such stem cells.

Animals↗

Mast-cell precursors in various haematopoietic colonies of mice produced in vivo and in vitro.

We have examined mast-cell precursors in various in vivo and in vitro haematopoietic colonies of mice. Cells from haematopoietic colonies of (WB x C57BL/6)F1- + +/+ mouse origin were injected into the skin of the congeneic W/Wv mice which are genetically depleted of tissue mast cells. The appearance of mast-cell clusters at the injection site indicated the presence of mast-cell precursors in the injected cell suspension. More than 40% of 12 d exogenous spleen colonies and 14 d in vitro mixed colonies contained mast-cell precursors, but only a small proportion of 7 d exogenous spleen colonies, 9 d in vitro erythroid bursts or 14 d large in vitro neutrophil-macrophage colonies contained mast-cell precursors. Neither transient endogenous erythroid spleen colonies examined at the fifth day nor 7 d in vitro neutrophil-macrophage colonies contained mast-cell precursors. Among 12 d spleen colonies mast-cell precursors were more frequent in the predominantly neutrophil than the predominantly erythroid colonies but 14 d in vitro mixed colonies, in which erythroid cells were predominant, contained mast-cell precursors more frequently than 14 d in vitro neutrophil-macrophage colonies. Therefore, differentiation of mast cells seems to be independent of either the neutrophil-macrophage or erythroid cell lineages.

Animals↗

Proliferative pattern of uterine cells from birth to adulthood in intact, neonatally castrated, and/or adrenalectomized mice, assayed by incorporation of [125I]iododeoxyuridine.

The proliferative pattern of uterine cells from birth to adulthood was investigated in mice. The uptake of 5-[125I] iodo-2'-deoxyuridine [( 125I]dUrd) by the whole uterus was used as an index of cell proliferation. Nearly parallel changes in uterine growth were found from days 0-25 after birth in both intact and neonatally castrated mice. In both groups of mice, the weight of the uterus increased (0.7-6 mg) and high [125I] IdUrd uptake values were found from days 0-15, while the weight remained nearly constant, and very low uptake values were found in the next 10 days. Additionally, we could demonstrate that adrenalectomy plus ovariectomy caused no significant effect on neonatal growth of the uterus. After day 25, the weight of uterus (6-50 mg) and [125I]IdUrd uptake increased again in the intact mice, but remained low in the neonatally castrated mice. The proliferative response of the uterine cells to exogenous 17 beta-estradiol was then examined. The injection of 17 beta-estradiol on days 0 (20 micrograms/mouse) and 10 (5 micrograms/mouse) induced significant increases in [125I]IdUrd uptake the next day. Neonatal castration had no significant effect on the responsiveness of the uterus to estrogen-induced growth in adult mice. These findings suggest that sex steroids secreted from both the ovaries and adrenals of neonatal and prepubertal mice play no significant role in the proliferation of uterine cells, and that a quiescent interval of cell proliferation occurs around day 20 after birth between the autonomous (days 0-15) and the ovary-dependent (after day 25) proliferation of mouse uterine cells.

Adrenalectomy↗

Effects of glucocorticoid on the ultrastructure of the mouse parathyroid gland.

Ultrastructural changes in the parathyroid glands of dexamethasone-treated mice were examined. Many chief cells of the treated mice contained a decreased number of prosecretory granules, secretory granules and storage granules, and an increased number of lipid droplets, compared with the control mice. In addition, myelin-like structures associated with cisternae of the granular endoplasmic reticulum were observed in the parathyroid glands of the treated mice. These findings suggest that cellular activity of the parathyroid gland may be suppressed by dexamethasone.

Animals↗

Increase in histidine decarboxylase activity in mouse skin after application of tumor promoters.

The activity of histidine decarboxylase (HDC) increased by a factor of 10 after a single application of 12-O-tetradecanoylphorbol-13-acetate (TPA). The HDC-inducing activity of other phorbol esters paralleled their tumor-promoting activity. Application of some indole alkaloids, which have been shown to be a new class tumor promoter, also induced the increase in HDC activity. The cell type responsible for this increase was examined. First, pieces of the skin were separated into epidermis and dermis after application of TPA. In contrast with ornithine decarboxylase, the HDC activity increased in the dermis. Second, genetically mast cell-deficient W/Wv and Sl/Sld mice were used. Although most histamine in the dermis is in the mast cells, the increase in HDC activity in W/Wv mice was comparable to that in congenic +/+ mice. However, no significant increase in HDC activity was detected in the skin of the Sl/Sld mice. Histological examination revealed that the magnitude of inflammatory cell infiltration was much less in the skin of Sl/Sld mice than in the skin of +/+ or W/Wv mice. The increase in HDC activity and the inflammatory cell response in the skin of W/Wv mice were abolished by prior X-ray irradiation, and were restored by subsequent bone marrow transplantation. Thus, inflammatory cells may be responsible for at least a part of the increase in HDC activity after application of tumor promoters.

Acrylamides↗

Different radiosensitivities of mast-cell precursors in the bone marrow and skin of mice.

Although tissue mast cells are derived from the bone marrow, some descendants of bone marrow-derived precursors retain the ability to proliferate and differentiate into mast cells even after localization in the skin. The purpose of the present study was to determine the D0 values for mast-cell precursors in the bone marrow and those localized in the skin. Bone marrow cells were removed from (WB X C57BL/6)F1-+/+ mice after various doses of irradiation and injected into the skin of the congenic W/Wv mice which were genetically without mast cells. Radiosensitivity of mast-cell precursors in the bone marrow was evaluated by determining the proportion of the injection sites at which mast cells did not appear. For the assay of the radiosensitivity of mast-cell precursors localized in the skin, pieces of skin were removed from beige C57BL/6 (bgJ/bgJ. Chediak-Higashi syndrome) mice after various doses of irradiation and grafted onto the back of the normal C57BL/6 mice. Radiosensitivity of mast-cell precursors in the skin was evaluated by determining the decrease of beige-type mast cells which possessed giant granules. Mast-cell precursors in the bone marrow were much more radiosensitive than those localized in the skin. D0 value was about 100 rad for the former and about 800 rad for the latter.

Animals↗

Bone marrow origin of mast cell precursors in mesenteric lymph nodes of mice.

Concentration of mast-cell precursors in the mesenteric lymph node of (WB X C57BL/6)F1 hybrid mice (WBB6F1) were evaluated by a limiting dilution method. Cells from WBB6F1-+/+ mice were injected directly into the skin of WBB6F1-W/Wv mice which genetically lack tissue mast cells. Concentrations of mast-cell precursors were calculated from the proportion of injection sites at which mast cells appeared. Although immunization with horse serum significantly increased the concentration of mast-cell precursors in the mesenteric lymph node, the concentration in the lymph node remained about 10% that observed in the peripheral blood mononuclear cells. Since the bone marrow origin of mast-cell precursors in the mesenteric lymph node was demonstrated by using giant granules of beige (C57BL/6-bgj/bgj) mice as a marker, the immunization seemed to increase the migration of bone-marrow-derived mast-cell precursors from the peripheral blood to lymph node.

Animals↗

Spontaneous gastric erosions in NOD and KK-A gamma.

Histopathological examinations of stomachs of insulin-dependent (NOD) and noninsulin-dependent (KK-A gamma) mice were carried out. Spontaneous erosions in the fundic area were observed in 31% of NOD and 35% of KK-A gamma mice. The morphological features of the erosions were similar to those of erosions produced by stress. Although no erosions were detected in nondiabetic C3H/Slc mice raised and maintained in the same animal room, the presence of hyperglycemia and glycosuria in NOD and KK-A gamma mice did not appear to have a direct correlation with development of erosions. NOD and KK-A gamma mice may be useful animal models for human stress ulcers.

Animals↗

Possible antiarrhythmic activities of trapidil.

Possible antiarrhythmic activities of 5-methyl-7-diethylamino-s-triazolo(1,5-a)pyrimidine (trapidil, Rocornal) were investigated in vitro and in vivo. Trapidil significantly increased the amount of aconitine or ouabain needed for production of ventricular arrhythmias in rats and guinea pigs. Trapidil also produced a significant increase in threshold current of electrical stimuli which induced ventricular tachycardia in dogs under acute myocardial ischemia. Electrophysiological examinations on effects of trapidil on isolated rabbit ventricular muscle cells showed shortening of the action potential duration (APD) and prolongation of the effective refractory period (ERP), resulting in an increase in the ratio of ERP/APD. The results indicate that trapidil will have a possible effectiveness in inhibiting ventricular arrhythmias.

Aconitine↗

Effect of adjuvant endocrine and adjuvant chemoendocrine therapies on metastasis of androgen-dependent Shionogi carcinoma 115.

Shionogi carcinoma 115 is an androgen-dependent tumor, defined by its failure to grow in either female or castrated male DS mice, and by its ability to grow in intact male DS mice as well as in female or castrated male DS mice given androgen. Since spontaneous lung metastasis was found in about 50% of intact male DS mice on the 40th day after s.c. transplantation of the tumor, we investigated the effect of various therapies on development of metastasis. Therapies were started on the 25th day after transplantation. Castration alone did not reduce the frequency of metastasis, and tumor excision alone reduced the frequency slightly. However, castration following the tumor excision showed an excellent effect. Chemotherapy (cyclophosphamide, 80 mg/kg body weight, three times) with or without tumor excision also showed a beneficial effect, and the combination of the tumor excision, castration, and chemotherapy was the most effective among various therapies examined. These results indicate that the Shionogi carcinoma 115 tumor is a useful model for therapy against metastasis of human hormone-dependent cancers.

Androgens↗

Tissue distribution of histamine in a mutant mouse deficient in mast cells: clear evidence for the presence of non-mast-cell histamine.

The contents of histamine in various tissues of mutant mice deficient in mast cells (W/Wv) and in congenic normal mice (+/+) were determined by high-performance liquid chromatography and were compared. In spite of the absence of mast cells in W/Wv mice, the histamine content of their whole bodies was about 5-10% of that of +/+ mice. The skin, heart and lungs of W/Wv mice contained negligible amounts of histamine (about 2% of that in +/+ mice), but the liver, kidneys and spleen contained appreciable histamine (8-15% of that in +/+ mice), and the brain and stomach contained much histamine (45 and 34%, respectively, of that in +/+ mice). These results indicate the presence of non-mast-cell histamine, especially in the brain and stomach, where it may play important physiological roles.

Animals↗

Concentration of mast-cell progenitors in bone marrow, spleen, and blood of mice determined by limiting dilution analysis.

When hematopoietic cells of congenic +/+ mice were injected into the skin of genetically mast-cell-depleted (WB X C57BL/6)F1-W/Wv mice, mast cells appeared at the injection site. The donor origin of developing mast cells was confirmed by using giant granules of C57BL/6-bgl/bgl mice as a marker. When the number of injected cells was decreased, the proportion of injection sites at which mast cells did not appear increased according to the expected frequency of null response in a Poisson distribution. Therefore, such proportions were used to calculate the concentration of mast-cell precursors in the bone marrow, spleen, and peripheral blood. The relative concentration of mast-cell precursors in these tissues was similar to that of spleen-colony-forming cells. The present method seems useful as a semiquantitative in vivo assay for a population of progenitor cells which are committed to differentiate into mast cells.

Animals↗