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Biomedical subjects

A Endo

Publications and source records attributed to A Endo.

At least 235 records · Page 13Linked to original sources
PubMed1987

[Potential role of phosphoprotein in collagen mineralization--an experimental study in vitro].

To examine the potential role of phosphoprotein in collagen mineralization, a series of experiments were carried out in vitro using native type collagen fibrils containing phosphoprotein. Ten different preparations of decalcified chicken bone were used for nucleation experiments, employing experimentally established metastable solutions of 10 mg/100 ml, ionic strength 0.165, at 25 degrees C. The specimens were analysed at regular intervals for their calcium and phosphorus content. Amino acid analyses including quantitation of phosphoserine and phosphothreonine were performed on all the samples. The time lag between the incubation of the sample in the metastable solution and the initiation of nucleation was found to be directly related to the concentration of the phosphoaminoacids. The data suggest that phosphoprotein has an effect on the speed of the collagen mineralization, thus playing a significant role in initiation of the tissue calcification.

Amino Acids↗
PubMed1986

Langerhans cells in the dermal infiltrate of hyperkeratosis lenticularis perstans.

Typical papules obtained from a patient with hyperkeratosis lenticularis perstans (HLP) were examined by light and electron microscopy. Dense cellular infiltrate, which consisted mainly of mononuclear cells, was observed in the dermis underlying the lesion. Electron microscopic studies revealed that these cells were mostly lymphocytic cells. In addition, several Langerhans cells were found in the infiltrate, some of which were apposed to the lymphocytic cells. These findings suggested that immunologic reactions via Langerhans cells might occur in HLP and further raises a possibility that Langerhans cells might be involved in the pathogenesis of HLP.

Aged↗
PubMed1986

Microbial conversion of compactin (ML-236B) to ML-236A.

Approximately 1,600 fungal strains were tested for ability to convert compactin (ML-236B) to ML-236A and Emericella unguis IFO 8087 was found to be the most active. E. unguis converted ML-236B to ML-236A with a yield of over 90%.

Ascomycota↗
PubMed1986

Monacolin M, a new inhibitor of cholesterol biosynthesis.

Monacolin M, a new specific inhibitor of cholesterol biosynthesis structurally related to monacolin K (mevinolin), was isolated from cultures of a strain of Monascus ruber. The structure of monacolin M was determined to be beta-hydroxybutyryl ester of monacolin J by a combination of physical techniques. It was suggested that monacolin M is derived from monacolin J via a synthetic pathway distinct from that for the synthesis of monacolin K, alpha-methylbutyryl ester of monacolin J. The inhibitory effect of monacolin M on beta-hydroxy-beta-methylglutaryl-CoA reductase was slightly lower than that of monacolin K.

Anti-Bacterial Agents↗
PubMed1986

Inhibition of liver acetyl-coenzyme-A carboxylase by 2-tetradecanylglutarate.

In a previous study (A. ENDO, et al., J. Antibiotics 38: 599 approximately 604, 1985), 2-alkyl glutarate and its derivatives isolated from cultures of Gongronella butleri were shown to inhibit animal acetyl-CoA carboxylase. In the present communication, the inhibition of liver acetyl-CoA carboxylase was investigated with several 2-alkyl glutarate and 2-alkyl succinate analogs. Their inhibitory potency increased with the chain length of the alkyl moiety, and 2-tetradecanylglutarate was most potent among the inhibitors tested. Kinetic analysis indicated that inhibition by 2-tetradecanylglutarate was non-competitive with respect to the substrates, ATP, HCO3- and acetyl-CoA, and competitive with respect to the allosteric regulatory citrate, giving a Ki value of 40 microM. Sucrose density gradient centrifugation analysis showed that the citrate-induced polymerization of the enzyme was inhibited by 2-tetradecanylglutarate.

Acetyl-CoA Carboxylase↗
PubMed1985

Cytogenetic and cytokinetic analysis of lymphocytes from patients with hereditary adenomatosis of the colon and rectum.

The frequencies of chromosome aberrations, sister chromatid exchanges (SCEs), and cell cycle kinetics were examined in cultured lymphocytes from five patients with hereditary adenomatosis of the colon and rectum (ACR) [three patients with Gardner's syndrome (GS) and two patients with familial polyposis coli (FPC)]. The frequency of numerical chromosome aberrations was no different in metaphase cells at the first and second replication cycles (M1 and M2) in the ACR patients and control subjects. The percentage of structural chromosome aberrations in both M1 and M2 cells was somewhat higher in the ACR patients as compared with the controls. Neither spontaneous nor mitomycin C-induced SCE frequencies in the patients with ACR were different from the controls, except for one patient with GS, who showed a remarkably high spontaneous SCE frequency. This patient is the mother of a son who had hepatoblastoma. The cell replication index (RI) was lower in the GS patients than in the controls. However, the RI in the FPC patients did not differ from that of the controls.

Adult↗
PubMed1985

Teratogenic effect of maternal zinc deficiency and its co-teratogenic effect with cadmium.

The teratogenic effects of feeding pregnant mice with the levels of zinc that were severely deficient (0.5 ppm), marginally deficient (10 ppm), or zinc replete (50 ppm) were studied. All groups of animals were fed the experimental diet from 1-18 days of gestation (dg) except for one additional group which received 0.5 ppm Zn diet from 5-14 dg. The effects of a single dose of 2.0 mg/kg of cadmium chloride (CdCl2) injected on 8 dg in mice fed the marginally zinc-deficient or the zinc-replete diets were also investigated. We found that more than 95% of fetuses exhibited a variety of external and skeletal malformations in the severely zinc-deficient groups and that the frequency of malformed fetuses in the marginally zinc-deficient group was similar to that of the control animals. Injection of CdCl2 produced a significant increase in the incidence of malformations in the marginally zinc-deficient mice, but not in zinc-replete animals. These results demonstrate that severe zinc deficiency is teratogenic in mice and that a marginal zinc intake influences the teratogenic potential of cadmium.

Abnormalities, Drug-Induced↗