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Biomedical subjects

A Hara

Publications and source records attributed to A Hara.

At least 487 records · Page 27Linked to original sources
PubMed1987

Altitude variation of cosmic-ray neutrons.

The altitude variation of the cosmic-ray neutron energy spectrum and the dose equivalent rate was measured at an average geomagnetic latitude of 24 degrees N by using the high-efficiency multi-sphere neutron spectrometer and neutron dose-equivalent counter developed by the authors. The data were obtained from a 2-h flight over Japan on 27 February 1985. The neutron energy spectra measured at sea level and at altitudes of 4,880 m and at 11,280 m were compared with the calculated spectra of O'Brien and with other experimental spectra, and they are in moderately good agreement with them. The dose equivalent rate increases according to a quadratic curve up to about 6,000 m and then increases linearly between 6,000 m and 11,280 m. The dependence of dose equivalent rates at sea level and at an altitude of 12,500 m on geomagnetic latitude also is given by referring to other experimental results.

Altitude↗
PubMed1987

Effect of exogenous gangliosides on amino acid uptake and Na+, K+-ATPase activity in superior cervical and nodose ganglia of rats.

The effects of some gangliosides on active uptake of nonmetabolizable alpha-aminoisobutyric acid (AIB) and Na+, K+-ATPase and Ca2+, Mg2+-ATPase activities in superior cervical ganglia (SCG) and nodose ganglia (NG) excised from adult rats were examined during aerobic incubation at 37 degrees C for 2 h. In NG, amino acid uptake was greatly accelerated with the addition of galactosyl-N-acetylgalactosaminyl-[N-acetylneuraminyl]-galactosylgluc osyl ceramide (GM1) (85%) and also with N-acetylgalactosaminyl-[N-acetylneuraminyl]-galactosylglucosyl ceramide (GM2) or [N-acetylneuraminyl]-galactosyl-N-acetylgalactosaminyl-[N-acetyl- neuraminyl]-galactosylglucosyl ceramide (GD1a) (43% each) compared with a nonaddition control at a 5 nM concentration. Under identical conditions, Na+, K+-ATPase activity was strongly stimulated with GM1 (180%) and GD1a (93%), whereas Ca2+, Mg2+-ATPase activity showed no change. In SCG, on the other hand, AIB uptake was apparently inhibited (-27%) by addition of GM1, with a slight decrease in Na+, K+-ATPase but no change in Ca2+, Mg2+-ATPase activity in the tissue. Both asialo-GM1, in which N-acetylneuraminic acid is deficient, and Forssman glycolipid, which is not present in nervous tissue, failed to produce any significant increase in both SCG and NG not only in amino acid uptake, but also in Na+, K+-ATPase activity. A kinetic study of active AIB uptake showed that GM1 ganglioside produced an increase in Km with no change in Vmax in SCG, whereas it caused a decrease in Km with a slight increase in Vmax in NG. Treatment of NG and SCG with neuraminidase from Vibrio cholerae, an enzyme that split off sialic acid from polysialoganglioside, leaving GM1 intact, caused little inhibition of the amino acid uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1987

Inhibition of hepatic 17 beta- and 3 alpha-hydroxysteroid dehydrogenases by antiinflammatory drugs and nonsteroidal estrogens.

Antiinflammatory agents and estrogens have been tested as inhibitors of two isozymes of guinea pig liver testosterone 17 beta-dehydrogenase (NADP) 1.1.1.64) and rat liver 3 alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50). Antiinflammatory steroids and estradiols were highly inhibitory to 3 alpha-hydroxysteroid dehydrogenase and one isozyme of testosterone 17 beta-dehydrogenase, respectively, but nonsteroidal antiinflammatory agents and nonsteroidal estrogens such as hexestrol, dienstrol, diethylstilbestrol and zearalenone showed potent inhibitions on all the enzymes. Although the inhibitory potency of indomethacin for one isozymes of testosterone 17 beta-dehydrogenase and 3 alpha-hydroxysteroid dehydrogenase decreased with changing pH from 9.7 to 7.0, that of the nonsteroidal estrogens for all the enzymes was little affected by pH. No additive effect in double inhibitor experiments with indomethacin and the nonsteroidal estrogens was observed, and the compounds were all competitive inhibitors with respect to steroidal substrate. The results suggest that there is a very similar region in substrate binding sites of the enzymes.

17-Hydroxysteroid Dehydrogenases↗
PubMed1987

Topographic diagnosis of facial paralysis by the assay of lysozyme concentration in tears.

Lysozyme in tears is secreted from the main lacrimal gland innervated by a parasympathetic nerve via the greater petrosal nerve. Lysozyme activity in tears was analysed in 10 cases of unilateral facial paralysis due to the cerebellopontine angle (CPA) tumor and 10 normal cases. The lysozyme concentration in tears on the paralysed side collected by Schirmer No. 2 test was significantly lower than that on the healthy side, or bilateral sides of normal subjects. This decreased concentration on the paralysed side is due to the interruption of the reflex are at the level of CPA. It is concluded that our new method is more useful for topographical diagnosis of facial paralysis than is the conventional Schirmer's filter paper test.

Adult↗
PubMed1987

The effects of nifedipine and captopril on renal function in patients with essential hypertension: comparison with sodium nitroprusside.

In comparison with a nonspecific vasodilator, sodium nitroprusside (SNP), we intended to deduce the characteristics of nifedipine (NIF) and captopril (CAP) in the treatment of hypertension. Ten patients with essential hypertension were hospitalized and kept on a constant sodium diet (10 g NaCl/day). Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured before and after the respective administration of SNP (0.9 +/- 0.5 mcg/kg/min), NIF (17 +/- 5 mg), and CAP (85 +/- 24 mg). SNP significantly reduced the mean blood pressure (MBP), the renal vascular resistance index (RVRI), urine volume (UV), urinary excretion of sodium (UNaV), and significantly raised active renin concentration (ARC), plasma norepinephrine (NE), and the heart rate (HR). RBF, GFR, and plasma epinephrine (E) were not changed. Compared with SNP, NIF significantly raised RBF, UV, UNaV, and fractional excretion of sodium (FENa) and significantly reduced RVRI. The differences between the increases in ARC, NE, and HR by NIF and those by SNP were not significant. GFR and E were not changed by NIF. Although CAP did not reduce MBP as much as SNP did, the increase in RBF by CAP was significantly greater than that by SNP. Changes in GFR, UV, UNaV, FENa, and E by CAP were not different than those by SNP. CAP increased ARC and did not raise E, NE, and HR. In conclusion, compared with SNP, NIF significantly raised RBF, UV, UNaV, and FENa and significantly reduced RVRI. On the other hand, the renal response to CAP was not very much different from the response to SNP. The characteristics of CAP were the suppressed sympathetic response to the decrease in blood pressure.

Adult↗
PubMed1987

An adult case of adrenoleukodystrophy with features of olivo-ponto-cerebellar atrophy: II. Lipid biochemical studies.

Different portions with or without demyelination or degeneration of formalin-fixed brain tissues of a patient with adrenoleukodystrophy and a control subject were applied to analyses of lipids, particularly sphingolipids and cholesteryl ester. Demyelinated area of the white matter in the occipital lobe showed marked decrease in cerebroside and sulfatide except for sphingomyelin and, conversely an accumulation of cholesteryl ester, whereas un-demyelinated white matter in the frontal lobe showed no abnormalities in lipids. Abnormalities of lipids in degenerated lateral nuclei of the thalamus were not so remarkable as the demyelinated white matter, whereas apparently normal dorsomedial nuclei of the thalamus showed no abnormalities in lipids. With regard to the fatty acid composition of abnormal lipids in the demyelinated white matter, all sphingolipids of cerebroside, sulfatide, and sphingomyelin showed remarkable reduction of their longer chain fatty acids and, conversely a significant increment of shorter chain fatty acids. However, these fatty acids in the degenerated lateral nuclei of the thalamus were not so different from those in the undemyelinated and apparently normal areas as well as in control brain. The fatty acids of cholesteryl ester contained mainly C18:1 and C16 acids, and very long chain fatty acids, namely fatty acids with chain length more than 22 carbons, by about 22% of the total fatty acids. In view of the analytical results of the fatty acid composition of brain lipids, it was inconceivable that this ALD patient brain showed especially the accumulation of very long chain fatty acids, and that the biochemical defect in this disease was related to the abnormal oxidation of very long chain fatty acids in peroxisomes. However, the neuropathological findings of demyelination, reactive astrocytosis, and massive infiltration of foam cells well correlated with the abnormalities in myelin lipids and the accumulation of cholesteryl ester. Also, the lower values of urinary 17-ketosteroid and 17-hydroxycorticosteroid suggested that the failure of ACTH to stimulate corticoid secretion seemed to indicate the relationship between the adrenocortical insufficiency and the affected areas of the central nervous system.

Adrenoleukodystrophy↗
PubMed1987

[Detection of polyamines by an enzymatic assay. (6). Fundamental and clinical studies of a simple enzymatic method for determining total polyamines in blood].

A simple enzymatic method for determining total polyamines in human blood was established. Polyamines in trichloroacetic acid extract from 1 ml of blood were isolated on an anion-exchange column and measured spectrophotometrically by the end point assay using polyamine oxidase and putrescine oxidase. The recovery was as high as 98.4% and within-run precision (coefficient of variance: 1.82%), and the values obtained by this method were in fair agreement with those obtained by high performance liquid chromatography and the enzymatic differential assay methods previously reported. The polyamine levels were not changed when the blood was stored at -20 degrees C. Blood polyamine levels were measured in 108 patients with genitourinary cancers, 29 patients with benign prostatic hypertrophy, 18 patients with benign urological diseases and 25 normal subjects. Although polyamines were not significantly elevated in the low stage of cancer, elevation was observed at a high stage of malignancy. These results indicate that the determination of total polyamines may be useful to determine biochemically the malignancy of cancers.

Biomarkers, Tumor↗
PubMed1986

Dihydrodiol dehydrogenases in guinea pig liver.

Four major and four minor dihydrodiol dehydrogenases, with similar apparent molecular weights of 28,000 to 34,000 but with different charges, were purified from male guinea pig liver cytosol. One of the minor enzymes catalyzed only the oxidation of benzene dihydrodiol with a high Km value of 5.0 mM and was identified immunologically with aldehyde reductase. The other enzymes oxidized xenobiotic alicyclic alcohols and 17 beta-hydroxysteroids as well as benzene dihydrodiol. These enzymes exhibited higher affinity for 17 beta-hydroxysteroids than for alicyclic alcohols and benzene dihydrodiol, and immunologically cross-reacted with testosterone 17 beta-dehydrogenase purified from the same source. Four major enzymes and one minor with Km values for benzene dihydrodiol of about 0.2 mM, possessed specificity for 5 beta-androstane--17 beta-hydroxysteroids and dual cofactor requirement, whereas the other two minor enzymes with high Km values of over 5 mM showed apparent NADP and 5 alpha-androstane specificity. The dihydrodiol dehydrogenase activity was localized in the cytosol of liver. The results indicate that the hepatic oxidation of dihydrodiols in the guinea pig is mediated by cytosolic testosterone 17 beta-dehydrogenase isozymes and aldehyde reductase. Testosterone 17 beta-dehydrogenase immunologically identical to the liver enzymes was detected only in kidney, whereas aldehyde reductase was detected in all tissues of the guinea pig.

Alcohol Dehydrogenase↗
PubMed1986

Isolation of multiple forms of indanol dehydrogenase associated with 17 beta-hydroxysteroid dehydrogenase activity from male rabbit liver.

Seven multiforms of indanol dehydrogenase were isolated in a highly purified state from male rabbit liver cytosol. The enzymes were monomeric proteins with similar molecular weights of 30,000-37,000 but with distinct electrophoretic mobilities. All the enzymes oxidized alicyclic alcohols including benzene dihydrodiol and hydroxysteroids at different optimal pH, but showed clear differences in cofactor specificity, steroid specificity, and reversibility of the reaction. Two NADP+-dependent enzymes exhibited both 17 beta-hydroxysteroid dehydrogenase activity for 5 alpha-androstanes and 3 alpha-hydroxysteroid dehydrogenase activity for 5 beta-androstan-3 alpha-ol-17-one. Three of the other enzymes with dual cofactor specificity catalyzed predominantly 5 beta-androstane-3 alpha,17 beta-diol dehydrogenation. The reverse reaction rates of these five enzymes were low, whereas the other two enzymes, which had 3 alpha-hydroxysteroid dehydrogenase activity for 5 alpha-androstanes or 3(17)beta-hydroxysteroid dehydrogenase activity for 5 alpha-androstanes, highly reduced 3-ketosteroids and nonsteroidal aromatic carbonyl compounds with NADPH as a cofactor. All the enzymes exhibited Km values lower for the hydroxysteroids than for the alicyclic alcohols. The results of kinetic analyses with a mixture of 1-indanol and hydroxysteroids, pH and heat stability, and inhibitor sensitivity suggested strongly that, in the seven enzymes, both alicyclic alcohol dehydrogenase and hydroxysteroid dehydrogenase activities reside on a single enzyme protein. On the basis of these data, we suggest that indanol dehydrogenase exists in multiple forms in rabbit liver cytosol and may function in in vivo androgen metabolism.

17-Hydroxysteroid Dehydrogenases↗