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K Nakagawa

Publications and source records attributed to K Nakagawa.

At least 19 recordsLinked to original sources
PubMed1979

Stereo-specific synthesis of 3-trifluoromethylcephalosporin derivative by microbial acylase.

Cephalosporin acylase (EC 3.5.1.11) obtained from Kluyvera citrophila ATCC 21285 was found to catalyze synthesis of 7-[2-(2-thienyl)acetamido]-3-trifluoromethyl-3-cephem-4-carboxylic acid from methyl thienylacetate and dl-7-amino-3-trifluoromethyl-3-cephem-4-carboxylic acid. The enzymatically-synthesized compound showed [alpha]25 D + 42.7 degrees (c 0.058, MeOH) and its biological activity was about twice as much as that of racemic 7-[2-(2-thienyl)acetamidol]-3-trifluoromethyl-3-cephem-4-carboxylic acid chemicall synthesized. As a result, N-acylation by this enzyme was demonstrated to be asymmetric synthesis.

Amidohydrolases↗
PubMed1979

[Computed tomography in crossed aphasia (author's transl)].

Crossed aphasia, first described by Bramwell, is aphasia due to the hemispheric damage on the side of handedness. Crossed aphasia in a dextral is rare, and in Japan, there have not been more than ten cases in which the lesion is localized clearly. The cases reported till now have been verified mainly by necropsy. However, the time lag between the appearance of aphasia and the necropsy may affect the conclusion subtly. We consider that computed tomography (CT) can obtain almost the same findings as that by necropsy. However, at present there have been few cases diagnosed by CT except two cases reported by April et al. and Wechsler. We have reported a 47-year-old man in a dextral, who shows left hemiparesis and Broca's aphasia. His lesion is diagnosed by cerebral angiography and CT as the right hemisphere infarction due to right middle cerebral artery occlusion. CT localizes the lesion on the right hemisphere mainly sited deep region and sited wedge shaped cortical area of the fronto-parietal region. On the other hand, it localizes no lesion on the left hemisphere. CT in aphasia has been already reported by Hayward et al. In their report they concluded that correlation of lesion located by CT with aphasia type supported Geschwind's concept of aphasia. In this report we have discussed CT in crossed aphasia analysing our case and the two cases by April et al. and Wechsler. Three cases including our case are all Broca's aphasia, and we compare the lesion location of these three cases with Hayward's lesion located on Broca's aphasia. As the result of this, we can draw the conclusion that the lesion location by CT of these three cases and that of Hayward's report are almost symmetric.

Aphasia↗
PubMed1978

A modulating role of taurine on release of acetylcholine and norepinephrine from neuronal tissues.

Effects of taurine (2-aminoethanesulfonic acid) on the uptake and release of 14C-acetylcholine (14C-ACh) and 3H-norepinephrine (3H-NE) in the superior cervical ganglion and cerebral cortex of the rat were studied. Taurine suppressed high potassium evoked release of 14C-ACh and 3H-NE from the rat superior cervical ganglia and cerebral cortical slices, while the drug did not modify per se the uptake and unstimulated (spontaneous) release of 14C-ACh and 3H-NE in these tissues. Furthermore, taurine inhibited the release of 3H-NE from the crude synaptosomal (P2) fraction of the rat brain without affecting the uptake. These results suggest that taurine may act as a modulator of neuronal activity, possibly by stabilizing excitable membrane and by suppressing the release of neurotansmitter at synapses.

Acetylcholine↗
PubMed1978

Morphine-induced changes in cyclic AMP metabolism and protein kinase activity in the brain.

The effects of consecutive oral administration of morphine on the cyclic AMP synthesizing system and cyclic AMP dependent protein kinase activity in the cerebral cortex of mice were examined. The administration of morphine (2--4 weeks) induced an increase of the cyclic AMP formation by activating adenylate cyclase, whereas responses of the cyclic AMP synthesizing system to biogenic amines (norepinephrine, dopamine and histamine) added in vitro was found to be significantly attenuated in these animals. Cyclic AMP dependent protein kinase activity in the cerebral cortex was also increased following a consecutive oral administration of morphine. These changes in the activities of adenylate cyclase and protein kinase were found mainly in crude mitochondrial and/or synaptosomal fractions. Morphine induced decrease in the response of the cyclic AMP synthesizing system to biogenic amines was rapidly reversed, and a significant increase of the cyclic AMP formation in the presence of added norepinephrine compared with that found in morphinized animals was observed following the administration of levallorphan, a narcotic antagonist. On the other hand, the changes in adenylate cyclase and cyclic AMP dependent protein kinase activities were not affected significantly by levallorphan administration. These results suggest that alterations in activities of cyclic AMP synthesizing system and of cyclic AMP dependent protein kinase may be involved in processes of the formation of morphine dependence. Possible involvement of abrupt increments in the sensitivity of "norepinephrine receptor-adenylate cyclase" system and a subsequent increase in cerebral cyclic AMP is also suggested as a cause of morphine withdrawal syndrome.

Adrenalectomy↗
PubMed1978

Enzyme-linked immunoassay of somatostatin.

An enzyme-linked immunoassay for somatostatin using somatostatin-alkaline phosphatase conjugate as "labeled" antigen was developed. Minimal detectable dose at present was 40 pg per tube. Serial dilutions of rat hypothalamic extract gave a gradual change of antibody-bound alkaline phosphatase activity which was parallel to that with standard somatostatin. Precision and accuracy of the method were comparable to those in radioimmunoassay reported by others. This method will be a useful tool for the determination of somatostatin, especially in tissues.

Alkaline Phosphatase↗
PubMed1978

The metabolites of procaterol HCl in urine and faeces of dog and man.

1. The metabolites of procaterol HCl in dog urine and faeces and in human urine were qualitatively analysed by an improved g.l.c.-mass spectrometric method. 2. Trimethylsilylated derivatives of procaterol metabolites were identified by mass fragmentography as procaterol glucuronide, 5-(2-amino-1-hydroxybutyl)-8-hydroxycarbostyril (desisopropylprocaterol), 5-formyl-8-hydroxycarbostyril, 8-hydroxycarbostyril and unchanged procaterol. 3. The metabolic pattern of procaterol HCl was species-independent in rats, dogs and man.

Administration, Oral↗