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Biomedical subjects

M Oishi

Publications and source records attributed to M Oishi.

At least 55 records · Page 3Linked to original sources

[A case of multiple cranial neuropathy with positive antinuclear antibody responded to steroid].

A 56-year-old woman was admitted to our hospital because of bilateral ptosis, total ophthalmoplegia, bilateral facial palsy and left hypoglossal nerve palsy. Antinuclear antibody (ANA) showed high titer of 1280 but other data were normal. With oral prednisolone therapy (40 mg/day), the symptoms improved gradually but ANA titer did not show any significant change. We thought multiple cranial neuropathy of the patient was due to autoimmune disease such as collagen disease or cranial nerve type of Guillain-Barré syndrome from her symptoms and positive ANA. In contrast to other reported cases of multiple cranial neuropathy with positive ANA, in our patient ANA titer was high, only motor cranial nerves were impaired, and total ophthalmoplegia was found. Steroid therapy was useful in accordance with other reports. Although our patient has no symptoms related to collagen diseases, a long follow-up of this patient is considered to be necessary.

Antibodies, Antinuclear↗

Effects of bunazosin hydrochloride sustained-release formulation on cerebral circulation.

BACKGROUND: We investigated the cerebral blood flow in mild to moderately hypertensive patients with chronic cerebral infarction before and after the administration of bunazosin hydrochloride sustained-release formulation, a selective sympathetic alpha1 receptor blocker. METHODS: Eleven mild to moderately hypertensive patients (mean age 65.6 years) with chronic cerebral infarction were studied. INTERVENTIONS: The patients were on enalapril maleate, an angiotensin converting enzyme inhibitor, for one week and then enalapril maleate was switched to bunazosin hydrochloride sustained-release formulation. MEASURES: The cerebral blood flow study was performed before and 8 weeks after starting the administration of bunazosin hydrochloride sustained-release formulation. Cerebral blood flow was measured using the stable xenon CT method. The picture analysis was performed using AZ-7000. The regional cerebral blood flow was measured by placing the region of interest on the CT images. The regional cerebral blood flows were measured before and 20 minutes after intravenous injection of 17 mg/kg acetazolamide. RESULTS: The blood flows in the parietal cortex and caudate nucleus 8 weeks after starting the administration of bunazosin hydrochloride sustained-release formulation were significantly greater than those before. The cerebrovascular acetazolamide reactivity in the occipital cortex and caudate nucleus was significantly lower after switching to bunazosin hydrochloride sustained-release formulation than before. CONCLUSIONS: Considering the reports that angiotensin converting enzyme inhibitors show little influence on cerebral blood flow, the present study suggests that bunazosin hydrochloride sustained-release formulation may show a good influence on cerebral blood flow in mild to moderately hypertensive patients with chronic cerebral infarction.

Acetazolamide↗

[A case of sarcoid myopathy presenting muscle pain and muscle weakness and with muscle MRI abnormality].

We experienced a 70-year-old female diagnosed as sarcoidosis. She complained bilateral femoral pain from 70-year-old. 3 months after the onset, she developed muscle weakness extending to her upper extremities with high fever of 38-39 degrees C. The erythema appeared at the right femoral region 4 months after the onset. She admitted to our hospital because of further evaluation. When she was admitted, she had tenderness on grasping the femoral muscles, proximal limb muscle weakness and Gowers' sign. On laboratory examination, CRP, aldorase, myoglobin, lysozyme were increased mildly. The EMG demonstrated a myogenic pattern. Muscle biopsy performed from the left quadriceps femoris muscle revealed non-caseating granuloma and muscle fiber necrosis. A diagnosis of muscle sarcoidosis was made from the biopsy findings and the clinical features. With oral prednisolone administration, muscle weakness and other clinical features improved gradually. On muscle MRI, multiple small high intensity areas were scattered in the femoral muscles. Muscle MRI is considered to be useful for differential diagnosis of muscle sarcoidosis.

Aged↗

[Acute transient swelling of the submandibular glands after laryngeal mask airway insertion].

A 40-year-old woman was scheduled for abdominal hysterectomy. Moderate difficulty in tracheal intubation was expected on preoperative evaluation. A size 3 laryngeal mask airway (LMA) was inserted after the induction of general anesthesia. The LMA insertion was accomplished smoothly at the first attempt and there was no air leakage during manual ventilation. Soon after the insertion, acute swellings were noted in the bilateral submandibular triangle regions. Enlargement and deformity of the submandibular glands were diagnosed by ultrasonography. The enlargements increased with elevated pressure of the LMA cuff, but disappeared completely in five minutes after removal of the LMA. Such enlargement did not occur with subsequent tracheal intubation. The patient had an uneventful postoperative course without any residual sequelae. We should pay attention to possible submandibular gland swelling by LMA insertion.

Adult↗

Cerebrovascular acetazolamide reactivity and platelet function in asymptomatic cerebral thrombosis.

In order to find out the relationship between the cerebrovascular acetazolamide reactivity and platelet function in asymptomatic cerebral thrombosis, 10 cases of asymptomatic cerebral infarction and 10 age-matched control subjects were studied. The cerebrovascular acetazolamide reactivity was measured using xenon computed tomography method. As markers of platelet function, the plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2 were determined. The cerebrovascular acetazolamide reactivity was significantly lower in the asymptomatic cerebral infarction group than in the control group. The plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2 were higher in the asymptomatic cerebral infarction group than in the control group. There was a significant negative correlation between the cerebrovascular acetazolamide reactivity and the plasma concentrations of platelet factor 4, beta-thromboglobulin, thromboxane B2, and 11-dehydrothromboxane B2. The low cerebrovascular acetazolamide reactivity is considered to be related to platelet activation in asymptomatic cerebral thrombosis.

Acetazolamide↗

Antibodies against the PH domain of phospholipase C-delta1 inhibit Ins(1,4,5)P3-mediated Ca2+ release from the endoplasmic reticulum.

The pleckstrin homology domain (PH domain) is now well known as a structural module for the binding of inositol compounds. In the present study, polyclonal antibodies against the peptide KVKSSSWRRERFYK, derived from the N-terminal of the PH domain of phospholipase C-delta1 (PLC-delta1), were raised in rabbits. These were then tested for their ability to inhibit the binding of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] to the binding proteins including the receptor molecule. The Fab fragment of the antibodies but not the whole molecule inhibited the binding of Ins(1,4,5)P3 not only to PLC-delta1 but also to the Ins(1,4,5)P3 receptor, indicating that the antibodies raised recognized the binding site for Ins(1,4, 5)P3 in the receptor. Rat basophilic leukemic cells were permeabilized with saponin and assayed for Ins(1,4,5)P3-mediated Ca2+ release. Pretreatment of permeabilized RBL cells with the Fab fragment of the antibodies diminished the release of Ca2+ caused by Ins(1,4,5)P3, and further absorption experiments using a variety of synthetic peptides suggested that the tripeptide KVK is the epitope of the antibodies. Structural information about KVK will help in screening for Ins(1,4,5)P3 antagonists.

Animals↗

Role of phosphorylation of Alzheimer's amyloid precursor protein during neuronal differentiation.

Alzheimer's amyloid precursor protein (APP), the precursor of beta-amyloid (Abeta), is an integral membrane protein with a receptor-like structure. We recently demonstrated that the mature APP (mAPP; N- and O-glycosylated form) is phosphorylated at Thr668 (numbering for APP695 isoform), specifically in neurons. Phosphorylation of mAPP appears to occur during, and after, neuronal differentiation. Here we report that the phosphorylation of mAPP begins 48-72 hr after treatment of PC12 cells with NGF and that this correlates with the timing of neurite outgrowth. The phosphorylated form of APP is distributed in neurites and mostly in the growth cones of differentiating PC12 cells. PC12 cells stably expressing APP with Thr668Glu substitution showed remarkably reduced neurite extension after treatment with NGF. These observations suggest that the phosphorylated form of APP may play an important role in neurite outgrowth of differentiating neurons.

Alzheimer Disease↗

Differences in regional cerebral blood flow in two types of leuko-araiosis.

Cerebral blood flow and cerebrovascular acetazolamide reactivity were investigated in patients with periventricular hyperintensity and in patients with leuko-araiosis in centrum semiovale. Fifteen patients with periventricular hyperintensity, 15 patients with leuko-araiosis in centrum semiovale and 15 age-matched controls without leuko-araiosis were studied. The regional cerebral blood flow was measured using the stable xenon CT method before and 20 min after intravenous injection of 17 mg/kg acetazolamide. The blood flow and the cerebrovascular acetazolamide reactivity in the area of leuko-araiosis were significantly lower in the periventricular hyperintensity group and the leuko-araiosis in centrum semiovale group than the control group. The blood flow in the cerebral cortex was significantly lower in the leuko-araiosis in centrum semiovale group than in the periventricular hyperintensity group and the control group. The cerebrovascular acetazolamide reactivity in the cerebral cortex did not show any significant difference among the three groups. The blood flow in the cerebral cortex was decreased in patients with leuko-araiosis in centrum semiovale but the cerebrovascular acetazolamide reactivity in the cerebral cortex was normal in patients with leuko-araiosis.

Acetazolamide↗

Corpus callosum atrophy and cerebral blood flow in chronic alcoholics.

The corpus callosum atrophy and cerebral blood flows were investigated in chronic alcoholics without Marchiafava-Bignami disease. Fifteen cases of chronic alcoholics and 15 age-matched healthy controls were studied. The sagittal plane of magnetic resonance imaging of the head was scanned into a computer and the corpus callosum was measured and the callosal index was calculated. Cerebral blood flows were measured using stable xenon computed tomography (CT) method. Regional cerebral blood flows in the frontal, temporal, parietal and occipital cortex, frontal, temporal and occipital white matter, caudate nucleus, putamen and thalamus were measured. The corpus callosum area, the thickness of the genu, the thickness of the trunk, the thickness of the splenium, and the callosal index were significantly smaller in the chronic alcoholic group than in the healthy control group. Blood flows in the cerebral cortex, thalamus and putamen were significantly lower in the chronic alcoholic group than in the healthy control group. Significant positive correlations were present between the corpus callosum atrophy and the cerebral cortex blood flows. Corpus callosum atrophy and decreased cerebral blood flows may be seen in chronic alcoholics without Marchiafava-Bignami disease.

Alcoholism↗

Physicochemical characteristics and toxicity of nickel oxide particles calcined at different temperatures.

The physicochemical characteristics and cytotoxicity of two types of commercial nickel oxide particles (black and green nickel oxide) and five types of nickel oxide particles prepared by calcination of the black nickel oxide at 600-1000 degrees C were studied. Thermal analysis with mass spectroscopy showed that the black nickel oxide particles contained approximately 1.4% impurity, which seemed to be basic nickel carbonate. The calcination treatment at 600 degrees C increased the nickel content and decreased the oxygen content, but these remained constant in the particles treated at higher temperatures (700-1000 degrees C) and in the green nickel oxide particles. The water solubility of black nickel oxide particles was markedly greater than that of the other particles, especially in the first 24 h after mixing with water. The solubility of the calcined particles decreased with increasing calcination temperature. The cytotoxicity of these particles was evaluated by the viability of rat alveolar macrophages and by the inhibition of cell proliferation in Chinese hamster ovary cells. The black nickel oxide was the most cytotoxic of the particles examined, and this may be attributable, at least in part, to a rapid dissolution of nickel from the contained impurity. The toxicity of the calcined particles decreased with increasing calcination temperature. These results indicate that water solubility, which depends on calcination temperature, modulates the acute cytotoxicity of nickel oxide particles.

Animals↗

Central motor conduction time in Parkinson's disease.

Central motor conduction time (CMCT) was analysed in 11 patients with Parkinson's disease and 10 age matched healthy controls. CMCT was measured during muscle relaxation, muscle contraction and in patients with Parkinson's disease before and 1 h after intravenous infusion of L-dopa (0.25%, 20 ml). Although the CMCT during muscle contraction did not differ significantly between Parkinson's disease and healthy controls, the CMCT during muscle relaxation was significantly shorter in Parkinson's disease than in healthy controls. The CMCT during muscle relaxation in Parkinson's disease was significantly longer after intravenous infusion of L-dopa than before, but the CMCT during muscle contraction did not differ significantly before and after intravenous infusion of L-dopa. The CMCT during muscle contraction was significantly shorter than the CMCT during muscle relaxation in healthy controls. However, in Parkinson's disease, the CMCT did not differ significantly between muscle relaxation and contraction. We consider that the central motor conduction pathway during muscle relaxation in Parkinson's disease is modified to be similar to that during muscle contraction in healthy subjects. Copyright 1999 Harcourt Publishers Ltd.

Journal Article↗

Regional differences in cerebrovascular reactivity to acetazolamide in Alzheimer's disease.

The cerebral blood flow and cerebrovascular reactivity to acetazolamide were investigated in Alzheimer's disease using stable xenon computed tomography (CT). Ten patients with Alzheimer's disease and 10 healthy controls were studied. The regional cerebral blood flow was measured using the xenon delivery and analysis system (AZ-7000 model, Anzai Sogyo, Tokyo, Japan) and CT (PreSage, Yokogawa Medical Systems, Tokyo, Japan). The subjects inhaled room air followed by a mixture of 30% xenon and 50% oxygen for 3 min. Serial scanning was performed once before xenon inhalation, three times in the wash-in process and five times in the washout process of 5 min. The xenon concentration in the end-tidal expired gas was recorded continuously by the thermoconductivity method. The regional cerebral blood flow was measured before and 20 min after i.v. injection of 17 mg/kg acetazolamide. The blood flows in the frontal lobe, parietal lobe and temporal lobe were reduced but the blood flows in the caudate nucleus, putamen and thalamus were normal in the Alzheimer's disease group. The cerebrovascular reactivity to acetazolamide was reduced in the frontal, parietal and temporal cortex but was normal in the other areas. There is a regional difference in the cerebral blood flow and the cerebrovascular reactivity to acetazolamide in Alzheimer's disease Copyright 1999 Harcourt Publishers Ltd.

Journal Article↗

Frontal lobe atrophy and central motor conduction time in chronic alcoholics.

The central motor conduction time (CMCT) was investigated in 12 cases of chronic alcoholism with frontal lobe atrophy, 12 cases of chronic alcoholism without frontal lobe atrophy, and 12 age-matched healthy controls. The CMCT was significantly prolonged in the chronic alcoholics with frontal lobe atrophy as compared to the chronic alcoholics without frontal lobe atrophy and the healthy controls. A significant positive correlation was noted between the CMCT and the degree of frontal lobe atrophy. The CMCT may be prolonged in chronic alcoholics with frontal lobe atrophy.

Alcoholism↗

[A case of post-infectious wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) syndrome].

The patient is a 72-year-old man who had tonsillitis and underwent incision on March 6, 1998. He complained headache and nausea from March 10 and double vision from March 12. He was admitted to our hospital on March 14. Neurological examination on March 18 revealed bilateral internuclear ophthalmoplegia with exotropia (WEBINO), bilateral ptosis and disturbance of convergence. Lumbar puncture revealed moderately elevated protein (46 mg/dl) with normal pressure and cells. The T2-weighted images of head MRI showed multiple high intensity lesions in anterior commissure and right pons. After he was treated with methylprednisolone, his headache and ptosis disappeared. The lesion in anterior commissure on MRI disappeared also. But WEBINO remained at the time of discharge. WEBINO syndrome is caused by lesion of pons and midbrain. The most common cause of bilateral internuclear ophthalmoplegia is multiple sclerosis in the European and American countries, but the frequency of vascular origin is higher in Japan than in the European and American countries. All the cases of WEBINO syndrome reported in Japan are vascular origin. This is the first case of WEBINO syndrome not of vascular origin.

Aged↗

Single lacunar brain infarction with transient signs versus those with long-lasting signs.

BACKGROUND: In order to find out the difference between single brain lacunar infarctions with transient signs and those with long-lasting signs, cerebral blood flow studies and blood tests were performed. METHODS: Ten cases of single lacunar infarction with transient signs and 10 of single lacunar infarction with long-lasting signs were studied. Subcortical cystic infarctions with a diameter of less than 1.5 cm were defined as lacunar infarction. Episodes lasting less than 24 hours were classified as transient signs and those lasting 24 hours or more as long-lasting signs. MEASUREMENTS: cerebral blood flows were measured using the stable xenon computed tomography method. The regional cerebral blood flows were measured before and 20 minutes after the intravenous injection of 17 mg/kg acetazolamide. Plasma fibrinopeptide A, platelet factor 4 and beta-thromboglobulin concentrations were determined at the Special Reference Laboratories. RESULTS: Blood flows in the cerebral cortex and cerebral white matter contralateral to the lacunar infarction were lower in the group with long-lasting signs than in that with transient signs. Cerebrovascular acetazolamide reactivity in the cerebral cortex and white matter contralateral to the lacunar infarction were lower in the group with long-lasting signs than in that with transient signs. Plasma fibrinopeptide A, platelet factor 4 and beta-thromboglobulin concentrations were higher in the long-lasting signs group than in that with transient signs. CONCLUSIONS: There may be some differences in pathogenesis between single lacunar infarction with transient signs and those with long-lasting signs.

Acetazolamide↗