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Biomedical subjects

H Imai

Publications and source records attributed to H Imai.

At least 343 records · Page 19Linked to original sources
PubMed1993

[A 77-year-old woman with myoclonus and epilepsy].

We present a 77-year-old woman with myoclonus and epilepsy. She was well until 35 years of age, when she noted an onset of trembling of the legs upon standing. Her symptom slowly progressed, and she felt a difficulty in standing when she was 39-year-old. She had a major motor seizure without an apparent focal onset when she was 46-year-old. She also developed tremor in her hands, and she felt difficulty in holding a glass filled with water. She was admitted to our service for the first time in 1965 when she was 51-year-old. She showed wide-based ataxic gait with truncal titubation. In finger to nose test, myoclonic jerks were induced in the upper extremities. Otherwise neurological examination was unremarkable. She was treated with primidone and phenobarbital, and was discharged for out patient follow up. Her symptoms slowly progressed, and gait and station became more difficult. Mentally she was sound. Three months prior to the present admission, she developed more difficulty in gait, and decrease in food intake. On the 14th of September in 1991, she was seen by a local physician who found an abnormal shadow in her chest X-ray, and she was admitted to our service for further work-up on September 18, 1991. On admission, the patient was a chronically ill and emaciated woman. Her blood pressure was 140/84 mmHg, heart rate 115/minutes and regular, and the body temperature 36.9 degrees C. The palpebral conjunctivae were anemic. No cervical adenopathy was noted. The lung fields were clear, and no heart murmur was audible. The abdomen was soft, and no organomegaly was present. On neurologic examination, she looked somnolent with disorientation to time and place. Her memory was poor, and she could not do well serial 7s. The disc was flat and the ocular movements appeared intact. Other cranial nerves were also unremarkable. She showed diffuse muscle wasting. She was unable to stand or walk. Maintaining the sitting position was also difficult. She was able to raise her arms, but almost unable to move her lower extremities. The precise muscle testing was impossible. No abnormal involuntary movement was seen. Finger to nose test could not be performed.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1993

[Festination and freezing].

Akinesia, the core symptom of parkinsonism, is a comprehensive term and a disorder characterized by poverty, slowness and also freezing of movement. Parkinson (1817) in his original essay pointed out the festinating gait. Festination is a tendency to speed up in parallel with a loss of normal amplitude of repetitive movement (petit pas, micrographia and inaudible speech). Freezing is a breakdown of repetitive voluntary movement emerging through festination or suddenly. Freezing of gait occurs either at the start (start hesitation), through festination of gait or suddenly when turning or going through the narrow doorway. Narabayashi and the present author reported the first 2 cases with pure akinesia or freezing symptom without rigidity or tremor and unresponsive to L-DOPA therapy as a new condition at the 14th annual meeting of this Society, 1973. Kinésie paradoxal was always accompanied by this type of akinesia. HVA level in the cerebrospinal fluid was not below normal. The author suggested that the main pathological structures of the condition are different from Parkinson's disease. L-threo-DOPS, a synthetic norepinephrine (NE) precursor, had a mild-to-moderate effect on some cases with freezing, and the NE hypothesis for freezing was proposed (Narabayashi). 35 cases with this condition have been known in our clinic to date. Slowly progressive supranuclear ophthalmoplegia appeared later in some patients, several of whom were clinically and two were pathologically diagnosed as progressive supranuclear palsy. The nosological position and responsible lesion sites of this condition are discussed.

Gait↗
PubMed1993

[Inferior branch palsy of the oculomotor nerve following clipping of basilar apex aneurysm].

A 67-year-old woman experienced a severe headache and vomiting. A computed tomographic (CT) scan showed a mild subarachnoid hemorrhage. Cerebral angiography revealed a saccular aneurysm at the apex of the basilar artery. Several days later, she noticed mild hemiparesis of the left extremities. She underwent a clipping operation on the aneurysm by approaching from the right temporal love. Postoperatively, she developed diplopia and dilatation of the left pupil. Cerebral angiography revealed an occlusion of the left posterior cerebral artery. She was admitted to another hospital in order to continue rehabilitation. General physical examination was normal. Neurological examination revealed paralysis of the left medial and left inferior rectus muscles and palsy of the left inferior oblique muscle. The pupil of the left eye was dilated, measuring 5 mm in diameter, and it did not constrict to any stimuli. The left superior rectus and levator palpebrae superioris functioned normally. Visual acuity and visual fields were normal except for the influence of a senile cataract. She had a mild left hemiparesis, slight left ataxia and slurred speech. She had numbness of the left half of the body. A CT scan showed small low density areas in the right thalamus and left cerebellar hemisphere. Her ophthalmologic findings were compatible with the inferior branch palsy of the oculomotor nerve. The ophthalmoplegia of this case seems to be due to partial damage of the oculomotor nerve induced by ischemia of vascular supply. It is supposed to be caused by a vasospasm of the left posterior cerebral artery following a clipping operation of the basilar apex aneurysm.

Aged↗
PubMed1993

[A 81-year-old man with dementia, gait disturbance, hemiparesis, and sympathetic apraxia].

We present a 81-year old male who developed dementia, gait disturbance and right hemiparesis. He was well until the age of 74 when he developed a hemorrhagic infarction in the right occipital region, which left him left homonymous hemianopsia. One year later he had one TIA attack consisting of dizziness, headache, and some clouding of consciousness. At that time, atrial fibrillation was found. At age 79, he was attacked by right hemiparesis. Cranial CT scans revealed a lesion consistent with a hemorrhagic infarct in the left middle cerebral artery territory. Two months prior to his final admission, he had a gradual onset of forgetfulness, labile affect, nocturnal agitation and hallucination which were followed by gait disturbance and urinary incontinence. On admission, he was alert but moderately demented. In addition he showed difficulty in repetition, limb kinetic and ideomotor apraxia of the left hand indicative of sympathetic apraxia, and constructional apraxia bilaterally. Granial nerves appeared intact except for left homonymous hemianopsia. His gait was wide-based and small stepped. No weakness or ataxia was noted. Deep reflexes were diminished on the left side. Plantar reflex was equivocally extensor of the left. Light touch and pain was slightly diminished on the right side. Cranial CT scans revealed a large low density area in the left fronto-temporo-parietal region. Also ventricular dilatation, diffuse low density change in the subcortical white matter, and diffuse cortical atrophy were seen. His clinical course was complicated by melena, anemia, pneumonia, cardiac failure and renal failure. He expired 2 months after his admission.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[Sparteine oxidation by hepatic cytochrome P-450 in patients with Parkinson's disease].

MPTP-induced parkinsonism has revived interest in the role of environmental factors in the etiology of Parkinson's disease. Many potentially neurotoxic substances are detoxified by hepatic cytochrome P-450 through oxidation. Barbeau et al. (1985) reported that significantly more parkinsonian patients than control subjects had defective 4-hydroxylation of debrisoquine. A close correlation between polymorphic oxidation of debrisoquine and sparteine had been observed in Caucasians, suggesting that the oxidative metabolism of these two drugs is under a common genetic control. We report here sparteine oxidation in 71 parkinsonian patients, including 26 young-onset subjects. Each subject was given 100 mg of sparteine sulfate orally, and urine was collected for 6 hours. Sparteine and its dehydrometabolites were analyzed in urine using the method of gas chromatography. Metabolic ratio (MR) was calculated from: (amount of sparteine)/(amount of 2-, plus 5-dehydrosparteine). Subjects with an MR greater than 20 were defined as poor metabolizers (PMs). No PM was observed in our parkinsonian subjects, but the distribution of MR in parkinsonian subjects was significantly deviated to the higher MR value (mean +/- SD: 1.19 +/- 1.27, range: 0.02-6.12) than healthy controls (0.60 +/- 0.61, 0.11-3.07). This is probably due to a higher frequency of intermediate metabolizers in parkinsonian patients having partial defect of sparteine oxidation. Mild negative correlation (rs = -0.45) was noted between the MR and the age of onset in parkinsonian subjects. When the 71 patients were divided into two groups according to the age of onset, a larger difference in the MR value was found when subjects were divided at the age of 45 years (p < 0.005) compared with subdivision at the age of 40 years (p < 0.02). Our results suggest that slower metabolism by hepatic debrisoquine-sparteine type cyt. P-450 is one of the contributory factors for the development of Parkinson's disease.

Adult↗
PubMed1993

[Intermittent high-dose vitamin C therapy in patients with HTLV-I-associated myelopathy].

The aim of this study was to determine the efficacy and safety of intermittent high-dose vitamin C therapy in patients with HTLV-I associated myelopathy (HAM). Seven HAM patients (4 men and 3 women, aged 36 to 81 years), who were repeatedly given a daily oral dose of 1.5 to 3.0 g of vitamin C (40 mg/kg/day) for 3 to 5 successive days followed by a two-day withdrawal period, were followed for a mean period of 9.7 +/- 5.8 months after the therapy. The therapeutic efficacy was evaluated by a 10-grade disability scoring (DS) system, short somatosensory evoked potentials (SSEP) elicited by tibial nerve stimulation and several immunological parameters before and at 2.0 to 14 months after the therapy. All HAM patients responded well to intermittent high-dose vitamin C therapy, 6 being excellent responders (DS improvement > or = 2 grades) and one being a good responder (DS improvement of one grade). The grade of DS was decreased at 9.7 +/- 5.8 months after the therapy from 5.9 +/- 1.6 (baseline) to 3.0 +/- 1.5 (p < 0.01), indicating an excellent clinical outcome. SSEPs were obtained before and after the therapy in 4 of the patients. On SSEP before therapy, all the patients showed abnormally prolonged P37 peak latency. N20 was not recorded in 2 patients. After the therapy, N20 appeared and prolonged P37 peak latency improved in 2 patients. Immunoglobulin concentrations, T-B lymphocyte subsets and HTLV-I antibody titer in serum did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

[A 70-year-old man with right hemiparesis and mutism].

We report a 70-year-old man who had a sudden onset of right hemiparesis and mutism. The lower extremity was more involved than the upper one. He had a long history of diabetes and chronic renal failure for which hemodialysis was necessary. On August 30, 1990, he had an sudden onset of right hemiparesis and mutism. Neurological examination revealed awake but mute in no acute distress. He could only respond to very simple commands such as opening his mouth or protruding his tongue. He did not appear to understand more difficult questions. In addition, he could not answer verbally. He was totally mute. Cranial nerves appeared intact except for slight right central facial paresis and severe diabetic retinopathy. He had complete paralysis of his right leg and a moderate weakness in his right upper extremity. Deep reflexes were diminished in both upper extremities and absent in the lower limbs. Frotal signs such as grasp and snout reflexes were present. Cranial CT scans revealed an ill-defined low density area in the left parasagittal subcortical area and a part of the anterior cerebral artery territory. The supplementary motor area appeared at least in part to be involved. He was treated with glycerol and other supportive cares, however, his clinical course was complicated by pneumonia, heart failure, septicemia, and he expired two months after his stroke. The patient was discussed in a neurological CPC, and the chief discussant arrived at a conclusion that he had an artery-to-artery embolism at the internal carotid bifurcation resulting in the cerebral infarction mainly in the territory of the anterior cerebral artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[Hemiballism-hemichorea caused by a putaminal hemorrhage with worsening after smoking--a case report].

A 65-year-old hypertensive man was admitted because of abnormal involuntary movements which had an onset one month prior to the admission. Neurological examination revealed an alert and intelligent male in no acute distress. Cranial nerves appeared intact except for dysarthria. His gait was wide-based. He had hemiballism-hemichorea in his left upper and lower extremities. Cranial CT scans revealed a high density area confined to the right putamen. After admission, his involuntary movements slowly improved without medication. After near complete disappearance of his abnormal movements two weeks after admission, he noted that smoking induced choreic movement in his left side transiently. The involuntary movement ceased soon after upon stopping smoking. This was repeatedly observed not only by him but also by us. Our observation may indicate that the inhibition of the subthalamic nucleus as the result of the decrease of the putaminal output to the external segment of the globus pallidus will induce hemiballism. The effect of smoking on his involuntary movements can be understood as a result of increase in the dopamine release from the nigrostriatal terminals induced by nicotine.

Aged↗
PubMed1993

Effect of low-osmolality contrast media on red cell filterability.

The effects of low-osmolality contrast media (CM) on red blood cell (RBC) filterability were investigated using a recently developed nickel mesh filtration method. The conventional hypertonic CM iothalamate, low-osmolality iohexol, and the recently synthesized iomeprol were studied. Among them, the osmolality of iomeprol was the lowest. The impact of CM osmolality, viscosity, and iodine content on the RBC filterability was analyzed. Under equal iodine content or viscosity condition, the filterability order of RBCs suspended in CM was iomeprol > iohexol >> iothalamate, because of the osmolality of CM. Iomeprol caused small echinocytic changes but these had a negligible influence on RBC filterability. In conclusion, the osmotic effect of CM on RBC filterability is more predominant than the other CM effects, and iomeprol is the preferred CM for RBC filterability.

Adult↗
PubMed1993

Altered localization of 73-kilodalton heat-shock protein in rat kidneys with gentamicin-induced acute tubular injury.

BACKGROUND: The constitutive 73-kilodalton heat-shock protein (HSP73) has been shown to have various essential functions in cells under both normal and stress conditions. In the present study, we observed serial localizations of HSP73 in rat kidneys with gentamicin-induced acute tubular injury. EXPERIMENTAL DESIGN: Sprague-Dawley rats received gentamicin (80 mg/kg/day) for 14 days, and developed acute proximal tubular injury. The intrarenal immunohistochemical distribution of HSP73 was examined by using a specific antibody against HSP73. In addition, HSP73 content in both isotonic buffer- and detergent-extractable renal fractions were measured by immunoblot analysis. RESULTS: After the gentamicin exposure, HSP73 moved from the nucleus to the cytoplasm, and accumulated in granules that were considered to be expressed within enlarged lysosomes in the injured proximal tubular epithelial cells. These granules started to appear from 36 hours after the first gentamicin exposure, enlarged in size until day 12, and gradually diminished after day 18. At day 27, the HSP73 localization pattern returned to that in the normal kidney. Moreover, significantly increased HSP73 protein bands were detected by immunoblot of detergent-extractable fractions from gentamicin-treated rat kidneys at from 36 hours to day 15 after the gentamicin exposure. CONCLUSIONS: Our findings suggest that HSP73 is rapidly induced as an insoluble form in injured lysosomes of the proximal tubular epithelial cells during gentamicin-induced acute tubular injury.

Animals↗
PubMed1992

Acyl-(acyl-carrier protein) hydrolase from squash cotyledons specific to long-chain fatty acids: purification and characterization.

Acyl-(acyl-carrier-protein) hydrolase (EC 3.1.2.14) releases fatty acids from the end-product of fatty acid synthesis in plastids for the subsequent synthesis of glycerolipids in the cytoplasm. Isoelectric focusing of chloroplast stroma proteins from squash cotyledons suggested that there were at least three isomeric forms of acyl-(acyl-carrier-protein) hydrolase having pI values of 4.5, 5.3 and 7.8. The pI 4.5 and pI 5.3 forms showed maximum activity at pH 9.8 whereas the activity of the pI 7.8 form increased within the range 6.2 to 10.2 but no optimum was seen. The pI 4.5 form was purified 100,000-fold from squash cotyledons. The highly purified fraction contained two polypeptides, whose molecular masses were estimated to be 35 kDa and 33 kDa by SDS-PAGE. It is suggested that the 33 kDa polypeptide was a degradation product of the 35 kDa polypeptide. Oleoyl-(acyl-carrier protein) was the preferred substrate of this enzyme over palmitoyl- and stearoyl-(acyl-carrier protein), whereas lauroyl-(acyl-carrier protein) was nearly inactive. These results indicate the enzyme is specific for long-chain acyl-(acyl-carrier protein).

Acyl Carrier Protein↗
PubMed1992

Assessment of chemoembolization therapy for primary liver cancer using a stabilized adriamycin-lipiodol suspension.

We formulated a new lipiodol-Adriamycin suspension (ADM/lipiodol, 50 mg/10 ml) that remained stable for 48 h (half-life, 25 +/- 3 days). In five cases of hepatocellular carcinoma (HCC) resected after intra-arterial infusion of this agent, the ADM concentration in the tumor was quite high and the tumor necrosis rate was more than 80% on histological examination. Over a 5-year period, 180 patients with unresectable HCC underwent transcatheter arterial embolization therapy (TAE) in the presence or absence of this agent. The regimens consisted of suspension injection alone (A, n = 54), suspension injection + TAE using gelatin sponge (B, n = 29), TAE followed by suspension injection (C, n = 34), and TAE alone (D, n = 63). The estimated 1-year survival values determined for patients treated with these regimens were 70%, 73%, 43%, and 39% respectively, and the corresponding 3-year survival values were 27%, 31%, 15%, and 10%. The survival achieved using suspension injection was thus superior to that obtained using conventional TAE, and combined therapy with suspension injection followed by TAE seemed to enhance survival, although there were some biases in tumor size and in the stage of tumor progression. For patients with tumors measuring 5 cm or more in diameter, the survival obtained using regimen A was lower than that achieved using regimen D, but the combination of TAE and suspension injection improved the 1-year survival value obtained using regimen D from 34% to 52%. For patients with tumors measuring less than 5 cm in diameter, the survival achieved using regimen A was markedly better than that obtained using regimen D, although no difference was found between the survival value achieved using regimen A and that obtained using regimens B and C. On the basis of these results, our newly formulated ADM-lipiodol suspension was surmised to be effective by itself against relatively small HCC tumors, whereas it enhanced the efficacy of conventional TAE in large lesions.

Aged↗
PubMed1992

Autotransplantation of peripheral cholinergic neurons into the brains of Alzheimer model rats.

Current hypotheses regarding Alzheimer's disease implicate cholinergic function. In this study, peripheral cholinergic neurons in the vagal nodosal ganglion were transplanted into the brains of Alzheimer model rats. Eighteen Sprague-Dawley strain rats were divided into three groups: 1) unoperated control rats, 2) rats that had undergone bilateral destruction of the nucleus basalis of Meynert (NBM) (Alzheimer model), and 3) the transplantation group in which the vagal nodosal ganglion was transplanted into the cerebral neocortex one week after the bilateral destruction of the Meynert nucleus. Seven weeks after the transplantation rat behaviour was assessed using psychological tests (spontaneous activity, passive avoidance response and the Hebb-Williams maze test). The Alzheimer model rats had a statistically significant increase in spontaneous activity in comparison with controls (P less than 0.01). The transplant rats showed some amelioration of this abnormal increase in spontaneous activity observed in the Alzheimer model rats. All of the control rats showed conditioned passive avoidance responses, while only one Alzheimer model rat retained is shocked-conditions behaviour before 24 hours (P less than 0.01). Three of the six transplanted rats showed complete improvement in the passive avoidance response test. In the Hebb-Williams maze test, the rats with NMB lesions made more errors than the control rats. The transplanted rats had a lower number of errors than NBM-lesioned rats but still more than the controls. Histological examination revealed many cholinergic cells in the transplanted tissue, especially in the area adjacent to the cerebral cortical surface. The present results indicate that autotransplantation of peripheral cholinergic cells ameliorates abnormal behaviour in Alzheimer model rats.

Alzheimer Disease↗
PubMed1992

Significance of fibrils in the formation of the Kimmelstiel-Wilson nodule.

The pathogenesis of the nodular lesion in diabetic glomerulosclerosis is described in association with fibrils. Thirteen diabetic patients with glomerular nodular lesions and 9 diabetics without the nodules were examined by electron microscopy using periodic acid-thiocarbohydrazide-silver proteinate staining. In cases of nodular glomerulosclerosis, abundant fibrillar structures mixed with electron-dense material were detected within the nodule and the mesangial matrix. They were also occasionally observed along the subendothelial space of the glomerular capillary walls. On the cross-section, these fibrils, including the lucent periphery, were 34 nm wide. Immunohistologically, collagen V and collagen VI were detected in nodular lesions. In contrast, in cases of the diffuse type of glomerulosclerosis, the widened mesangium was composed of dense material, which resembled the original mesangial matrix. The above fibrils were not detected in the mesangium. These findings suggest that the accumulation of the peculiar fibrils in the glomerular mesangium is a major pathogenic factor in the formation of Kimmelstiel-Wilson nodules.

Adult↗