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Biomedical subjects

T Yuasa

Publications and source records attributed to T Yuasa.

At least 127 records · Page 7Linked to original sources

Identification of regions on the hemagglutinin-neuraminidase protein of human parainfluenza virus type 2 important for promoting cell fusion.

The hemagglutinin-neuraminidase (HN) and fusion (F) glycoproteins of two paramyxoviruses, human parainfluenza virus type 2 (PIV2) and simian virus 41 (SV41), were expressed in HeLa cells by transfecting with recombinant plasmid harboring each glycoprotein gene. Expressed F proteins could not induce cell fusion by themselves, but evoked prominent cell fusion when coexpressed with homologous HN proteins. It was also proved that PIV2 HN protein could weakly promote SV41 F-mediated cell fusion. By analyzing the fusion-promoting function of chimeric HN proteins of PIV2 and SV41, it was revealed that the N-terminal region (about 16% of total amino acids) of either PIV2 HN or SV41 HN protein could define the type-specific fusion-promoting function for homologous F protein. Analyses of additional chimeras indicated that the N-terminal region in PIV2 HN protein (designated region I, consisting of 94 amino acids) could be reduced to a 58-amino-acid region (region I') which was located at the membrane-proximal end of the ectodomain. Furthermore, PIV2 HN protein proved to promote cell fusion mediated by PIV4A F protein. Unexpectedly, analyses of another set of chimeras revealed that the promoting function of PIV2 HN protein for PIV4A F-mediated cell fusion was not merely carried by its region I but also by another region ranging from residue 148 to 209 (region II). Finally, it was indicated that regions I' (in the presumed stalk domain) and II (in the globular head) in PIV2 HN protein might play important roles in promoting cell fusion mediated by the F proteins.

Amino Acid Sequence↗

Suppression of motor cortical excitability by magnetic stimulation of the cerebellum.

EMG responses of the relaxed right thenar muscle evoked by magnetic stimulation over the sensorimotor cortex were suppressed by magnetic conditioning stimulation over the occiput. The optimal interstimulus interval for reduction of the EMG amplitude was 4-6 ms. The optimal conditioning position and induced current direction were 3-4 cm below the inion when the induced current in the center of the figure-8 coil flowed from right to left horizontally. It differed from that for activating the descending motor pathway. We consider this suppression to be due to the inhibition of motor cortex excitability caused by stimulation of the dentato-thalamo-cortical pathway at the dentate nuclei or superior cerebellar peduncle.

Adult↗

A cell fusion-inhibiting monoclonal antibody binds to the presumed stalk domain of the human parainfluenza type 2 virus hemagglutinin-neuraminidase protein.

Previously, we obtained a neutralizing monoclonal antibody directed against the hemagglutinin-neuraminidase (HN) protein of human parainfluenza type 2 virus (PIV2), which was able to prevent cell fusion without affecting the hemagglutinating and neuraminidase activities. In this study, four escape mutants of PIV2 have been obtained under pressure of the monoclonal antibody. Intriguingly, the HN protein of each mutant proved to have two amino acid substitutions, one of which is at 83Asn or 91Lys, and another one is at 150Leu, 160Ala, or 186Met. One mutant designated F13, which has substitutions at 83Asn and 186Met in the HN protein, could not cause cell fusion in HeLa cells despite its multiple replication, while the other mutants formed typical syncytial cells. The deduced amino acid sequence of F13 fusion (F) protein proved to be identical to that of wild-type F protein, and furthermore, protein expression analyses have revealed that the low-fusion phenotype of F13 was due to its mutated HN protein, whose antigenicity to the monoclonal antibody was abolished by the single mutation at 83Asn. These observations have suggested that the principal epitope for the monoclonal antibody resides in the presumed stalk domain of the HN protein, which may play an important role in promoting cell fusion.

Amino Acid Sequence↗

Lactate rise in the basal ganglia accompanying finger movements: a localized 1H-MRS study.

To investigate whether motor activation can cause lactate elevation, we observed the metabolic changes in seven right-handed volunteers by localized 1H-magnetic resonance spectroscopy (MRS). The volume of interest (VOI) was centered on a region including portions of the putamen and globus pallidus. Finger opposition movements were applied as the motor tasks. On the side contralateral to the finger movements, lactate rose in all subjects. No lactate rise occurred in basal ganglia ipsilateral to the movements.

Basal Ganglia↗

Nitrite, nitrate and cGMP in the cerebrospinal fluid in degenerative neurologic diseases.

To investigate whether nitric oxide (NO) plays a role in degenerative neurologic disease (DND), we measured nitrite, nitrate and cyclic GMP in cerebrospinal fluid (CSF) samples from patients with Parkinson's disease (PD), spinocerebellar ataxia (SCA) and amyotrophic lateral sclerosis (ALS). We found no significant change in CSF nitrite, nitrate or cyclic GMP in patients with any DND compared with control values. These results suggest that NO production is preserved in PD, SCA and ALS.

Aged↗

Effects of MCI-225 on memory and glucose utilization in basal forebrain-lesioned rats.

The effects of MCI-225 on amnesia, the cerebral glucose metabolism, and choline acetyltransferase (ChAT) activity in basal forebrain (BF)-lesioned rats were studied in comparison with those of tacrine. Bilateral BF lesions with ibotenic acid impaired the performance in passive avoidance (PA) tasks. Single administration of MCI-225 (10 mg/kg, PO) after a 2-week postoperative recovery period, increased the escape latencies in the PA task, but was not statistically significant. Repeated administration of MCI-225 (0.3 and 1 mg/kg, PO for 6 days) significantly reversed the PA failure. The BF-lesioned rat exhibited a marked decrease in the local cerebral glucose utilization (LCGU) in the frontal cortex, parietal cortex, and caudate-putamen. MCI-225 (1 mg/kg, PO for 5 days) significantly ameliorated the reduction of the LCGU in the parietal cortex. MCI-225 did not change the decrease in the cortical ChAT activity induced by the BF lesion. Repeated administration of tacrine reversed the PA failure (0.3 mg/kg, PO) but failed to prevent the decrement in the LCGU and the ChAT activity. These results suggest that MCI-225 could be effective in the treatment of senile dementia of the Alzheimer type, which is accompanied with both deficit in the BF-cortex cholinergic neuron and cerebral glucose hypometabolism.

Animals↗

Mutism developing after bilateral thalamo-capsular lesions by neuro-Behçet disease.

We described a 44-year old right-handed man showing mutism, left hemiplegia and pseudobulbar palsy after CT and MRI documented bilateral thalamo-capsular lesions by neuro-Behçet disease. Single photon emission tomography (SPECT) and Xenon CT revealed hypoperfusion of the bilateral frontal lobes. The pathophysiological mechanism of mutism was discussed and we postulate that mutism might occur as the result of frontal lobe dysfunction due to the disconnection of thalamocortical fiber from thalamus to frontal cortex and that it could be interpreted as an incomplete form of akinetic mutism.

Adult↗

Cyclic guanosine monophosphate (cGMP), nitrite and nitrate in the cerebrospinal fluid in meningitis, multiple sclerosis and Guillain-Barré syndrome.

Recent evidence suggests the involvement of nitric oxide (NO) in inflammation and demyelination in the brain. To test this hypothesis, we measured NO markers in the cerebrospinal fluid from patients with bacterial meningitis (BM), aseptic meningitis (AM), multiple sclerosis (MS), and Guillain-Barré syndrome (GBS). Subjects with non-inflammatory neurologic diseases served as the controls. NO markers were cyclic guanosine monophosphate (cGMP) measured with an enzyme immunoassay, and nitrite and nitrate measured with the Griess reaction. Except for BM, cGMP was not increased in AM, MS or GBS compared with the controls. Nitrite and nitrate were unaltered in any of the groups studied. These results do not support the hypothesis that NO is increased in the brain in meningitis, MS or GBS. Otherwise cGMP, nitrite and nitrate in the cerebrospinal fluid do not reflect the increase in NO in the brain.

Adult↗

Trigeminal neuralgia associated with venous angioma--case report.

A 35-year-old male presented with trigeminal neuralgia associated with venous angioma at the root entry zone. Magnetic resonance imaging and angiography demonstrated a venous angioma with a dilated petrosal draining vein, and displacement of the anterior inferior cerebellar artery (AICA). The AICA and dilated petrosal vein were both decompressed, resulting in complete relief from symptoms of trigeminal neuralgia for 30 months. Microvascular decompression rather than resection of venous angioma is recommended for treatment of such cases. The possibility of a venous anomaly should be considered in younger patients with trigeminal neuralgia.

Adult↗

[Surgical treatment for ischemic mitral regurgitation in patients with poor left ventricle].

Results of CABG with and without mitral valve surgery were analyzed retrospectively in 81 patients with ischemic mitral regurgitation (MR) to determine the effects of severity of MR and surgical treatment on survival. Seven of 81 patients had severe MR (more than Sellers III degrees/IV). Of these 7 patients, 5 patients underwent mitral valve replacement and 1 patient underwent mitral annuloplasty. Only one patient did not undergo valve surgery. This patient had slight improvement of the functional classification after CABG, but died of congestive heart failure 5 years after surgery. There were 3 hospital deaths and 5 late deaths in 81 patients. Among the 29 patients with poor left ventricle (EF < or = 0.3), there were 3 hospital deaths and 2 late deaths. Postoperatively, 12 patients had Sellers II degrees/IV or III degrees/IV MR. In 4 patients of these 12, the severity of MR was aggravated in comparison with the preoperative severity. Three of these 4 patients had perioperative myocardial infarction (PMI). IABP was utilized preoperatively in patients with poor left ventricle to keep the stable hemodynamics and prevent PMI. In these patients, there were no PMI, no hospital death, or no aggravation of MR. In conclusion, patients with Sellers I degree/IV or II degrees/IV MR require CABG only, whereas those with Sellers III degrees/IV or IV degrees/IV MR need CABG combined with mitral valve surgery. Preoperative use of IABP is useful for preventing PMI and aggravation of MR in patients with poor left ventricle.

Aged↗

[Experience of modified Bentall's procedure for annulo-aortic ectasia].

To reduce the incidence of false aneurysm formation at the suture lines, a known complication with the inclusion technique such as Bentall's procedure or Cabrol's procedure, modified Bentall's procedure (Carrel patch technique), which is identical to Inberg's procedure, has been selected as treatment for annulo-aortic ectasia since 1991. This operation was carried out in 6 consecutive patients with annulo-aortic ectasia from July 1991 to August 1992. The aortic valve and the aneurysm were resected, the coronary ostia were dissected free, mobilized, and then implanted to the composite graft. It was necessary for one patient to undergo coronary artery bypass grafting for myocardial ischemia due to injury of the right coronary ostium. Thereafter, the button of coronary ostium was cut into a big size and then trimmed just before the implantation to the composite graft in order to prevent injury of the button of the coronary ostium. There was no hospital mortality. No pseudo-aneurysm at the coronary ostia or the distal aortic anastomosis was observed at control aortography carried out 1 month after surgery. One patient died 1 year after the first operation because of low cardiac output after the re-operation for pseudo-aneurysm at the proximal aortic anastomosis and infection of the composite graft. All the other patients have been symptom free during follow-up. The use of gelatin impregnated dacron graft and the reinforcement of the suture lines by Teflon felt strips minimized bleeding. One patient underwent this operation without blood transfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Cerebellar nitric oxide synthase, cGMP and motor function in two lines of cerebellar mutant mice, Staggerer and Wriggle Mouse Sagami.

We investigated the hypothesis that nitric oxide (NO) is involved in the cerebellar motor function, by measuring nitric oxide synthase (NOS) activities and cGMP in the cerebellum using two lines of mutant mice having motor dysfunction, Staggerer (SG) and Wriggle Mouse Sagami (WMS). In SG, the NOS activity per cerebellum was reduced to 5.8% of that of the controls, while no significant change was observed in WMS. The cerebellar cGMP in SG was reduced to 3.3% of that of the controls and to 43% in WMS. In contrast with these neurochemical markers of NO, the locomotor dysfunction and the number of falls were greater in WMS than in SG. The reductions of the neurochemical markers of NO are consistent with the results of the previous neuropathological studies in SG and WMS whereas the cerebellar motor dysfunction was independent of these neurochemical and neuropathological changes.

Amino Acid Oxidoreductases↗

Regional cerebral blood flow measured with N-isopropyl-p-[123I]iodoamphetamine single-photon emission tomography in patients with Joseph disease.

Regional cerebral blood flow (rCBF) was measured in five Japanese patients who were clinically diagnosed as having Joseph disease, also called Machado-Joseph disease or Azorean disease, using N-isopropyl-p-[123I]iodoamphetamine (IMP) and single-photon emission tomography (SPECT). Cerebellar atrophy was evaluated by a five-step rating scale as defined on X-ray computed tomography (X-CT). Compared with ten age-matched normal controls (mean cerebellar CBF +/- SD: 66.9 +/- 6.6 ml/100 g/min), rCBF in patients with Joseph disease was significantly decreased in the cerebellum (mean +/- SD: 50.2 +/- 7.3 ml/100 g/min). No significant relationship, however, was found between the decrease in rCBF in the cerebellum and the degree of cerebellar atrophy on X-CT. rCBF in the cerebellum was minimally decreased in one patient who had severe cerebellar atrophy and in two patients with moderate atrophy. These data may support the findings that Purkinje cells in the cerebellum are almost normal in Joseph disease, and that the granular and molecular layers remain intact in spite of cortical atrophy of the cerebellum. It is concluded that [123I]-IMP SPET is able to identify pathological and metabolic changes in the cerebellum that do not appear on X-CT or magnetic resonance imaging, and thus is useful for the diagnosis of Joseph disease.

Adult↗

Motor neuron disease with multi-system involvement presenting as tetraparesis, ophthalmoplegia and sensori-autonomic dysfunction.

We carried out a postmortem examination on two Japanese patients, 64- and 80-year-old men whose survival was prolonged with an artificial respirator. They had no family history of neuropsychiatric disorders and were suspected, clinically, as having a motor neuron disease that differed from amyotrophic lateral sclerosis (ALS). As well as upper and lower motor neuron impairment, they showed a variety of symptoms, such as sensory disturbances, hypohidrosis, impotence, ophthalmoparesis and/or atonic neurogenic bladder, and their protein content in cerebrospinal fluid was elevated markedly. Pathological examination revealed the following extensive nervous system involvement: (1) the upper and lower voluntary motor systems, including the IIIrd, IVth and VIth cranial nerve nuclei: (2) the reticular formation and its major afferent pathways; (3) the vestibulospinal and tectospinal systems; (4) the spinocerebellar system and the exteroceptive somatic afferent pathways; (5) the dentatorubral and pallidoluysian systems; and (6) the substantia nigra, locus ceruleus and intermediolateral and Onufrowicz's nuclei. Neither Bunina bodies, Lewy body-like hyaline inclusions nor ubiquitin immunoreactive skein-like structures were observed. The distribution of the lesions was quite different from that in patients with ALS and the other known related diseases. Recently, seven autopsied cases with clinical and histopathological similarities to our patients have been reported in Japan. Our conclusion is that our two and these seven patients should be classified as having a new motor neuron disease entity, which can be is differentiated from ALS.

Aged↗