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Biomedical subjects

T Yanagihara

Publications and source records attributed to T Yanagihara.

At least 235 records · Page 13Linked to original sources
PubMed1989

Corrosion properties of soldered joints. Part I: Electrochemical action of dental solder and dental nickel-chromium alloy.

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. The initial equilibrium was induced between high resistance Ni-Cr alloys and both solders by less current density, which implies a smaller degree of corrosive current than that in low-resistance alloys. Corrosion was observed in the silver solder coupled with high-resistance Ni-Cr alloy, but was not found in the gold solder coupled with both alloys. In soldering Ni-Cr alloy, it is better to use a gold solder and a high-resistance Ni-Cr alloy for corrosion resistance.

Chromium↗
PubMed1989

The development of a computer-aided perinatal information system.

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. This system also supports the telephone line network. Further, we have developed a highly convenient portable CTG that can easily be operated by the patient at home. Through the use of this portable CTG and the computer system, the information about fetal heart rate and uterine contractions of high-risk pregnancy can be easily and directly transmitted to the hospital from the patient's home. This system is indispensable to reducing the perinatal morbidity and mortality.

Computer Communication Networks↗
PubMed1988

Weakness of the lower extremity in carotid occlusive disease.

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. Based on clinical profiles, angiographic findings, and cerebral blood flow patterns, we concluded that the pathophysiologic mechanism was hypoperfusion in the border zone between the anterior cerebral artery and the middle cerebral artery and that patients with progressive weakness had more extensive compromise in cerebral circulation. Following surgical treatment in 17 patients, progressive and episodic weakness disappeared and the majority of them (76.4%) became asymptomatic. However, the patients with stenosis at the siphon and those with progressive weakness from occlusion at the origin appeared to be at increased risk for cardiac death.

Adult↗
PubMed1988

Immunohistochemical investigation of ischemic and postischemic damage after bilateral carotid occlusion in gerbils.

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. The ischemic and postischemic lesions in the cerebral cortex, thalamus, and caudoputamen were partially or completely reversible if the ischemic period was 5 minutes, whereas delayed degeneration occurred in the pyramidal cells of the medial CA1 region after reperfusion for 48 hours (delayed neuronal death). After 10 minutes' ischemia and subsequent reperfusion, delayed neuronal death extended from the medial to the lateral CA1 region; the ischemic and postischemic lesions in the cerebral cortex, thalamus, and caudoputamen also expanded during reperfusion. Our investigation demonstrates that selective vulnerability existed in global cerebral ischemia as in incomplete or regional ischemia and suggests that neurons in many areas of the brain possessed the potential for recovery, progressive deterioration, and even delayed neuronal death depending on the severity and duration of cerebral ischemia.

Animals↗
PubMed1988

Prediction of stroke before and after unilateral occlusion of the common carotid artery in gerbils.

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. With the cumulative neurologic score, gerbils could be divided into classes with no, mild, moderate, and severe symptoms, mostly after 10 minutes. Severely symptomatic gerbils were identified in 3 minutes. Extensive ischemic damage was observed in severely symptomatic gerbils, but no immunohistochemical lesion was detected in mildly symptomatic gerbils. Cerebral blood flow was markedly reduced in severely symptomatic gerbils but more selectively reduced in the cortical structures of moderately symptomatic gerbils. This prediction method is useful for investigating early cerebral ischemia and for evaluating the effectiveness of pharmacologic agents.

Animals↗
PubMed1988

Intracerebral hemorrhage after carotid endarterectomy.

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. All hemorrhages occurred within the first 2 weeks after operation and were ipsilateral to the side of the operation. Eight patients died, and only two made a good recovery. Significant risk factors are hypertension and chronic hemispheric hypoperfusion with impaired autoregulation. The "normal pressure-hyperperfusion breakthrough" syndrome was considered to be operative in 12 of the 14 patients. Nine patients had documented hyperperfusion (at least 100% increase of baseline cerebral blood flow) at the time of surgery. In an additional three patients, normal perfusion-pressure breakthrough was inferred by the clinical course and radiological findings, as well as by the absence of alternative explanations. Patients at risk for postendarterectomy intracerebral hemorrhage include those who have a clinical history suggestive of hemodynamic cerebral ischemia, severe carotid stenosis with limited hemispheric collateral flow, and postendarterectomy hyperperfusion, as measured by intraoperative cerebral blood flow. To minimize the risk of hemorrhage in these patients, strict maintenance of blood pressure at normotensive or even relatively hypotensive levels during the intraoperative and early postoperative periods is advised.

Aged↗
PubMed1987

A combined method for measurement of cerebral blood flow and immunohistochemistry for investigation of cerebral ischemia.

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. The results also suggested that the pathophysiological mechanism of selective tissue vulnerability might be different from one site to another in cerebral ischemia. This method will be useful for autoradiographic measurement of other physiological and biochemical parameters in combination with the immunohistochemical method for demonstration of not only the structural damage, but also the alteration of cell-specific functions.

Animals↗
PubMed1987

Transient global amnesia and epilepsy. Electroencephalographic distinction.

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. The majority (60.8%) of waking records were normal during or after episodes of TGA. Mild or moderate and nonfocal abnormalities were found in a minority. Genuine epileptiform activity was observed only among patients who had seizure disorders. Amnestic episodes attributable to seizures were more brief and more apt to be repeated than TGA and usually responded to anticonvulsant drugs. Differentiation of TGA from epilepsy is essential for appropriate management.

Amnesia↗
PubMed1987

Focal cerebral ischemia: pathophysiologic mechanisms and rationale for future avenues of treatment.

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.

Anticoagulants↗
PubMed1987

Elevation of serum creatine kinase B-subunit levels by radiographic contrast agents in patients with neurologic disorders.

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 0.01). Eight of the 11 patients had recent ischemic cerebrovascular diseases, and 7 of the 11 had undergone CT scanning. On the basis of the information available in the literature, elevation of the serum CKB levels may be interpreted as reflecting breakdown of the blood-brain barrier and neural damage. Intravascularly administered radiographic media are generally safe, but the results of the current investigation suggested the potential for detrimental effects, particularly in patients with recent cerebrovascular diseases.

Brain↗
PubMed1987

Early detection of cerebral ischemic damage and repair process in the gerbil by use of an immunohistochemical technique.

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. The reaction for tubulin was the most sensitive for detection of the neuronal ischemic damage. After an ischemic period of 30 minutes and subsequent reestablishment of cerebral circulation, the immunohistochemical lesions affecting the neuronal structure expanded during the first 3 hours and then slowly afterward for up to 12 hours. Reactive astrocytes were already identified 24 hours after reperfusion. The current investigation demonstrated that early ischemic damage can be clearly visualized by use of the immunohistochemical technique soon after the onset of cerebral ischemia but that considerable heterogeneity exists not only in different anatomic regions but also within the neuronal structure. This technique has potential for further investigation of cerebral ischemia or other pathophysiologic conditions when used in combination with other morphologic, physiologic, or biochemical techniques.

Animals↗
PubMed1987

Transient global amnesia: clinical characteristics and prognosis.

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 14.1% and cerebrovascular diseases in 11.2% of patients, but these conditions were usually not temporally linked to TGA. Characteristic antecedent events and activity such as exertion existed in 33.4%. The incidence of TGA was 5.2 per 100,000 per year in Rochester, MN. Although 23.8% of the patients had recurrent episodes, they were not at increased risk for subsequent stroke.

Aged↗
PubMed1987

High resolution two-dimensional polyacrylamide gel electrophoresis of cerebrospinal fluid in patients with neurological diseases.

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. The appearance of 10 spot areas in the light chain region of 2-DE gels seem to be connected with the diagnosis of multiple sclerosis. The sensitivity and the specificity of these spot areas for the diagnosis of multiple sclerosis are described. Proteins within the ten spot areas are immunoglobulin light chains or substances which cross-react very strongly with light chain antibodies as demonstrated by immunoblotting and immunoabsorption.

Adolescent↗
PubMed1987

Immunohistochemical investigation of cerebral ischemia after middle cerebral artery occlusion in gerbils.

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. The earliest lesion in the caudoputamen evolved after 30 minutes of ischemia. After reestablishment of cerebral circulation, the immunohistochemical ischemic lesions in the neuronal structure disappeared if the ischemic period was 10 minutes or less and partially disappeared even after ischemia for 15 minutes in the cerebral cortex, while the postischemic lesion in the caudoputamen disappeared even after ischemia for 15 minutes. Reactive astrocytes were detected in the cerebral cortex and caudoputamen as early as 24 hours after reperfusion, both in the areas with and without the neuronal lesions. No lesion was identified in the hippocampus or thalamus. This experimental model is suitable for investigation of rapidly progressive regional ischemia in the cerebral cortex and for comparison with other regional or global cerebral ischemia in the gerbil or other animal species.

Animals↗
PubMed1986

Cerebral ischemia in the gerbil: transmission electron microscopic and immunoelectron microscopic investigation.

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. After ischemia for 30 min to 1 h, the pyramidal cell bodies showed mitochondrial swelling, distension of endoplasmic reticulum and disaggregation of polyribosomes. The immunoelectron microscopic procedure for tubulin revealed irregularity of reaction products associated with microtubules after ischemia for 5 min in the dendritic terminals in the stratum moleculare and in the stratum radiatum after ischemia for 10 min. Reaction products in the pyramidal cell bodies became sparse after ischemia for 30 min to 1 h. The present investigation revealed early onset of ischemic damage in the dendritic terminals and subsequent proximal extension, with disintegration of microtubules and mitochondrial swelling.

Animals↗
PubMed1986

Immunohistochemical investigation of regional cerebral ischemia in the gerbil: occlusion of the posterior communicating artery.

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. The staining with hematoxylin-eosin was much less sensitive in detection of early ischemic lesions. After re-establishment of blood flow to the posterior communicating artery, the ischemic lesions which were visualized with the reaction for tubulin or creatine kinase BB-isoenzyme disappeared or reduced the size, if the ischemic period was brief. Beyond a certain ischemic period, the lesion expanded further during the early postischemic period. The reaction for astroprotein visualized reactive astrocytes even in the area without any abnormalities with other reactions, an evidence of subtle ischemic insults.

Animals↗