Publications by authors named "Yanagihara T"

The corrosion properties of contact between six Ni-Cr alloys and two dental solders were evaluated. Ni-Cr alloys with low Cr content coupled with silver solder induced continuous galvanic current, whereas Ni-Cr alloys with high Cr and some Mo content coupled with silver or gold solder induced galvanic current for a short time. Six Ni-Cr alloys were divided into two groups according to the dissolution of Ni, one with low resistance and the other with high resistance.

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Loss of consciousness is rare in the absence of transient or persistent insult to the diencephalon or mesencephalon. We found three patients with severe atherosclerotic stenosis or occlusion of both internal carotid arteries who experienced brief loss of consciousness. Common characteristics were the absence of clinical or electroencephalographic seizure activities, significant cardiovascular disease, or a history suggestive of vasovagal syncope.

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In the perinatal center of Kagawa Medical School, we have newly developed and introduced a computer-aided perinatal information system to realize an ideal management system for high-risk pregnancies. The system comprises 5 microcomputer subsystems. With this system, not only can the continuous full monitoring of the fetus during labor and delivery be easily realized, but also can the management of outpatients and perinatal statistics.

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We investigated progression and recovery of neuronal damage during and after global cerebral ischemia in gerbils after bilateral occlusion of the common carotid arteries, using the immunohistochemical method (reaction for tubulin and creatine kinase BB-isoenzyme). The earliest, but reversible, ischemic lesions occurred after 3 minutes' ischemia in the subiculum-CA1 and CA2 regions of the hippocampus. The lesions became irreversible after 4 minutes' ischemia.

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A method was developed to predict the severity of cerebral ischemia before permanent occlusion of a common carotid artery in gerbils by observing the diameter and appearance of the artery after temporary occlusion and observing clinical signs after permanent occlusion. The severity of cerebral ischemia was confirmed by a sensitive immunohistochemical method and measurement of focal cerebral blood flow after 30 minutes' ischemia. All gerbils with greater than 40% reduction of the diameter and a white arterial margin distal to temporary occlusion developed severe neurologic signs following permanent occlusion, but no gerbils with reduction of less than 30% and a red arterial margin developed neurologic signs.

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A series of 14 patients with intracerebral hemorrhage after carotid endarterectomy is reviewed. This complication occurred in 0.6% of 2362 consecutive carotid endarterectomies performed at the Mayo Clinic from 1972 through 1986.

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Nineteen patients experienced progressive or episodic weakness of one lower extremity caused by severe stenosis or occlusion of the internal carotid artery. The majority of patients (84.2%) had occlusion or severe stenosis at the origin.

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A combined method was established where measurement of cerebral blood flow (CBF) by quantitative autoradiography and detection of morphologic ischemic damage by immunohistochemistry could be accomplished simultaneously with the same brain. The method was applied to the gerbil brain 15 min after occlusion of the right common carotid artery which demonstrated that the reduction of focal CBF can be heterogenous at an early ischemic period, that the residual focal CBF was below 8.0 ml/100 g/min in some areas with ischemic lesions but other areas were tolerant of severe hypoperfusion.

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Progression and recovery of ischemic and postischemic damage after occlusion of the middle cerebral artery and subsequent reperfusion were investigated in the gerbil. This study was performed by immunohistochemical reaction testing for tubulin and creatine kinase BB-isoenzyme to visualize the neuronal structure and by immunohistochemical reaction testing for astroprotein (an astrocyte-specific protein) to visualize reactive astrocytes. The earliest ischemic lesion became visible in the frontoparietal cortex after 7 minutes of ischemia as a laminar loss of the reaction for tubulin involving the neuropil, neuronal perikarya, and dendrites.

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Electroencephalographic recordings were obtained during 13 episodes of transient global amnesia in 13 patients. Eight were entirely normal; none showed seizure discharges or other epileptiform activity. Electroencephalographic recordings were also obtained after 103 episodes of amnesia in 96 patients with transient global amnesia (TGA) alone, five patients who had both TGA and epilepsy independently, and three patients with amnesia related to epilepsy.

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After occlusion of the right common carotid artery in the gerbil, we monitored the progression of ischemic damage and postischemic damage and the repair process in the brain immunohistochemically by using tubulin, creatine kinase BB-isoenzyme (CK-BB), and neuron-specific enolase as the neuronal markers and astroprotein, glial fibrillary acidic protein, and CK-BB as the astrocytic markers. The earliest ischemic lesion was detected in the hippocampus and the cerebral cortex after ischemia for 5 minutes as loss of the reaction in the neuropil, nerve cell bodies, and dendrites. The reaction disappeared more promptly in the dendrites than in the nerve cell bodies.

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We studied the clinical characteristics of transient global amnesia (TGA) in 277 patients with an average follow-up of 80 months. The syndrome occurred most frequently after age 50. There was a history of migraine in 14.

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The effect of radiographic contrast agents on the central nervous system was evaluated by measurement of serum creatine kinase B-subunit (CKB) levels with use of radioimmunoassay in 58 patients who underwent computed tomographic (CT) scanning and 46 patients who underwent cerebral angiography for evaluation of cerebrovascular diseases, brain tumors, and other neurologic disorders. In 11 patients (10.6%), the CKB increased to abnormally high levels within 4 hours after the radiographic procedures, and the median value after 30 minutes was significantly higher than the corresponding precontrast value (P less than 0.

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The protein pattern of cerebrospinal fluid (CSF) of 334 patients with various neurological and systemic diseases was investigated by high resolution two-dimensional electrophoresis (2-DE). 2-DE gels of normal CSF contain proteins which are not detectable in 2-DE gels of serum. Disturbances of the blood-brain or blood-CSF barrier, and degenerative diseases of the brain and malignant diseases produce specific changes on 2-DE gels of the CSF.

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Although approximately 500,000 patients suffer from a stroke each year in the United States, treatment of these patients to date has consisted primarily of prevention, supportive measures, and rehabilitation. The modification of experimental cerebral infarction by new pharmacologic agents, along with encouraging results from the restoration of blood flow to areas of focal ischemia in both laboratory and clinical trials, suggests that a more aggressive approach might be considered in selected patients with acute stroke.

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Three cases of ongoing intracerebral hematoma are reported. In all cases, a very small hematoma on the initial CT taken within 2 hours after onset increased in size to such an extent that surgical intervention was necessary. A round radiolucent zone in high density clots was seen on the initial CT of all cases.

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Progression of cerebral ischemia from 5 min to 3 h after occlusion of a common carotid artery was investigated in the subiculum-CA1 region of the hippocampus of the gerbil by transmission electron microscopic and immunoelectron microscopic technique. The earliest change was found after 5 min in the periphery of the apical dendrites in the stratum moleculare, where mitochondrial swelling and disintegration of microtubules were clearly seen inside swollen dendritic processes. After ischemia for 10 min, similar abnormalities were observed in the more proximal part of the apical dendrites, and the basal dendrites also became similarly affected.

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Evolution, progression and recovery of neural damage during and following cerebral ischemia were investigated in the gerbil after occlusion of a posterior communicating artery and by using the immunohistochemical reaction for tubulin and creatine kinase BB-isoenzyme which are enriched in the neuronal structure and the reaction for astroprotein which is specific for astrocytes. The transcardiac perfusion study with India ink revealed marked hypoperfusion diffusely in the hippocampus and moderately in the thalamus on the occluded side. The earliest immunohistochemical lesion, manifested as loss of the reaction for tubulin and creatine kinase BB-isoenzyme in dendrites and nerve cell bodies, was found in the CA1 and CA2 region of the hippocampus after ischemia for 4 min, while it took 10 min before the earliest lesion became visible in the ventral nucleus of the thalamus and it took over 1 h before scattered lesions evolved in granular cells of the dentate gyrus.

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The concentration of carcinoembryonic antigen (CEA) in cerebrospinal fluid (CSF) was determined by using an enzyme immunoassay for 204 patients with various nonneoplastic neurologic disorders, 8 patients with systemic infectious diseases, 19 patients with systemic neoplastic diseases without involvement of the nervous system, and 35 patients with neoplastic neurologic disorders. The highest CEA level in CSF among patients without neoplastic neurologic disorders was 0.6 ng/ml.

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Immunohistochemical methods for the determination of tubulin, creatine kinase BB-isoenzyme, and astroprotein-glial fibrillary acidic protein were used to investigate recovery of the ischemic lesion after temporary occlusion of a common carotid artery in the gerbil and the evolution of the postischemic lesion following reperfusion. One group of gerbils was followed from 15 minutes to one month after an ischemic period of 30 minutes, and another group was examined after 7 days following an ischemic period of 5 to 30 minutes. It was found that the postischemic lesion, visualized as loss of the immunohistochemical reaction for tubulin and creatine kinase BB-isoenzyme, evolved within 60 minutes after reperfusion in the hippocampus and cerebral cortex and within 3 hours in the caudoputamen and thalamus.

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