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Biomedical subjects

K Hirota

Publications and source records attributed to K Hirota.

At least 487 records · Page 27Linked to original sources
PubMed1981

Androgen receptor in human placental villi.

In studies with a synthetic androgen, R 1881, an androgen-binding component was found in the cytosol of human placental villi. Kinetic analysis indicated that the Kd value of this component was 1.4 nM at 0-4 degrees C and that binding of R 1881 amounted to 277 +/- 73 fmol/mg protein. glycerol density gradient ultracentrifugation showed a peak of binding activity in the 8S region in a medium of low ionic strength, but in the 4.5S region in a medium containing 9.5 M KCl. The R 1881-binding component was inactivated by mild heat- or trypsin-treatment, but not by treatment with DNase or RNase. Most of the R 1881-binding activity was sedimented at 20 to 40% saturation of ammonium sulfate. These findings indicate that the R 1881-binding component in human placental cytosol is quite similar in its characteristics to androgen receptors, which are present in various androgen-responsive organs. Testosterone was a more potent competitor of R 1881-binding than DHT or cyproterone acetate. Scatchard plots indicated that the binding site of testosterone was identical with that of R 1881. These findings suggest that the androgen receptor in placental cytosol is specific for testosterone. The Kd value for testosterone was calculated to be 3.2 nM.

Cell Membrane↗
PubMed1981

Genetic and clinical patterns of heritable cerebellar ataxias in adults. II. Clinical manifestations.

Clinical data on 244 probands with spinocerebellar types, 163 with late cortical cerebellar atrophies (LCCA), and 180 with olivopontocerebellar atrophies (OPCA) were analysed. Spinocerebellar cases were divided into three according to their estimated genetic mechanisms: recessive, dominant, or sporadic. Ages of onset were identical in sporadic spinocerebellar types, LCCA, and OPCA, the average being about 50. They showed highly correlated clinical patterns. In the light of other evidence, these diseases may represent a premature aging process in the central nervous system, probably determined multifactorially. Recessive spinocerebellar cases were very few. There were 127 cases of spinocerebellar types with dominant inheritance, characterised by age of onset around 33, colourful ocular signs, and spasticity. A large family with this disease was described in which 34 patients were affected through five generations. The computed tomograms showed an almost normal cerebellum and electronystagmograms indicated patterns of vestibulocular impairment. No necropsied case was available among the present material, but in pathological reports of similar cases, major lesions were found in the ventral and the dorsal spinocerebellar tracts, Clarke's columns, and the posterior columns in the spinal cord. This disease, or hereditary spastic ataxia, represented a fairly well-defined entity inherited dominantly among a group of cases with spinocerebellar types, and it was separable from LCCA or OPCA, not only on clinical and genetic grounds, but by a predominantly spinal involvement.

Age Factors↗
PubMed1980

Improved gas chromatographic method of determining diclofenac in plasma.

Diclofenac was converted into either its methyl or ethyl ester in methanol or ethanol containing 0.1% or 0.5% sulfuric acid, respectively. The ester was extracted and subjected to gas--liquid chromatography with electron-capture detection. The esterification resulted in an increased sensitivity of the gas chromatographic detection, three times better than that previously reported for the formation of indolone ring in trifluoroethanol containing 0.5% sulfuric acid.

Chromatography, Gas↗
PubMed1980

Demonstration of IgG EA (early antigen) and IgM MA (membrane antigen) antibodies in CMV infection of healthy infants and in those with liver disease.

The sequence of antibody production to various virus-specific antigens in CMV infection in infancy was studied. In healthy infants, IgG EA antibody was demonstrated in 18% of cord sera, and disappeared within two months after birth in all cases not shedding virus. The nonmaternal EA antibody was produced following virus excretion and decreased rapidly following cessation of virus excretion. Thus, demonstration of EA antibody in infants after 2 months of age was found to indicate acquired CMV infection, even when CMV could not be isolated. IgM MA antibody did not persist as long as EA antibody, disappearing before cessation of virus excretion. Both IgG EA and IgM MA antibodies were more frequently demonstrated in infants with hepatitis than in healthy infants. These findings suggest the possible association of CMV with hepatitis in infants.

Antibodies, Viral↗
PubMed1980

Friedreich's ataxia in Japan: clinical and genetic analyses in 52 cases.

Among 844 proband cases with various types of spinocerebellar degenerations reported to us by about 200 major neurological clinics in Japan, there were 26 males and 26 females with Friedreich's ataxia. Genetic analysis disclosed recessive transmission of these cases. Clinical patterns were almost identical with the cases observed in Europe and Canada.

Adolescent↗
PubMed1980

Synthesis and antiherpesviral activity of 5-C-substituted uracil nucleosides.

Reaction of 2'-deoxy-5-hydroxyuridine with some Wittig reagents gave 5-alkoxycarbonylmethyl-, 5-carbamoylmethyl-, 5-cyanomethyl-and 5-acetonyl-2'-deoxyuridines. The corresponding 1-beta-D-arabinofuranosyl derivatives were prepared from 1-beta-D-arabinofuranosyl-5-hydroxymethyluracil. The latter was also converted to 1-beta-D-arabinofuranosyl-5-vinyluracil via triphenylphosphonium salt, and then to 5-(2-halogenovinyl)derivatives. Some of these compounds showed marked antiherpesviral activity in vitro.

Antiviral Agents↗
PubMed1979

Nucleosides. 110. Synthesis and antiherpes virus activity of some 2'-fluoro-2'-deoxyarabinofuranosylpyrimidine nucleosides.

A series of 5-substituted 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl)cytosines 7a-d and their corresponding uracils 9a-d,f were prepared by condensation of 3-O-acetyl-5-O-benzoyl-2-deoxy-2-fluoro-D-arabinosyl bromide (5) with appropriately trimethylsilylated pyrimidines followed by saponification of the protected nucleosides 6 or 8. 1-(2-Deoxy-2-fluoro-beta-D-arabinofuranosyl)-5-iodocytosine (7e) was obtained by iodination of 7a. Iodination of 8a followed by removal of the protecting acyl-protecting groups afforded the 5-iodo nucleoside 9e. Several of these 2'-fluoro-substituted nucleosides completely obviated replication of herpes simplex virus type 1 (HSV-1) in monolayers of Vero cells at concentrations of 10-100 microgram/mL. The 5-iodocytosine analogue 7e was the most effective, showing 99.5% suppression of viral replication even at concentrations of 0.1 microgram/mL. The cytotoxicity of 7e to L5178Y or P815 cells in culture was minimal. A comparison of the efficacy of 7e against HSV-1 with other known nucleoside antiviral agents indicates that further in vitro and in vivo evaluation of 7e is warranted.

Antiviral Agents↗
PubMed1979

Augmentation of puerperal lactation by oral administration of sulpiride.

The effect of oral administration of sulpiride on PRL secretion and initiation of puerperal lactation was studied in 130 randomly selected primiparous nursing mothers. Sixty-six women were given 50 mg sulpiride orally twice a day during the first 7 days of the puerperium (sulpiride group). Sixty-four women were given a placebo in the same way (control group). The mean (+/-SE) total milk yield during the first 5 postpartum days in the sulpiride group (1211.7 +/- 65.0 ml) was significantly greater than that in the control group (916.0 +/- 66.0 ml). Every other day determinations of serum PRL levels revealed significantly higher concentrations in the sulpiride group than in the control group. A single oral dose of 50 mg sulpiride raised serum PRL levels for 12 h, with a peak level at 2 h after dosing in 7 women on the second postpartum day. These data suggest that sulpiride given orally promotes the initiation of lactation in puerperal women by stimulating PRL secretion.

Adult↗
PubMed1978

Oxidative degradation of haemoglobin by nitrosobenzene in the erythrocyte.

Substitutions on the benzene ring of nitrosobenzene did not have the same effect on oxidative haemolysis as substitutions on phenylhydrazine. We previously found that the haemolytic effect of arylhydrazines paralleled their oxidative conversion into ligands of ferrihaemoglobin. In contrast, although most substituted nitrosobenzenes that are ligands of ferrohaemoglobin caused haemolysis and most that are not ligands failed to cause nitrosoarenes appeared to be related more closely to the ease of their reduction to arylhydroxylamines than to their properties as ligands. We propose a mechanism of oxidative degradation whereby the cyclic formation of phenylhydroxylamine from nitrosobenzene within an erythrocyte leads to the accumulation of H2O2, which then reacts with ferrohaemoglobin to initiate the oxidative cleavage of haem. The posulated active intermediate in this reaction is the same as that previously proposed in the oxidative degradation of haemoglobin by phenylhydrzine and in the coupled oxidation of ascorbic acid and haemoglobin.

Animals↗
PubMed1978

Influence of ring substituents on the binding of nitrosobenzene by ferrohemoglobin.

The affinity of a substituted nitrosobenzene for ferrohemoglobin and the visible absorption spectrum of the resulting compound was influenced by the nature, position, and number of substituents on its benzene ring. Alkyl ring substituents inhibited the binding of nitrosobenzene to ferrohemoglobin, and binding was blocked by an ortho tertbutyl group or by a pair of ortho methyl groups. A single halogen atom increased binding affinity except that iodine decreased affinity, more at the ortho than at the para position. Binding occurred with a pair of ortho fluorine atoms but not with a pair of ortho chlorine or bromine atoms. These results favor a model of nitrosoarene ferrohemoglobin in which the iron of ferroheme is bonded to the nitrogen atom of the nitroso group since a bond to the oxygen atom would not be hindered by ortho substituents. The presence of a carboxylate substituent resulted in prevention of binding, which was reversed by esterification of the group. Large neutral para substituents, which cannot directly affect formation of the Fe-NO bond, inhibited binding, although not to the same degree as ortho substituents. It thus appears that the affinity of a substituted nitrosobenzene for ferrohemoglobin depends on interactions of the nonbonding part of the ligand molecule with the heme crevice as well as on the ability of its nitroso group to form a bond with the iron of heme. Nitrosoarenes also exhibited in varying degrees the property of removing an electron from ferrohemoglobin to form ferrihemoglobin.

Hemoglobins↗