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Biomedical subjects

M Ohashi

Publications and source records attributed to M Ohashi.

At least 397 records · Page 22Linked to original sources
PubMed1985

Multipotent mutator strain of mouse teratocarcinoma cells.

A mutator strain [AraCr (1.5)4], isolated from mutagenized cultures of multipotent mouse teratocarcinoma cells (embryonal carcinoma stem cells), exhibited a dNTP pool imbalance, with more than a 10-fold relative increase in the intracellular concentration of dCTP. The increase in the spontaneous rate of mutation for 6-thioguanine resistance was 3.6-fold and for ouabain resistance, 7.9-fold. Normalization of the dCTP/dTTP ratio by addition of thymidine and deoxycytidine to the media was associated with normalization of the mutation rates. AraCr (1.5)4 cell retained its multipotency (including chimerization potential) when injected into blastocysts. Moreover, its differentiated progeny expressed the dNTP pool imbalance and mutator phenotype in vitro. The preliminary finding of an increased frequency of morphologically abnormal embryos derived from a series of transplanted blastocysts injected with AraC2 (1.5)4 stem cells is consistent with significant phenotypic effects in vivo.

Animals↗
PubMed1985

Possible mechanisms of inhibitory action of sodium nitroprusside on histamine-induced contractile responses in isolated rabbit aorta compared with basilar artery and taenia coli.

Possible mechanisms of the inhibitory actions of sodium nitroprusside (NaNP) on histamine-induced contractile responses of isolated rabbit aorta, basilar artery and taenia coli were studied. NaNP (3 X 10(-5) M) reduced maximum contractile response to histamine in the aorta, whereas a concentration (10(-4) M) of NaNP slightly shifted the concentration-response curve for histamine towards its higher concentrations, but did not influence the maximum response in the basilar artery and taenia coli. The reduction in the maximum response of the aorta by NaNP was reversed by removal of the endothelium, or treatment with indomethacin (5 X 10(-6) M) or quinacrine (5 X 10(-6) M), but not by nordihydroguaiaretic acid (NDGA) (5 X 10(-5) M). Prostaglandin (PG) E1, PGE2 and PGI2 produced a relaxation in histamine-contracted basilar artery and taenia coli, whereas PGE1 and PGE2 produced a weak relaxation in histamine-contracted aorta. PGD2 relaxed taenia coli contracted by histamine, but had no influences in aorta and basilar artery. From these results, it is concluded that the inhibitory action of NaNP on histamine-induced contractile response in isolated rabbit aorta may be mediated at least partly by endothelium-derived arachidonic acid metabolite(s) via the cyclooxygenase pathway which must not involve PGI2. Furthermore, the difference in the inhibitory actions of NaNP between the tissues used in this study must be attributed to the absence of such mechanisms both in the basilar artery and taenia coli.

Animals↗
PubMed1985

Prostacyclin production reduced in diabetics with vascular complications.

Concentrations of plasma 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable metabolite of prostacyclin, were measured by radioimmunoassay before and after 3 min of induced ischemia in 45 diabetics and 23 controls matched for age. In the 45 diabetics, 15 had no vascular complications (group I), 10 had a macroangiopathy (group II), 10 had a microangiopathy (group III) and 10 had both macroangiopathy and microangiopathy (group IV). Plasma levels of 6-keto-PGF1 alpha before forearm ischemia were significantly lower in group IV diabetics than in non-diabetic controls (188 +/- 17 pg/ml and 245 +/- 14 pg/ml, respectively). After 3 min of ischemia, plasma 6-keto-PGF1 alpha concentrations were increased in control subjects by 34% and by 21% in group I diabetics. In group III diabetics as well as diabetics with atherosclerotic vascular lesions (groups II and IV), no significant change was observed after 3 min of ischemia. These results suggest that impaired vessel wall prostacyclin production may to some extent be responsible for the development of diabetic retinopathy and nephropathy as well as atherosclerotic vascular complications.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Do D 600 and diltiazem interact with serotonin receptors in rabbit vascular tissues?

This study investigates the interactive effects of Ca antagonists and responses to serotonin (5-HT) in isolated rabbit aorta and basilar artery. Isolated strips of rabbit aorta and of basilar artery were studied in organ baths containing 20 ml of Krebs-buffer solution. D 600 or diltiazem caused parallel rightward shifts of concentration-response curves for 5-HT in isolated rabbit aorta, but each reduced the 5-HT-induced maximum response in basilar artery. The slope values from Schild plot analyses in aorta were 1.11 +/- 0.05 and 1.22 +/- 0.37 in D 600 and diltiazem, respectively. Dibenamine pretreatment caused reduction of maximum response to 5-HT in both tissues. Such reduction was diminished markedly by the presence of D 600, diltiazem or 5-HT in aorta but not in basilar artery. Also, the antagonistic effects of D 600 and diltiazem were diminished by elevation of bath Ca in basilar artery but not in aorta. These results strongly suggest that the two Ca entry blockers used in this study might compete with 5-HT at 5-HT receptors in rabbit aorta and that the pharmacomechanical property of 5-HT receptors in rabbit aorta might be distinct from that in rabbit basilar artery.

Animals↗