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Biomedical subjects

Y Ide

Publications and source records attributed to Y Ide.

At least 145 records · Page 8Linked to original sources
PubMed1979

Limb muscle endplates in ocular myasthenia gravis: quantitative ultrastructural study.

Motor endplate ultrastructure in the biceps brachii was quantitatively analyzed in five patients with ocular myasthenia gravis (56 endplates), six patients with generalized myasthenia gravis (83 endplates), and five controls (64 endplates). Ultrastructural changes of the motor endplates were observed in nonweak limb muscles of patients with ocular myasthenia gravis as well as in generalized myasthenia; these changes were mostly restricted to the postsynaptic region. Decrease of the mean presynaptic and postsynaptic membrane length, and postsynaptic membrane density, were more remarkable in generalized myasthenia than in ocular myasthenia. Widening of the primary and secondary synaptic clefts was also observed more frequently in generalized myasthenia. There was no correlation between ultrastructural alterations and the duration of symptoms or treatment, severity of disease, or titers of antiacetylcholine receptor antibody.

Adolescent↗
PubMed1979

Neuromuscular defect after suppression of ion conductance.

In rat skeletal muscle, trimetazidine (TMZ) caused a transmission defect without directly blocking binding of acetylcholine--ionophore impairment. In vivo, TMZ produced low-amplitude and cumulative depression of successive muscle responses, and immediate posttetanic exhaustion. These features differed from the effects of alpha-bungarotoxin (alpha-BuTx) or immunization with acetylcholine receptor (experimental autoimmune myasthenia gravis [EAMG]). In vitro, TMZ-induced block was similar to both alpha-BuTx-induced block and EAMG in many respects, but there were differences in endplate potentials evoked during and after rapid repetitive activations. These differences suggest that antibodies to the acetylcholine receptor do not affect the ionophore.

Acetylcholine↗
PubMed1977

[Effects of somatostatin on pancreatic isolated islets and peripheral tissues of rats].

This study was performed in order to evaluate the effects of somatostatin on insulin releasing mechanisms and on glucose uptake in peripheral tissues using isolated pancreatic islets, isolated rat diaphragms and epididymal fat pads. Insulin release by various concentrations of glucose were examined, and it was found that 100 ng/ml of somatostatin significantly inhibited insulin release at the glucose concentration of 200 mg/dl. Somatostatin also significantly inhibted insulin release by the administration of 5microgram/ml of glucagon with 200 mg/dl of glucose concentration and 20 mM of orginine with 200mg/dl of glucose concentrations. But at the glucose concentration of 50mg/dl, no significant inhibition of somatostatin on insulin release was observed even when various concentrations of glucagon or arginine were added. The influence of somatostatin on peripheral tissues was examined in vitro, and no significant change on glucose uptake compared with the control group was shown in either tissues. The results indicated that somatostatin directly inhibited insulin release from rat pancreatic islets but had no effect on glucose uptake in peripheral tissues. The inhibitory effect of somatostatin on insulin release may act through the common mechanism of both glucose and other substances in leading to insulin release.

Animals↗