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Biomedical subjects

K Komiya

Publications and source records attributed to K Komiya.

At least 37 records · Page 2Linked to original sources
PubMed1990

[A case of three-year-old boy with periodic apnea during waking and sleep, severe psychomotor retardation and hypotonia].

We presented a 3-year-old boy, a product of consanguineous parents, with periodic apnea during waking and sleep states, severe psychomotor retardation and hypotonia. According to polysomnographical recordings, he exhibited frequent central apneas which decreased in frequency and regularity in the stage REM. He showed abnormal background EEG, undifferentiated sleep stage and very short duration of stage REM. The initiation of breathing after apnea was often accompanied with generalized muscles contraction like a startle response. In the waking state the apnea induced generalized muscular hypotonicity and the decline of wakefulness. Arterial CO2 and O2 saturation was within normal limits. It was suggested that the malfunction of the brain stem responsible for the control of breathing, sleep-wakefulness cycle and determination of sleep stages was closely connected with the pathogenesis of abnormal breathing patterns.

Apnea↗
PubMed1989

The spectrum of cytoplasmic body myopathy: report of a congenital severe case.

A 6-year-old girl presented with a myopathy--she was floppy since birth and developed progressive respiratory failure for which she required mechanical ventilation at age 6 months. Biopsy showed cytoplasmic bodies in about 15% of both type 1 and 2 muscle fibers. Of the 18 cases of cytoplasmic body myopathy (CBM) reported in the literature, 3 had symptoms at birth and in all of them the course was benign. Four clinical patterns emerged; a) congenital severe, b) congenital benign, c) juvenile severe and d) adult severe forms.

Child↗
PubMed1989

[Stellate ganglion block therapy against progressive facial hemiatrophy].

A typical case with progressive facial hemiatrophy was treated with a new therapeutic trial, stellate ganglion block. The present case, a Japanese girl, suffered from progressive atrophy involving the soft tissue of the left buccal region, with onset at the age of 6 following a minor local trauma. She visited our hospital at the age of 9, and as soon as the diagnosis was made, left stellate ganglion block was initiated. Local injection of lidocaine was performed 53 times over the period of 1 year and 4 months. During this period of therapy and the subsequent follow-up period of 4 years, the state of atrophy remained unchanged and nonprogressive. Stellate ganglion block as a therapy against progressive facial hemiatrophy was considered to be worth further evaluation, although it was impossible to judge, based solely on our experience, whether the arrest of progression was attributable to the therapy. The rationale of this therapy was also discussed. It was based upon the assumption that atrophy may result from irritation of the cervical sympathetic nerve, one of the most popular theories regarding the pathomechanism of progressive facial hemiatrophy.

Autonomic Nerve Block↗
PubMed1988

A case of juvenile metachromatic leukodystrophy--the third case in Japan.

We report here a case of juvenile metachromatic leukodystrophy. The patient is an 8-year-old boy with motor and mental deterioration, which began at about age 3. He has also suffered from astatic seizures since age 8. Arylsulfatase A activity in the patient was markedly decreased in peripheral leukocytes, cultured fibroblasts and urine. Sulfatide was detected in urine from the patient by thin-layer chromatography. Peripheral motor and sensory nerve conduction velocities were markedly reduced. Computerized tomography of the brain showed low density areas in the periventricular white matter which were not enhanced by intravenous contrast material. His parents' arylsulfatase A activities were about half those of normal controls. This is the third case of juvenile metachromatic leukodystrophy in Japan.

Brain↗
PubMed1986

Cerebellar infarction.

Here is reported a rare case of a child with cerebellar infarction confirmed by vertebral angiography and computed tomography (CT). Following the sequential CT scan, new hypodense areas developed twice in the later stages. This finding has not been previously reported neither in infra- nor in supra-tentorial infarction.

Cerebellum↗
PubMed1981

Properties of the mercury and selenium complex formed in rat plasma in vivo.

Properties of the mercury and selenium complex (Hg-Se Complex) produced in plasma after the simultaneous injection of mercuric chloride and sodium selenite were investigated by means of pronase digestion and isoelectric focusing. When the gel chromatographic fraction containing the HG-Se complex was digested with Pronase E and chromatographed on a Sephadex G-200 column, the resulting derived proteins contained no mercury and very low percentage of selenium. Most of mercury and selenium in the digest of the Hg-Se complex remained at the top of column, but the content of proteins (derived proteins) found at the same site of column was only trace amount. In contrast, the derived proteins obtained from proteins containing mercury or selenium in serum by the same digestion contained mercury and high percentage of selenium respectively. These results indicated that the Hg-Se complex in plasma did not contain protein as a component. When the isoelectric focusing of the serum containing the Hg-Se complex was carried out, the peak containing both mercury and selenium was present in the position of pH2 and pH4. The former peak was independent of the serum proteins, the latter peak overlapped the distribution of that. Similar behavior of mercury and selenium was observed in the isoelectric focusing of the mercuric selenide colloid dispersed in the solution containing bovine serum albumin. The properties of the Hg-Se complex in these studies supported the hypothesis that it is a mercuric selenide colloid.

Animals↗
PubMed1976

Hyperalaninemia hyperpyruvicemia and lactic acidosis due to pyruvate carboxylase deficiency of the liver; treatment with thiamine and lipoic acid.

A 16-month-old female infant with severe mental and motor retardation, clinically diagnosed as Leigh's encephalomyelopathy, forms the basis of this study. This infant was found to have lactic acidosis, low cerebrospinal fluid glucose, hyperalaninemia, and increased levels of urine lactate, pyruvate and alanine. These laboratory studies suggested an inborn error in gluconeogenesis. Further investigation revealed a low level of hepatic pyruvate carboxylase activity. The patient's elder sister who also had mental and motor deterioration was then also found to have an elevated blood lactate. These two siblings clinically and biochemically showed improvement with treatment consisting of thiamine and lipoic acid.

Acidosis↗