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Biomedical subjects

K Onoda

Publications and source records attributed to K Onoda.

At least 91 records · Page 5Linked to original sources

Pituitary enlargement with target organ deficiency: hypothyroidism and hypogonadism.

Three women with pituitary enlargements associated with preexisting target organ failures are reported. Two pituitary enlargements owing to primary hypothyroidism and one to primary hypogonadism were shown to be regressed on computed tomography after the replacement therapy. Clinically and pathologically, the differentiation of a pituitary hyperplasia from a pituitary adenoma is often very difficult. Moreover, the treatments for these conditions are quite different. Adequate medication can diminish a pituitary enlargement because of the feedback mechanism. Existence of the target organ deficiency should always be checked before the management of pituitary tumor.

Adult↗

Selective modulation of calcium-dependent myosin phosphorylation by novel protein kinase inhibitors, isoquinolinesulfonamide derivatives.

Ca2+-dependent myosin phosphorylation by Ca2+/calmodulin-dependent myosin light chain kinase (MLC-kinase) and protein kinase C were studied using selective inhibitors, isoquinolinesulfonamide derivatives. Both protein kinases were potently inhibited by 1-(8-chloro-5-isoquinolinesulfonyl)piperazine (HA-156) and its derivatives. Kinetic analysis indicated that HA-156 inhibited both enzymes competitively with respect to ATP, and Ki values of HA-156 for MLC-kinase and protein kinase C were 7.3 and 7.2 microM, respectively. To clarify molecular mechanisms of the isoquinolinesulfonamides to inhibit the Ca2+-dependent protein kinases, we examined the structure-activity relationships of HA-156 and its derivatives. The dechlorinated analogues, HA-100 and HA-142, markedly decreased the affinity for MLC-kinase, suggesting that the inhibitory effect of isoquinolinesulfonamide derivatives depends upon hydrophobicity of the compounds. There is a good correlation between MLC-kinase inhibition and hydrophobicity determined by reverse phase chromatography. In contrast, HA-140 and HA-142 showed weak inhibition of protein kinase C, suggesting that the electron density of the nitrogen in the isoquinoline ring of the compounds correlates with the potency to inhibit protein kinase C activity. These pairs of isoquinolinesulfonamides will aid in elucidating the biological roles of Ca2+-dependent myosin phosphorylation in intact cells. HA-156 and HA-140 inhibited myosin light chain phosphorylation in platelets exposed to collagen, whereas HA-142 and HA-100 did not, significantly. These isoquinolinesulfonamide derivatives should prove to be useful tools for distinguishing between the biological functions of Ca2+-activated, phospholipid-dependent, and Ca2+/calmodulin-dependent myosin light chain phosphorylation, in vivo.

Adenosine Triphosphatases↗

[Follow-up CT myelography of severe cervical spinal cord injury].

There are many reports describing gross anatomical and microscopical findings of severely injured cervical cords in autopsy of the acute and chronic state, but no morphological findings of a severe cervical spinal cord injury in a chronic state by follow-up CT myelography have been found in the literature so far. The sagittal and transverse diameters of the cervical spinal cord and subarachnoid space of 9 out of 14 severe cervical spinal cord injury patients were measured with CT myelography within 7.5 years after the trauma and their size compared with a control group which was made up of 29 patients with slight radiculopathy due to cervical spondylosis and whiplash injuries. Injured cord levels were C4 4 cases, C5 4 cases and C6 1 case. Remarkable spinal cord atrophy was recognized in the sagittal diameter from C1 to C7 and in the transverse diameter below C4 and narrowing of the cervical subarachnoid space in the sagittal diameter from C2 to C5. The significance level was set at 1-5%. From these findings, we have concluded that atrophy appeared not only in the injured segment but also the whole cervical cord after the trauma. There was less cord atrophy in a good functional prognosis than in a poor prognosis.

Adolescent↗

An adult case of adrenoleukodystrophy with features of olivo-ponto-cerebellar atrophy: I. Clinical and pathological studies.

A male patient was suspected as olivo-ponto-cerebellar atrophy from the clinical and computed tomographic features at 34 years of age. Afterwards, his dysarthria and limb ataxia were slowly and steadily worsened. He was finally bed-ridden and unresponsive, and died of hyperpyrexia and general wasting at 37 years of age. It was noted that laboratory investigation gave lower values of urinary 17-ketosteroids and 17-hydroxycorticosteroids in comparison with those of normal subjects. Pathological investigation in autopsy showed that he had pathological features consistent with adrenoleukodystrophy accompanying the olivo-ponto-cerebellar atrophy; diffuse demyelination in the cerebrocerebellear white matter, distorted architecture and cytoplasmic striations in the adrenal cortex, and in addition, a pseudosystemic degeneration of the olivo-ponto-cerebellar system and subcortical gray matter.

17-Hydroxycorticosteroids↗

Simple management of cerebrospinal fluid rhinorrhea after pituitary surgery.

A simple procedure for managing postoperative cerebrospinal fluid rhinorrhea after pituitary surgery is described. Under local anesthesia, a needle is introduced manually through a nostril toward the sella turcica and EDH adhesive or fibrin glue is injected into the sellar cavity or sphenoid sinus, or both. This procedure is simple and safe to perform, acceptable to the patient, and can be done in a short hospital stay.

Aprotinin↗

Reevaluation of thyroid function in low birth weight infants based on free triiodothyronine and triiodothyronine.

We attempted to analyze the physiological meaning of abnormally low thyroid hormones in low birth weight (LBW) infants on the basis of cross-sectional data on free triiodothyronine (free T3) and T3 in addition to the other thyroid hormones. In LBW infants, the levels of free T3 and T3 were lower than those of normal infants, similar to the relation between free thyroxine (free T4) and T4. The ratio of free T3/T3 or free T4/T4, however, was not different between the groups. The levels of thyroid-stimulating hormone, thyroid hormone-binding globulin and reversed T3 in LBW infants were not significantly different from those of normal infants.

Humans↗

Studies on nitrosamine formation by the interaction between drugs and nitrite. II. Hepatotoxicity by the simultaneous administration of several drugs and nitrite.

The alterations of biochemical parameters, namely, glutamic oxaloacetic transaminase and glutamic pyruvic transaminase in serum, hepatic microsomal drug oxidation systems, glucose-6-phosphate dehydrogenase and lysozomal enzymes in hepatic soluble fraction were investigated for the purpose of semiquantitatively estimating the hepatotoxicity caused by the interaction of several drugs and sodium nitrite in rats. The simultaneous administration of aminopyrine and sodium nitrite induced the alterations of these parameters. However, these alterations were not induced by the administration of antipyrine and sodium nitrite. Therefore the alterations were thought to be mainly due to N-nitrosodimethylamine formed. The administration of 0.4 mmole/kg of aminopyrine and 1.0 mmole/kg of sodium nitrite was thought to induce the alterations to almost the same extent as induced by 0.15 mmole/kg of N-nitrosodimethylamine. The simultaneous administrations of sodium nitrite and several other drugs with tertiary amino groups, namely oxytetracycline, diphenhydramine, oleandomycin, erythromycin and minocycline induced small alterations of these parameters. However, these alterations were not thought to relate to the hepatic injury induced by N-nitrosodimethylamine. Therefore the amount of N-nitrosodimethylamine formed from these drugs in rats was thought to be rather small. We also investigated the effect of several antioxidants on the alterations of biochemical parameters induced by aminopyrine and sodium nitrite. Ascorbic acid, sodium erythorbate and propyl gallate inhibited these alterations. On the other hand, sorbic acid did not.

Aminopyrine↗

The inhibition and potentiation of procarbazine on hepatic mixed-function oxidases in phenobarbital tolerant and nontolerant mice.

The effect of procarbazine on mixed-function oxidases was investigated in naive and pentobarbital tolerant mice. In mice receiving procarbazine, 200 mg/kg, i.p. 1 hr earlier, metabolisms of pentobarbital, aniline and ethylmorphine in vitro and cytochrome P-450 content of hepatic microsomes were significantly decreased. The drug binding of either aniline or pentobarbital to cytochrome P-450 was also decreased. However, procarbazine failed to exert this effect after the enzymes had been induced by continuous administration of pentobarbital. Interestingly, procarbazine enhanced the barbiturate induced hepatic microsomal mixed-function oxidase activities when it was administered before the implantation of pentobarbital pellet. Both cytochrome P-450 and cytochrome b5 content after pentobarbital pellet implantation were further increased by pretreatment with procarbazine. This finding was further substantiated by the increase in pentobarbital and aniline binding to cytochrome P-450. The present studies may provide another model for studying the nature of hepatic mixed-function oxidase induction process.

Animals↗