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Biomedical subjects

K Maeyama

Publications and source records attributed to K Maeyama.

102 records · Page 6Linked to original sources
PubMed1982

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↗
PubMed1982

Deciduoma formation in uterus of genetically mast cell-deficient W/Wv mice.

The role of mast cells in deciduoma formation in the uterus of mice was investigated by using genetically mast cell-deficient (WB x C57BL/6)F1-W/Wv (hereafter called WBB6F1-W/Wv) mice. Deciduoma formation occurred in castrated WBB6F1-W/Wv mice after estradiol-progesterone injection and traumatization in spite of their deficiency of mast cells. Injection of diphenhydramine, which blocks histamine receptors, inhibited deciduoma formation in WBB6F1-W/Wv mice as well as in congenic +/+ mice. THe uterus of WBB6F1-W/Wv mice contained about 10% of the amount of histamine found in the uterus of +/+ mice. These results suggest that mast cells are not essential for formation of deciduomata and that histamine originating from sources other than mast cells may be important in deciduoma formation.

Animals↗
PubMed1982

Endometrial argyrophil cell adenocarcinoma with indole- or catecholamine precursor uptake and decarboxylation.

The capacity for indole- or catecholamine precursor uptake and decarboxylation of the argyrophil cell adenocarcinoma of the endometrium was examined by fluorescence microscopy, microspectrofluorometry, and biochemical analyses. Both argyrophil and nonargyrophil cell adenocarcinomas of the human endometrium have been grown serially in nude mice. With the use of the formaldehyde-induced wet-histofluorescence method, yellowish green fluorescence was demonstrated in the cytoplasm of some cells of the argyrophil cell adenocarcinomas after exposure in vitro and in vivo to L-dopa. When 5-hydroxytrytophan was administered in vitro and in vivo to these tumors, an intense yellow fluorescence was also obtained in the cytoplasm. These fluorescent products were located in the argyrophil cells and corresponded to argyrophil granules. Microspectrofluorometrical and biochemical analyses strongly suggested that the yellowish green fluorescent products were dopamine and the yellow ones were serotonin, produced by decarboxylation of each amine precursor.

APUD Cells↗
PubMed1981

Absence of increase of histidine decarboxylase activity in mast cell-deficient W/W mouse embryos before parturition.

The histidine decarboxylase (L-histidine carboxylase, EC 4.1.1.22) activity of whole W/W mouse embryos, which are devoid of mast cells, remained very low and did not show the rapid increase before birth (17-20 days of gestation) seen in wild-type +/+ embryos. During the same period, the histamine content also remained very low and no mast cells were detected in the W/W embryos, in the contrast to the large increase in both histamine content and number of mast cells in wild-type embryos. These findings imply that the histamine in embryos is largely derived from mast cells. In +/+ mice, histidine decarboxylase activity decreased rapidly soon after birth without concomitant decrease in histamine content or number of mast cells, suggesting that the enzyme activity in mast cells is regulated by some unknown mechanism.

Age Factors↗
PubMed1980

Spontaneous stomach ulcer in genetically mast-cell depleted W/Wv mice.

Histamine has been implicated in the pathogenesis of gastroduodenal ulcers. Since mast cells contain a considerable amount of histamine as well as heparin and other biologically active substances, it seems reasonable to speculate that they are involved in this process. In fact, development of gastroduodenal ulcers was reported in dogs with mastocytoma, and an increase in mast-cell number was described in the vicinity of human gastroduodenal ulcers. Y.K. et al. have recently found that the number of mast cells in a unit length of the skin of W/Wv mutant mice is less than 1% of the value for the congeneic +/+ mice and that no mast cells are detected in the intestinal canal of W/Wv mice. Therefore, this mutant mouse was used to investigate the role of mast cells in the induction of gastroduodenal ulcers. As a preliminary experiment, we examined the stomach and duodenum of W/Wv mice without any treatments. Unexpectedly, we found the spontaneous development of perforating stomach ulcers in W/Wv mice, suggesting that mast cells do not necessarily have aggravating effects on the production of stomach ulcers.

Age Factors↗
PubMed1978

Further studies on endo-beta-N-acetylglucosaminidase D1.

The purification procedure for endo-beta-N-acetylglucosaminidase D was improved to yield an enzyme preparation which was homogeneous upon gel electrophoresis. The molecular weight of the enzyme as estimated by Sephadex G-200 column chromatography was 280,000, while SDS-gel electrophoresis after reduction with 2-mercaptoethanol gave a value of 150,000. The purified enzyme did not show any chitinase, hyaluronidase or lysozyme activity. In the presence of exoglycosidases removing peripheral sugars, the endoglycosidase acted on serum glycoproteins such as transferrin and fetuin. The enzyme also hydrolyzed an oligosaccharide, (Man)5(GlcNAc)2, indicating that the peptide portion of substrates does not have much effect on susceptibility to the enzyme.

Acetylglucosaminidase↗
PubMedDate not supplied

1173C>T polymorphism in VKORC1 modulates the required warfarin dose.

The response to warfarin is highly variable among individuals and such variability is likely to have some genetic basis. We evaluted the effect of VKORC1 polymorphisms on warfarin response among Japanese, taking advantage of its unique population structure in which CYP2C9 *2 and *3 alleles are relatively rare. Thirty-one patients (12-34 years old; median, 22) on warfarin were recruited from a pediatric cardiology clinic. Genotyping of the C>T polymorphism at position 1173 in intron 1 of VKORC1 revealed that 26 patients (84%) were T/T homozygotes at nucleotide 1173, whereas 5 (16%) were C/T heterozygotes. Complete linkage disequilibrium was observed between the 1173C > T polymorphism and another polymorphism, the 3730G > A, in the 3' untranslated region. The C/T heterozyogtes at the 1173C > T polymorphism tended to require more warfarin than the T/T homozygotes, when adjusted for international normalized ratio (p = 0.003). Both the 1173C > T polymorphism and the 3730G > A polymorphism are likely to be inert from a functional standpoint. Rather, based on the complete linkage disequilibrium between 1173C > T and 3730G > A polymorphisms, we suspect that the actual change that defines the relative resistance to warfarin may be present in the proximity of these two polymorphisms.

Adolescent↗
PubMedDate not supplied

Isolation of the third component of complement and its derivative with anaphylatoxin-like activity from the plasma of the newt Cynops pyrrhogaster.

The third component of complement (C3) of a newt, Cynops pyrrhogaster, was purified using a fast protein liquid chromatography technique. The purified newt C3 consists of two polypeptide chains (the molecular masses of the alpha and beta-chains of C3 were 120,000 and 70,000, respectively) linked by disulfide bonds. The alpha-chain retained an internal thiolester bond that was cleaved with methylamine, and the N-terminal amino acid sequence of the alpha-chain was XVQLIDAKAGKAAKF. Digestion of newt C3 with trypsin yielded fragments that induced significant histamine release from newt peritoneal cells. These results indicate that newt C3 retains structural and functional properties shared with mammalian C3.

Amino Acid Sequence↗