Search PubMed⌕ Search

Biomedical subjects

M Shimada

Publications and source records attributed to M Shimada.

At least 865 records · Page 48Linked to original sources
PubMed1980

Formation of heterotopic granule cell in mouse cerebellum after neonatal administration of cytosine arabinoside.

The mice, ICR-JCL strain, were injected s.c. with 30 mg/kg body weight of cytosine arabinoside at the age of 2, 3, and 4 days. The external granular layer of these mice was destructed selectively, and subsequently these mice developed abnormal cytoarchitecture in the cerebellum, such as disarrangement of Purkinje cells and heterotopic granule cells in the molecular layer. This study was undertaken to elucidate the mechanism in the formation of heterotopic granule cells. In the cerebellum of the treated mouse, some mossy fibers and glomerular collaterals of climbing fibers extended abnormally even into the molecular layer by the age of 10 days, since no granule cells migrated to the inner granular layer until about 10 days when granule cell production started again in the regenerated external granular layer. Subsequently, these fibers, i.e. axons which extended into the molecular layer, established synapses in the molecular layer with the dendrites of migrating granule cells. These granule cells had no need to migrate to the inner granular layer, and so they remained in the molecular layer as heterotopic granule cells.

Age Factors↗
PubMed1980

Neuronal depletion of cerebellum in late infantile metachromatic leukodystrophy.

The cerebellums of two children with late infantile metachromatic leukodystrophy were investigated by light and electron microscopy. These observations showed that the morphological abnormalities were comprised not only of severe demyelination and presence of metachromatic granules but also marked loss of Purkinje cells and granule cells. The depletion of Purkinje cells is considered to have resulted from demyelination of their myelinated axons. On the other hand, the reduction of granule cells is considered to be caused by the loss of Purkinje cells and presynaptic elements such as mossy fibers and glomerular collaterals of climbing fibers. The depletion of these neurons induced destruction of synaptic connection in the cerebellum.

Cerebellar Diseases↗
PubMed1980

Intracellular redox state and stimulation of gluconeogenesis by glucagon and norepinephrine in the perfused rat liver.

The role of the cellular redox state in the hormonal stimulation of gluconeogenesis was studied in hemoglobin-free perfused rat liver, by fluorimetric measurement of the redox states of intracellular pyridine nucleotides. The maximum rate of glucose production from lactate/pyruvate mixture was observed with a lactate/pyruvate ratio of 10/1, which corresponds to the ratio observed in vivo. Increased reduction of pyridine nucleotides on infusion of ethanol or octanoate was associated with an increased production of glucose from pyruvate, whereas glucose production from lactate decreased. Stimulation of gluconeogenesis from lactate by glucagon was affected by the lactate/pyruvate ratio; a decrease of the lactate/pyruvate ratio resulted in a decrease of the efficacy of glucagon. Stimulation by glucagon of glucose production from pyruvate was abolished during octanoate infusion, although it was still observable during ethanol infusion. In contrast to glucagon, the stimulatory effect of norepinephrine on gluconeogenesis was unaffected by the ratio of lactate to pyruvate. Norepinephrine in the presence of octanoate and ethanol still induced stimulation of glucose production from lactate and pyruvate, which was always accompanied by a transient reduction of pyridine nucleotides. The results demonstrate that the regeneration of NADH in the cytosol is one of the regulatory factors in gluconeogenesis, and that the effects of glucagon and norepinephrine on gluconeogenesis and on the redox state of pyridine nucleotides are not identical.

Animals↗
PubMed1980

Effects of calcium ions on the activation of gluconeogenesis by norepinephrine in perfused rat liver.

The effects of calcium ions on the activation of gluconeogenesis by norepinephrine were studied in the perfused rat liver. The norepinephrine-mediated enhancement of gluconeogenesis was accompanied by a transient increase in the reduction level of pyridine nucleotides. There was a positive correlation between the increases in the rate of glucose production and the reduction level of pyridine nucleotides induced by norepinephrine. These changes were "dose-dependent" with respect to the norepinephrine concentration from 5 nM to 1 muM and were mimicked by phenylephrine. The omission of calcium from the perfusate did not modify the basal rate of gluconeogenesis from lactate and pyruvate or the increased rate of glucose production induced by glucagon and isoproterenol. The extents of the responses to norepinephrine and phenylephrine, however, were decreased markedly in liver perfused with a calcium-free medium and/or with phentolamine. Infusion of calcium into the calcium-deficient liver caused an abrupt elevation of glucose production together with a transient reduction of pyridine nucleotides, and the original extent of the response to norepinephrine was recovered. The data presented provide evidence indicating that stimulation of gluconeogenesis by norepinephrine is mediated through an alpha-adrenergic and calcium-dependent mechanism in which redox changes of mitochondrial pyridine nucleotides are involved.

Animals↗
PubMed1980

Coincidental development of forestomach papilloma and prepyloric ulcer in nontreated mutant mice of W/Wv and SI/SId genotypes.

A double gene dose of mutant alleles at either the W or Sl locus produces the pleiotropic effects of anemia, sterility, lack of hair pigmentation, and lack of tissue mast cells. Coincidental development of forestomach papilloma and prepyloric ulcer was observed in about 40% of nontreated (WB X C57BL/6) F1-W/Wv mice raised in our laboratory. The stomach lesions of the W/Wv mice could be detected at the 15th day after birth, and such lesions never appeared in the W/+, Wv/+, and +/+ littermates maintained under the same laboratory conditions. Since the stomach lesions were also observed in (WC X C57BL/6) F1-Sl/Sld mice purchased from The Jackson Laboratory, phenotypes common to both W/Wv and Sl/Sld mice seem to play an essential role in the spontaneous development of the forestomach papilloma and prepyloric ulcer.

Anemia↗
PubMed1979

Distribution of mast-cell precursors in hematopoeitic and lymphopoietic tissues of mice.

Two experimental systems were used to investigate the origin of precursor cells which differentiate into tissue mast cells in vivo. (a) Increase of mast cell number was examined in the skin, stomach, cecum, and mesentery of genetically mast cell-depleted WBB6F1 (WB X C57BL/6)-W/WV mice after the injection of various hematolymphoid cells of congenic +/+ mice. (b) Appearance of mast cells with giant granules was studied in irradiated C57BL/6-+/+ mice after the injection of lymphoid cells of C57BL/6-bgJ/bgJ (beige, Chediak-Higashi syndrome) mice. Concentrations of mast cell precursors in the thymus, lymph node and Peyer's patch were less than 0.1% of the concentration in the bone marrow. Neither treatment of donor bone marrow cells with anti-Thy-1.2 serum and complement nor thymectomy of the recipient mice affects the development of mast cells in the skin, stomach, cecum, and mesentery. Moreover, the number of mast cells increased to normal level when the skin of WBB6F1-W/WV mice was grafted on the back of nude athymic (BALB/c-nu/nu) mice. These results indicate that mast cell precursors are derived from hematopoietic tissues rather than lymphopoetic ones and that the differentiation of the precursor cells does not depend on T lymphocytes or the thymus.

Animals↗
PubMed1979

Electron microscopic examination of skin and conjunctival biopsy specimens in neuronal storage diseases.

Skin and conjunctival biopsy specimens from fourteen patients with neuronal storage diseases were investigated using an electron microscope. The diseases were Tay-Sachs disease, ceroid-lipofuscinosis (Jansky-Bielschowsky type), Niemann-Pick disease (type B), highly suspected adrenoleukodystrophy, I-cell disease, mucolipidosis of the beta-galactosidase deficient type, Hurler disease, Hunter disease and Morquio disease. This examination provided valuable diagnostic information on some neuronal storage diseases but not on Morquio disease or highly suspected adrenoleukodystrophy. False negative results may sometimes occur using this examination method. However, this examination suggests the usefulness of skin and conjunctival biopsy specimens as a diagnostic tool in some neuronal storage diseases.

Adolescent↗