[Zollinger-Ellison syndrome].
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Biomedical subjects
Publications and source records attributed to H Iwasa.
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Local changes in cerebral glucose utilization during the postictal phase of amygdaloid-kindled generalized seizures were studied with the quantitative autoradiographic 2-[14C]deoxyglucose method in conscious rats. Measurement was initiated either just after termination of a behavioral seizure (GS-I) or 30 s after seizure termination (GS-II) to determine dynamic metabolic changes in the postictal phase. Although glucose utilization of the neocortex was remarkably depressed in both GS-I and GS-II, that of the hippocampus significantly increased in GS-I and then decreased in GS-II as compared with control. These changes of hippocampal glucose utilization were observed in all sectors of the pyramidal cell layer (CA 1-4) and in the molecular layer. Because metabolic changes associated with development of amygdaloid-kindled seizures begin in the limbic structures including the hippocampus, the transient increase in hippocampal glucose utilization observed in the early postictal phase indicates that the hippocampus is one of the key structures not only for initiating and maintaining but also for terminating kindled seizures.
We examined the changes in pertussis toxin (PTX)-catalyzed ADP-ribosylation in amygdaloid-kindled rats to clarify the role of G proteins in the basic mechanisms of epilepsies. Autoradiographic analysis showed a remarkable increase in PTX-catalyzed ADP-ribosylation in 39-41-kDa proteins in hippocampus and cerebral cortex of kindled animals. The 39- to 41-kDa proteins were shown to be alpha-subunits of Gi and Go by immunoblotting with specific anti-Gi alpha and anti-Go alpha. The increase in ADP-ribosylation of these proteins was observed on stimulated and unstimulated sides of brains 24 h after the last generalized seizure and persisted for at least 3-4 weeks. These results suggest that persistent alterations in signal transduction through Gi and Go might be related to acquisition of long-lasting epileptogenesis.
Thirty-two patients with lobar hematoma were encountered during a period of six and a half years. Of these patients, 13 had arterial hypertension, 7 had other etiologies, and the remaining 12 were without apparent etiology. In 5 of these patients, cryptic angiomas were suspected from angiograms and CT scans. In one young patient, there was a later recurrence of hemorrhage that resulted in death. Our experience in this series and a review of the literature have led us to conclude that, in young normotensive patients with lobar hematoma, surgical intervention may be a reasonable consideration so that evacuation of the hematoma may be accomplished and a detailed search for small angiomatous malformations may be carried out with a view to preventing recurrences.
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This report presents three cases of primary intracranial germ cell tumor encountered in unusual sites, or essentially non-midline structures. The three provided the opportunity to examine surgically obtained tissues with the electron microscope. The histological diagnosis was initially made by light microscopic observations. The first case was a 10-year-old boy in whom the tumor occupied the right thalamic and basal ganglionic region and was diagnosed as a yolk sac tumor. The second an 11-year-old boy who presented with a mass lesion on the left thalamic and basal ganglionic region, diagnosed as germinoma. The third was a 39-year-old man who presented with multiple tumors in the ventricular system and posterior fossa, also diagnosed as germinoma. Among the three cases, neither diabetes insipidus nor ophthalmologic disorder was manifested. Extensive examination and autopsy findings indicated that these intracranial lesions had not metastasized from primary extracranial tumors, including those of the genital organs.