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Biomedical subjects

M Hashimoto

Publications and source records attributed to M Hashimoto.

At least 973 records · Page 54Linked to original sources
PubMed1987

FK-506, a novel immunosuppressant isolated from a Streptomyces. I. Fermentation, isolation, and physico-chemical and biological characteristics.

FK-506, a novel immunosuppressant, has been isolated from the fermentation broth of Streptomyces tsukubaenis No. 9993 as colorless prism and the molecular formula was determined as C44H69NO12.H2O. The compound suppressed immune responses in vitro and in vivo with mice. This immunosuppressive effect was more potent than that of ciclosporin.

Animals↗
PubMed1987

[Effect of the TRH analog DN-1417 on the appearance of frontal midline theta activity (Fm0)].

The distinct 0 rhythm which appears in the frontal midline area during the performance of mental tasks is called Fm0. The appearance of Fm0 shows individual differences and a close relationship to the personality traits of the subject. It is also reported that administration of diazepam or alcohol brings about an increase of Fm0 along with lowering of the anxiety level. In the present study, the TRH analog DN-1417 (80 mg) was administered to 8 healthy male students for 15 days. They were all extrovert in nature and had no great neurotic tendencies as measured by the Maudsley Personality Inventory (MPI). EEG recording, determination of the blood concentration of DN-1417, and Spielberger's State-Trait Anxiety Inventory-I (STAI-I) were carried out before, during, and after drug administration. The appearance of Fm0 showed significant increase during and just after drug administration. As to anxiety, the STAI-I score showed no significant change. There was no correlation between blood concentration and Fm0. From these results, we considered that the change of appearance of Fm0 due to drug administration was not necessarily associated with change of the anxiety level, and that DN-1417, a DA releaser, increased the appearance of Fm0.

Adult↗
PubMed1987

[The propensity to malignancy of dispermic, heterozygous moles].

Complete hydatidiform moles may originate from either the fertilization of an empty egg by a haploid sperm followed by duplication (producing a monospermic, homozygous mole) or the fertilization of such an egg by 2 haploid sperm (producing a dispermic, heterozygous mole). This difference in the mechanism leading to the formation of complete moles raises the question of whether the risk of subsequent malignancy is influenced by the zygosity of the mole. In the research reported here, we compared the incidence of postmolar sequelae between patients with homozygous and heterozygous moles. Using chromosomal heteromorphism, HLA and PGM1 polymorphisms, we established the androgenetic origin of complete mole in 82 of 91 cases. Homozygosity was confirmed in 51 moles, and we found 10 heterozygous moles. Five of 10 patients with heterozygous moles developed postmolar trophoblastic disease, whereas only 2 of the 51 patients with homozygous moles had postmolar trophoblastic disease (an additional 5 patients showed signs of degenerating residual trophoblasts). A high incidence of sequelae after the expulsion of heterozygous moles suggests that the heterozygous constitution of allelic genes plays an important role in the process of malignant transformation of trophoblasts.

Female↗
PubMed1987

[MTX resistant mechanisms in human choriocarcinoma cells].

Choriocarcinoma cells grown in the presence of MTX have developed resistance in two ways. The HCCM derived sublines (relatively high MTX resistant) produced enhanced levels of DHFR and had relatively unimpaired transport of MTX, though altered transport was the primary determinant of response in the CC1 derived sublines (low MTX resistant). Since the selection procedure used was identical, it was assumed that altered MTX transport was insufficient to account entirely for various degrees of resistance. Increased DHFR activity was necessary for the development of high MTX resistance. The overproduction of DHFR was the consequence of amplification of the DHFR gene sequence. The incidence of DMs in metaphases paralleled the degree of resistance. Since DMs were also present in the cells not showing DHFR gene amplification, mechanisms other than DHFR gene multiplication were responsible for the de novo synthesis of DMs.

Cells, Cultured↗