Search PubMed⌕ Search

Biomedical subjects

Y Yonemasu

Publications and source records attributed to Y Yonemasu.

At least 109 records · Page 6Linked to original sources
PubMed1988

[Somatosensory evoked potential and local cerebral glucose utilization in the transient MCA-occluded rat].

Wistar rats were used through the experiments. Preparatory operations for the autoradiography and somatosensory evoked potential (SEP) were performed under 1.5% halothane anesthesia. After a control measurement of SEP, the left MCA was occluded with a micro clip. The animals were divided into 2 groups. In the 1st group (n = 8), the clip was removed 1 hour after MCA occlusion and 4 rats were used for the measurement of local cerebral glucose utilization (LCGU) by 14C-DG autoradiography. Another 4 rats were allowed to recover from anesthesia and used for the histopathological examination after 72 hours. In the 2nd group (n = 8), the clip was removed 2 hours after occlusion and the same procedures were performed. SEP was monitored throughout the experiment. Two positive and one negative peaks were recorded before MCA occlusion. SEP diminished immediately after MCA occlusion. Following the removal of the clip, complete recovery of SEP was observed in the 1st group of rats. However, in the 2nd group, recovery of SEP was minimal. In the 1st group, LCGU in the sensorimotor cortex at 30 minutes after reperfusion showed 22% reduction compared to that of the contralateral homologous area. In the 2nd group, in the contrast, 66% reduction of LCGU was observed. Experimental results indicate that SEP and LCGU in the early recovery period of ischemia are able to predict the reversibility of ischemic brain.

Animals↗
PubMed1988

[Regional cerebral blood flow during development of limbic seizures induced by kainic acid (KA) microinjection into unilateral amygdala in chronic cats].

Regional cerebral blood flow (rCBF) was studied by means of electrolytic hydrogen clearance method in chronically prepared adult cats during development of limbic seizures induced by KA microinjection into the unilateral amygdala. Stereotaxic operation was carried out on 7 adult cats. Bipolar electrodes were placed in the lateral nuclei of bilateral amygdala (LA: left amygdala, RA: right amygdala), and in the ipsilateral dorsal hippocampus (LH). Teflon needles with inner stainless steel needle guides were placed in LA, RA, LH and left anterior sigmoid gyrus (LCx) so as to introduce platinum electrodes for rCBF measurements. The teflon needle placed in LA was also utilized for KA microinjection (1 microgram). Measurements of rCBF were done before (control) and after KA microinjection. Control rCBF were as follows; LA: 41.6 15.9, RA: 40.7 12.2, LH: 39.1 10.9, LCx: 55.4 20.7 (ml/100 g/min). After KA microinjection, measurements of rCBF were made during limbic seizure stage (LSS) and transfer stage (TS). TS was divided into two stages; early TS and late TS. In LSS, 50 to 92% increase of rCBF were noted as follows; LA: 79.7 23.7, RA: 66.1 18.1, RH: 58.6 17.6, LCx: 91.4 17.8 (ml/100 g/min). In early TS, rCBF in all recorded sites returned to the same level as control rCBF. In late TS, rCBF in LA and LH were slightly lower than the level of control rCBF. Pathological examination of LA and LH in early and late TS showed different features. In late TS, astrocytic proliferation was remarkable while it was mild in early TS.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1987

Unilateral exophthalmos caused by an invasive pituitary adenoma.

A case of pituitary adenoma associated with unilateral exophthalmos is reported. An intraorbital infiltrative tumor growth was verified by histopathological study. The mechanism of exophthalmos is discussed, and edema of the intraorbital tissue secondary to an inflammatory reaction or venous stasis associated with tumor cell infiltration is considered to be the cause of exophthalmos in this patient.

Adenoma, Chromophobe↗
PubMed1987

[Epileptogenic properties of quisqualic acid: microinjection into the unilateral amygdala in cats].

The present studies demonstrated that the microinjection of quisqualic acid (QA) into unilateral amygdala in chronically implanted cats resulted in various types of limbic seizures in accordance with injected doses. The epileptogenic potency of QA in the induction of epileptic seizures was lower then that of kainic acid (KA), which has also been demonstrated in our previous studies. Electroencephalographic changes and clinical manifestations of QA-induced epilepsy were less prominent as compared with those of KA-induced epilepsy. Five micrograms of QA resulted in pure amygdaloid seizures. The moderate dose administration of QA (15 micrograms) was suitable to observe limbic status. Both doses of QA elicited similar characteristic epileptic patterns on EEG, which was quite distinguishable from those of KA. In pathological study, mild degeneration of hippocampal pyramidal cell layer was observed in the cases injected 15 micrograms of QA. These electro-clinical and pathological features are interesting in similarities to those of human complex partial seizures, mesial temporal sclerosis. In conclusion, the strict dose dependency of QA in the production of limbic seizures is a valid advantage for an experimental model of a complex partial epilepsy in man.

Amygdala↗
PubMed1987

[Ibotenic acid-induced limbic seizures and neuronal degeneration].

Electrographic and clinical observations were made as long as 2 months after the injection of ibotenic acid (IBO) solution (50 micrograms in 1 microliter of phosphate buffer solution) through a chronically implanted cannula into unilateral amygdala of freely moving and non-anesthetized cats. The control group (phosphate buffer group) showed no change during the observation period. About 30 to 60 minutes after the injection of IBO, focal amygdaloid seizures occurred and propagated to the adjacent limbic structures. Clinically, attention and ipsilateral mydriasis were observed. The seizures occurred only 2 to 5 times and ceased within 4 hours. Cats became electroclinically normal afterwards. Histopathological examination revealed a small necrosis at the injected site of the amygdala. Remarkable pyknosis and gliosis were noted around the necrosis. Remote lesions such as neuronal cell loss and pyknosis were observed in the ipsilateral pyramidal cell layer of the hippocampus. But these changes were mild and not so severe as compared to our previous report of kainic acid microinjection in cats. Authors emphasized that IBO should be an excellent tool for lesion making and also suggested that an aseptic manipulation was essential in the lesion study in cats.

Amygdala↗
PubMed1987

[Serial changes in evoked potentials in kainic acid (KA)-induced limbic seizures in chronic cats].

On the basis of careful histological works including the use of experimental techniques, nearly all of the workers came to the conclusion that no neuronal connections between amygdala and hippocampus exist, regardless of close topographical localization or intimate functional cooperation. We examined ipsilateral amygdalo-hippocampal responses (A-H), hippocampo-amygdaloid responses (H-A) and amygdalo-cortical responses (A-Cx) in normal or epileptic cats by means of evoked potential method. Stereotaxic operations were carried out in ten adult cats. Bipolar electrodes were placed in the left amygdala and ipsilateral dorsal hippocampus, and stainless screws on the dura over the bilateral anterior sigmoid gyrus. A teflon needle with an inner needle guide was also inserted obliquely into the ipsilateral amygdala. The bipolar electrodes allowed both to stimulate and to record the electrical activity. Two hundred rectangular pulses (0.3 msec, 5 V, 2 Hz) were given and evoked responses summed and averaged by a computer. These evoked studies were made before and after KA injection (1 microgram) into the ipsilateral amygdala. In controls, only A-H were observed. During limbic status stage, H-A began to appear and peak latencies of A-H shortened in accordance with seizure development. During generalized seizure stage, A-Cx was newly observed and peak latencies of both A-H and H-A shortened. Peak latencies of the evoked potentials began to shorten soon after development of limbic seizure, and stepwise shortening of peak latencies were recognized in some cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1987

[The effects of hyperglycemia on ischemic brain edema].

The effects of hyperglycemia on ischemic brain edema in rats were studied by measuring the local changes in water content of brain and cerebrovascular permeability using a transient middle cerebral artery (MCA) occlusion model. Rats, fasted except for water for 12-16 hours, were used. They were anesthetized with halothane and the stem of the left MCA was occluded for 2 hours by a microclip. Reperfusion was performed by removal of the clip. The rats were allowed to awake from anesthesia after removal of the clip. Hyperglycemia was induced by intraperitoneal injection of 50% glucose and same volume of physiological saline was injected intraperitoneally 20 minutes before MCA occlusion in control rats. Cerebrovascular permeability was measured by quantitative autoradiography using 14C-alpha-amino-isobutyric acid (14C-AIB) 2 hours after reperfusion. The specific gravity of cerebral tissue, determined by the gradient column with bromobenzene and kerosene, was used to study local changes in brain water content 2 hours after MCA occlusion and 2 hours after reperfusion. In hyperglycemic rats, plasma glucose content-ration rose to over 500 mg/dl at the peak and then declined. A hyperglycemic state around 300 mg/dl was maintained during the experiments. Elevation of hematocrit and plasma osmolarity were observed in hyperglycemic rats. At 2 hours after MCA occlusion, specific gravity of the brain was decreased in the left MCA territory, especially in the frontal cortex, in both groups. The decrease in the frontal cortex in hyperglycemic rats was statistically significant compared with that in the control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[A case of idiopathic brain stone presenting as psychomotor epilepsy].

A rare case of idiopathic brain stone with psychomotor epilepsy is reported. On December 9, 1982, a 29-year-old man with 18 years' history of psychomotor epilepsy was admitted to our neurosurgical service. He had no history of neonatal asphyxia, trauma or other neurological diseases. No neurological deficit was disclosed. Skull x-ray films and plain CT scan demonstrated a calcified mass in the right temporal lobe. No contrast enhancement was noted. Despite an extensive search, the etiology of the calcified mass was not revealed. Conventional EEG showed focal spike discharges in the right anterior temporal lead and telemetered EEG monitoring for 24 hours disclosed sharp wave burst in the right temporal lobe. In spite of appropriate medication, seizures persisted. At surgery, electrocorticogram and stereo-electrocorticogram showed paroxysmal epileptiform events in the right temporal lobe. Anterior temporal lobectomy with excision of calcified mass was done. Histopathological examination demonstrated thick collagen fibers and gliosis around the stone, and diagnosis of idiopathic brain stone was made. We reviewed five previously reported cases. We also emphasized an epileptogenicity of idiopathic brain stone and indication of surgical excision which may result in an excellent control of epilepsy.

Adult↗
PubMed1986

[The effect of hyperglycemia on ischemic brain damage: relevance to the local cerebral blood flow].

The effect of hyperglycemia on ischemic brain damage in rats was studied by measuring the local cerebral blood flow (LCBF) using a transient middle artery (MCA) occlusion model. Rats, fasted except for water for 12-16 hours, were used. They were anesthetized with halothane and the stem of the left MCA was occluded for 2 hours by a microclip. Reperfusion was performed by removal of the clip. The rats were awaken from anesthesia after removal of the clip. Hyperglycemia was induced by intraperitoneal injection of 50% glucose and same volume of 50% D-mannitol or physiological saline were injected intraperitoneally 20 minutes before MCA occlusion in control rats. LCBF was measured by quantitative autoradiography using 14C-iodoantipyrine 2 hours after clipping and 2 hours after reperfusion. Some rats were prepared for neuropathological observation 72 hours after reperfusion. In hyperglycemic rats, plasma glucose concentration rose to over 500 mg/dl at the peak. A hyperglycemic state around 300 mg/dl was maintained during the experiments. Elevation of hematocrit and plasma osmolarity to the same degree were observed in both hyperglycemic and mannitol pretreated rats. On histological study ischemic neuronal cell damage was found to be more extensive in hyperglycemic rats than in the saline pretreated rats. At 2 hours after MCA occlusion, LCBF in the ischemic focus decreased significantly in hyperglycemic rats compared with the control. The reduction of LCBF was observed also in the contralateral non-ischemic side (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Quisqualic acid-induced hippocampal seizures in unanesthetized cats.

An intrahippocampal injection of quisqualic acid (QA) was made in chronically implanted freely moving unanesthetized cats and electrographic and clinical observations were made. Fourteen to 40 micrograms of QA injection resulted in a mild limbic seizure within 24 h after QA injection. Some cats demonstrated a pure hippocampal seizure on an electroencephalogram. Electrographic changes and clinical manifestations were less prominent as compared with those of kainic acid. Histopathological examination showed a selective loss of pyramidal cell layer of the CA3 portion in the injected side of the dorsal hippocampus. A mild but constant epileptogenic potency of QA has an advantage for an experimental model of temporal lobe epilepsy in man.

Animals↗
PubMed1985

Spontaneous secondarily generalized seizures induced by a single microinjection of kainic acid into unilateral amygdala in cats.

Electrographic and clinical observations were made for 6 months after the injection of kainic acid (KA) solution (1 microgram in 1 microliter of phosphate buffer solution) through a chronically implanted cannula into a unilateral amygdala of freely moving and non-anesthetized cats. The control group (phosphate buffer group) showed no change during the observation period. After the injection of kainic acid, focal status epilepticus in the limbic system was observed for 3 days. Cats recovered clinically but persistent IIDs were observed at the injected site of the amygdala. These IIDs increased in amplitude and frequency and began to trigger spontaneous amygdaloid seizures. Secondary epileptogenic foci were then established in the contralateral amygdala, and amygdaloid seizures began to occur alternatively on both sides and finally trigger frequent limbic seizures from 20 to 40 days after KA injection. Spontaneous secondarily generalized seizures developed about 30 days after KA injection and occurred once or twice a week thereafter. The animals were completely normal in their behavior during the interictal phase. This is an excellent model of experimental epilepsy for the investigation of the mechanism of limbic seizure development and further study using this model will provide informations useful for the therapy of temporal lobe epilepsy in man.

Amygdala↗
PubMed1985

[Squamous cell carcinoma of the frontal sinus caused osteomyelitis of the frontal bone].

A case of the squamous cell carcinoma of the frontal sinus complicated with osteomyelitis of the frontal bone was reported. A 47-year-old male was admitted to Asahikawa Medical College Hospital because of a bulging of forehead and remittent fever of a six-month history and general convulsive seizures on the day before admission. On physical examination, a bulging of forehead with redness, tenderness and fluctuation was noted. Sense of smell diminished bilaterally. Oto-laryngological examination disclosed paranasal sinusitis. Skull X-P and CT scan suggested osteomyelitis of the frontal bone secondary to frontal sinusitis. However, a frontal sinus tumor with osteomyelitis was also possible. Operation was performed and a granulomatous mass attached to the dura with thick epidural abscess was noted. The mass and affected bone edge were removed. Pathological examination of the specimens disclosed findings of squamous cell carcinoma and osteomyelitis. Recurrence of the tumor rapidly occurred and reoperation was performed a month after the first operation. Postoperative irradiation and chemotherapy with pepleomycin were done but failed to control the growth and recurrence occurred immediately. The tumor penetrated the skin of the forehead and the patient died of cachexy 7 months after the first surgery. Osteomyelitis usually occurred in the metaphysis of long tubular bone and rarely in short bone or flat bone such as a skull. This is attributed to the difference of distribution of the bone marrow vessels. Embolization and subsequent growth of bacteria in the blood flow is less liable to occur in short bone and flat bone.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma, Squamous Cell↗
PubMed1984

[Quantitative double tracer autoradiographic technique for the simultaneous measurement of local cerebral blood flow and local cerebral glucose utilization using 14C-IAP and 18F-FDG].

We have reported a quantitative double tracer autoradiographic technique for the simultaneous measurement of local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) using 14C-IAP and 18F-FDG respectively. Six awake normal rats and 3 left middle cerebral artery (MCA) occluded rats were used for this experiments. A 50-hold greater radioactivity of 18F was administered and the first exposure was done for 2 hours to obtain a 18F image. Three days later (39 half-lives of 18F), a second exposure was done for 5 to 6 days to obtain the 14C image. Tissue concentration of 14C was measured relative to the commercially available 14C-methyl methacrylate standards. 18F standards were prepared in each experiment. Cross contamination of 14C in the first exposure was less than 2% in the normal state and less than 4% even in the uncoupling condition. The values obtained by this methods for LCBF and LCGU agreed closely with those obtained by a single tracer technique previously reported in the literature. The technique outlined in this paper also provided local glucose utilization flow ratio (LGFR) for the first time. LGFR was obtained by dividing the LCGU image by LCBF image and was expressed as percent mumol/ml. The mean LGFR of control rats was 76 +/- 8% mumol/ml. In a MCA occlusion group, LGFR of ischemic cortex increased until 2 to 3 times higher than that of contralateral non-ischemic cortex. Oxygen glucose index image which was obtained from the LCGU and A-V differences of O2 showed that approximately half of the glucose was metabolized anerobically.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

[Regional cerebral blood flow in limbic seizures induced by microinjection of kainic acid into amygdala in cats].

The relationship between neuronal epileptic activity and regional cerebral blood flow was studied by means of hydrogen clearance method (rCBF). Measurements of rCBF in the limbic structure and cerebral cortex were performed during limbic seizures induced by a microinjection of kainic acid to the left amygdala under concurrent monitoring of polygraph. Pentobarbital (35 mg/kg, i.p.) anesthesia was induced and cats were artificially ventilated. Physiological parameters such as blood pressure, body temperature, PaO2, PaCO2 and HCO3 were kept stable. After fixation of the cat's head in a stereotaxic device, stainless screw electrodes were placed over bilateral anterior sigmoid gyrus so as to touch the dura mater for cortical EEG monitoring. Bipolar needle electrodes were stereotaxically placed to both amygdala and the left dorsal hippocampus. Platinum electrodes were stereotaxically placed to the left amygdala, dorsal hippocampus and sensorimotor cortex. After measurements of control rCBF, a microsyringe was stereotaxically inserted into the left amygdala and kainic acid solution (2 micrograms) was injected. Polygraphic monitoring followed. Five to 30 minuted after kainic acid injection, continuous multiple spikes appeared in the left amygdala. Forty to 120 minutes later, continuous multiple spikes transmitted to the left hippocampus. Two to five hours later, limbic seizure occurred. The limbic seizure lasted five to eight hours and interictal discharges appeared. Repeated measurements of rCBF were done. In the left amygdala, rCBF increased about two-fold of the control immediately after development of continuous multiple spikes and remained increased as long as the seizure persisted.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗
PubMed1984

[Pituitary oncocytoma].

Since the first reports of pituitary oncocytoma by Kovacs and Horvath, and Landolt and Oswald increasing numbers of cases have been reported with the advent of electron microscopy. It has been posturated that more cases were not precisely diagnosed because of lack of electron microscopic study. We reported two cases of pituitary oncocytoma and discussed clinicopathological aspects. Case 1 A 66-year-old woman had a 6 year history of visual impairment. Neurological examination revealed loss of vision on the left and decreased visual acuity (0.3) with temporal hemianopsia on the right. The endocrinological study revealed moderate panhypopituitarism. Plain skull X-ray, computed tomography and cerebral angiography showed the findings of a pituitary tumor with suprasellar extension. Subfrontal removal of the tumor followed by irradiation was performed. Case 2 A 50-year-old man was well until 8 years previously, when he experienced loss of libido. Three years before entry, the left sided exophthalmos and ptosis were noted. Neurological examination showed a severe visual impairment with a bitemporal field defect, bilateral optic atrophy and disturbance of eye movements on the left. Endocrinological study revealed panhypopituitarism. Radiological studies showed a pituitary tumor with a suprasellar extension and an invasion into the left orbital cavity. Transcranial and then transsphenoidal partial removal of the tumor were done followed by irradiation. Histological examination of the tumors revealed a poorly granurated adenoma with very weak affinity to acid dyes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗