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Biomedical subjects

M Tabuchi

Publications and source records attributed to M Tabuchi.

At least 55 records · Page 3Linked to original sources
PubMed1998

Spontaneous dural carotid cavernous sinus fistula presenting isolated ophthalmoplegia: evaluation with MR angiography.

We describe three patients with spontaneous dural carotid cavernous sinus fistula presenting an isolated ophthalmoplegia where magnetic resonance angiography demonstrated abnormal flow-related enhancements in the cavernous sinus with extension into the inferior petrosal sinus. Magnetic resonance angiography is of value in evaluation of patients with isolated ophthalmoplegia.

Arteriovenous Fistula↗
PubMed1998

[The role of the right hemisphere on recovery from Wernicke's aphasia].

We report a rare case of severe Wernicke's aphasia who showed a rapid and surprisingly good recovery despite of a large infarct involving the left posterior language area. A 68-year-old right-handed woman without a family history of left-handedness developed a severe comprehension difficulty and paraphasic output following a large infarct in the left posterior temporoparietal region. However, in 6 weeks, naming, comprehension, and repetition of words became almost normal. Spontaneous speech also became almost normal, although comprehension and repetition of sentences remained slightly impaired. The lesion size remained unchanged. A dichotic listening test 4 months after the onset showed clear left ear superiority. We speculate from these observations that the dormant language function in the right hemisphere might have played a role for rapid and good recovery of this case.

Aged↗
PubMed1997

The Schizosaccharomyces pombe gms1+ gene encodes an UDP-galactose transporter homologue required for protein galactosylation.

In a previous study, we isolated a Schizosaccharomyces pombe mutant defective in protein galactosylation (Takegawa, K., Tanaka, N., Tabuchi, M. and Iwahara, S. (1996) Biosci. Biochem. Biotech. 60, 1156-1159). From an S. pombe genomic library, we cloned the gms1+ gene which restored the galactosylation of cell wall glycoproteins. Gms1 protein shares significant sequence similarity with human UDP-galactose and murine CMP-sialic acid transporters. The fission yeast strains deleted for the gms1+ gene lacked galactose residues in sell surface glycoproteins and were significantly decreased in UDP-galactose transport activity. These results showed that the gms1+ encodes an UDP-galactose transporter, and this protein appears to be an essential role for the incorporation of UDP-galactose into the lumen of Golgi in s. pombe.

Amino Acid Sequence↗
PubMed1997

Cloning, sequencing, and expression of Arthrobacter protophormiae endo-beta-N-acetylglucosaminidase in Escherichia coli.

The gene encoding endo-beta-N-acetylglucosaminidase from Arthrobacter protophormiae (Endo-A) was cloned, and its nucleotide sequence was determined. A single open reading frame consisting of 1935 base pairs and encoding a polypeptide composed of signal peptides of 24 amino acids and a mature protein of 621 amino acids was found. The primary structure of Endo-A exhibited significant homology with FO1F.10 gene product from Caenorhabditis elegans and weak homology with peptide-N4-(N-acetyl-beta-D-glucosaminyl)asparagine amidase from Flavobacterium meningosepticum and chitinase from Streptomyces olivaceoviridis. However, the enzyme had no significant homology with any previously reported endo-beta-N-acetylglucosaminidases. Transformed Escherichia coli cells carrying the 4.5-kb fragment expressed Endo-A activity. This enzyme activity was detected in the medium as well as in the periplasmic space of cells under the control of the Endo-A gene promoter. The recombinant Endo-A was efficiently isolated from the periplasmic space of the cells. N-terminal sequence analysis revealed that native and recombinant Endo-A have the same N-terminus. Recombinant and native Endo-A also showed very similar optimum pH profiles and transglycosylation activity.

Amino Acid Sequence↗
PubMed1997

Vacuolar protein sorting in fission yeast: cloning, biosynthesis, transport, and processing of carboxypeptidase Y from Schizosaccharomyces pombe.

PCR was used to isolate a carboxypeptidase Y (CPY) homolog gene from the fission yeast Schizosaccharomyces pombe. The cloned S. pombe cpy1+ gene has a single open reading frame, which encodes 950 amino acids with one potential N-glycosylation site. It appears to be synthesized as an inactive pre-pro protein that likely undergoes processing following translocation into appropriate intracellular organelles. The C-terminal mature region is highly conserved in other serine carboxypeptidases. In contrast, the N-terminal pro region containing the vacuolar sorting signal in CPY from Saccharomyces cerevisiae shows fewer identical residues. The pro region contains two unusual repeating sequences; repeating sequence I consists of seven contiguous repeating segments of 13 amino acids each, and repeating sequence II consists of seven contiguous repeating segments of 9 amino acids each. Pulse-chase radiolabeling analysis revealed that Cpy1p was initially synthesized in a 110-kDa pro-precursor form and via the 51-kDa single-polypeptide-chain intermediate form which has had its pro segment removed is finally converted to a heterodimer, the mature form, which is detected as a 32-kDa protein on sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing conditions. Like S. cerevisiae CPY, S. pombe Cpy1p does not require the N-linked oligosaccharide moiety for vacuolar delivery. To investigate the vacuolar sorting signal of S. pombe Cpy1p, we have constructed cpy1+-SUC2 gene fusions that direct the synthesis of hybrid proteins consisting of N-terminal segments of various lengths of S. pombe Cpy1p fused to the secreted enzyme S. cerevisiae invertase. The N-terminal 478 amino acids of Cpy1 are sufficient to direct delivery of a Cpy1-Inv hybrid protein to the vacuole. These results showed that the pro peptide of Cpy1 contains the putative vacuolar sorting signal.

Base Sequence↗
PubMed1997

Inhibition of octapeptide N-myristoylation by acyl amino acids and acyl alkanolamines.

Several acyl amino acids and acyl alkanolamines were prepared and screened for their inhibition of octapeptide N-myristoylation and HIV-1 replication in MT-4 cells. Of the 62 acyl derivatives tested, N-myristoyl-O-caproyl-L-serine, N-myristoyl-O-caproyl-D-serine and N-decanoyl-O-myristoyl-L-serine were found to be uncompetitive inhibitors of N-myristoylation, but did not prevent HIV-induced cytopathicity in MT-4 cells. However, other acyl derivatives such as N-3-hydroxymyristoyl ethanolamine, N-3-hydroxymyristoyl-D-serine and N-myristoyl-L-cysteine, which did not inhibit N-myristoylation, suppressed the cytopathicity in the infected cells. The acyl derivatives described here may serve as lead compounds for antiviral agents.

Acylation↗
PubMed1997

["Forced mouth opening reaction" associated with corticobasal degeneration].

Corticobasal degeneration (CBD) is a slowly progressive disorder characterized by an asymmetrical akinetic-rigid syndrome, supranuclear ophthalmoplegia, dystonia, often accompanied by involuntary movements, particularly myoclonus, and associated with lateralized cortical signs such as alien limb behavior and apraxia. Computerized tomography demonstrates asymmetrical frontoparietal cortical atrophy in the later stages of the illness. Neuropathological examination reveals neuronal loss, gliosis and swollen achromatic neurons within the frontal and temporal cortices, and the substantia nigra. We discuss here a unique phenomenon not described so far in three patients with clinical features of CBD, one with subsequent autopsy observations. When awake, they all showed a common behavior, their mouth opened constantly and immediately, when a tongue-depresser was approached in front of it by the examiner. In two of them, their mouth also opened when its corner was stroked by a tongue-depressor. They could not control these phenomena at all, even they were asked not to open their mouth. We would like to call these phenomena "forced mouth opening reactions" because they were uncontrollable voluntarily. They may be divided into two groups, i.e. visual and tactile "forced mouth opening reactions". In all the patients the neurological, neuro-imaging and neuropathological data showed that the frontal lobes were damaged. Additionally, they had some frontal lobe release signs such as forced grasping, forced groping, or alien limb sign. We would like to apply the mechanism for these release signs to the "forced mouth opening reactions". Thus, we speculate that the frontal lobe contains a higher motor control mechanism for normal mouth opening movement, and the "forced mouth opening reactions" result from impairment of this control.

Basal Ganglia Diseases↗
PubMed1997

[Occlusive lesions of carotid and intracranial arteries in patients with symptomatic lacunar infarction--evaluation by MR angiography].

The purpose of this study is to elucidate the prevalence and degree of occlusive lesions of carotid and intracranial arteries in patients with symptomatic lacunar infarction. We performed carotid and intracranial MR angiography, and T2-weighted MRI on 65 patients with symptomatic lacunar infarction. Stenosis of more than 25% narrowing of the diameter was found in 12 patients (18.5%) in the extracranial carotid arteries and in 14 patients (21.5%) in the intracranial arteries. Most of the stenotic lesions were mild. Multiple logistic regression analysis showed that age was significant and independent predictor for carotid artery stenosis, and that diabetes mellitus was predictor for intracranial artery stenosis. The incidence of intracranial artery stenosis was statistically higher in patients with asymptomatic lacunar infarctions in subcortical white matter area on T2-weighted MRI than in patients without such lesions. Coexistence of carotid artery stenosis should be suspected in aged patients with symptomatic lacunar infarction, and the possibility of intracranial artery stenosis should be considered in patients with diabetes mellitus or asymptomatic lacunar infarctions in subcortical white matter area.

Adult↗
PubMed1996

Asymptomatic occlusive lesions of carotid and intracranial arteries in Japanese patients with ischemic heart disease: evaluation by brain magnetic resonance angiography.

BACKGROUND AND PURPOSE: The purpose of this study was to elucidate the prevalence and degree of asymptomatic occlusive lesions in the carotid and intracranial arteries in Japanese patients with ischemic heart disease (IHD). METHODS: We performed carotid and intracranial MR angiography (MRA) on 67 patients (49 men, 18 women; age range, 40 to 78 years; mean age, 60.1 years) who had received selective coronary angiography for the clinical diagnosis of IHD. On the basis of these images, degree of stenosis in the regions of the bilateral carotid artery bifurcation and five regions of the intracranial arteries, ie, bilateral intracranial portions of the internal carotid arteries and the middle cerebral arteries and the basilar artery were estimated. RESULTS: Stenosis of more than 25% narrowing of the diameter of the target arteries was found in 15 patients (22.4%) in the extracranial carotid arteries and in 11 patients (16.4%) in the intracranial arteries. Most of the stenotic lesions were mild. The incidence of extracranial carotid stenosis and the severity of coronary atherosclerosis showed a significant correlation. The mean age of the patients with intracranial arterial lesions was statistically higher than those without intracranial lesions. CONCLUSIONS: Our data suggest that asymptomatic occlusive lesions in the carotid and intracranial arteries are fairly common in Japanese patients with IHD, although the degree of stenosis is relatively mild. Coexistence of carotid atherosclerosis should be suspected in IHD patients with severe coronary atherosclerosis, and the possibility of atherosclerosis in the intracranial arteries should be considered in aged IHD patients.

Adult↗
PubMed1996

Isolation and characterization of a glycosylation mutant from Schizosaccharomyces pombe.

N-Linked oligosaccharides were elongated by glycosylation with mannose and galactose residues in the secretory pathway of Schizosaccharomyces pombe. The wild-type S. pombe cells were agglutinated by the additions of not only concanavalin A lectin, which is specific for mannose residues, but also PNA (from Arachis hypogaea) and RCA (Ricinus communis) lectins, which are specific for terminal galactose residues. By PNA-binding selection, we isolated an S. pombe mutant defective in protein glycosylation. The mutant cells, named gms1, were not agglutinated by PNA or RCA. In contrast, agglutination of the gms1 cells by the addition of concanavalin A was markedly increased. Structural studies on N-linked oligosaccharides from gms1 mutant cells showed that the number of alpha-1,2-linked galactose residues wes markedly reduced, and unsubstituted alpha-1,6-linked polymannose outer chains were attached to the core oligosaccharides.

Anti-Bacterial Agents↗
PubMed1996

[Trigeminal motor paralysis and dislocation of the temporo-mandibular joints].

A 64-year-old woman with diabetes mellitus was admitted to our hospital with left hemiparesis of sudden onset. A brain MRI demonstrated a cerebral infarction in the ventral part of the right lower pons. When left hemiparesis worsened, she had dislocation of the temporo-mandibular joints repeatedly. Then, her lower jaw deviated to the right when she opened her mouth. Also, there was decreased contraction of the right masseter when she clenched her teeth. These findings suggest that there was trigeminal motor paralysis on the right side resulting from involvement of the intrapontine trigeminal motor nerve. She has no history of dislocation of the temporo-mandibular joints. An X-ray film showed that the temporo-mandibular joints were intact. Thus, it is possible that deviation of the lower jaw was the cause of this dislocation. We suspect that dislocation of the temporo-mandibular joints may occur as a complication of unilateral trigeminal motor paralysis. This has not been reported to our knowledge.

Cerebral Infarction↗
PubMed1995

Synthesis of neoglycoproteins using oligosaccharide-transfer activity with endo-beta-N-acetylglucosaminidase.

We describe a novel method for the enzymatic synthesis of neoglycoproteins. Endo-beta-N-acetylglucosaminidase from Arthrobacter protophormiae (Endo-A) had high levels of transglycosylation activity. The enzyme activity of Endo-A was markedly increased by adding 4-L-aspartyl-glycosylamine (GlcNAc-Asn) to the reaction mixture. Digesting (Man)6(GlcNAc)2 with the enzyme in the presence of GlcNAc-Asn gave a mixture of hydrolytic ((Man)6GlcNAc) and transglycosylic ((Man)6(GlcNAc)2-Asn) products. By means of transglycosylation, (Man)6GlcNAc was transferred en bloc to the partially deglycosylated ovalbumin glycopeptide (EEKYN(GlcNAc)LTSVL) concomitant with the hydrolysis of (Man)6-GlcNAc)2Asn. The structure of the transglycosylation product was designated as (Man)6(GlcNAc)2-peptide by amino acid composition and sequence analysis as well as ion mass spectrometry. The enzyme also transferred oligosaccharide to partially deglycosylated ribonuclease B (GlcNAc-protein) during the hydrolysis of (Man)6-(GlcNAc)2Asn. Native ribonuclease B had (Man)5-9 (GlcNAc)2 as its heterogeneous N-linked sugar chains. High performance liquid chromatography showed that all of the N-linked sugar chains of the synthetic neoribonuclease of the pyridylamino derivatives were modified to (Man)6(GlcNAc)2.

Amino Acid Sequence↗
PubMed1995

Isolation and characterization of a novel endo-beta-galactofuranosidase from Bacillus sp.

A soil bacterium capable of growing on a polysaccharide-containing beta(1-->6)galactofuranoside residues derived from the acidic polysaccharide of Fusarium sp. as a carbon source has been isolated. From various bacteriological characteristics, the organism was identified as a Bacillus sp. The bacterium produced beta-galactofuranosidase inductively in the culture media. The most effective inducer for the beta-galactofuranosidase production was a polysaccharide containing beta(1-->5) or beta(1-->6)-linked galactofuranoside residues, but gum arabic, gum guar, gum ghati, arabinogalactam, araban, and pectic acid did not induce the enzyme. The enzyme had three different molecular weight forms. The low molecular-weight form was purified by a combination of Toyopearl HW-55 and DEAE-Toyopearl 650S column chromatographies, and preparative polyacrylamide gel electrophoresis. The molecular weight of the enzyme was estimated to be 67,000 by SDS-polyacrylamide gel electrophoresis. The enzyme was most active at pH 6 and 37 degrees C, and was stable between pH 4 to 8 at 5 degrees C. The action of the enzyme was inhibited by the addition of Cd2+, Co2+, Hg2+, Zn2+, iodoacetic acid, and EDTA. The purified enzyme cleaved beta(1-->5) and beta(1-->6)-linked galactofuranosyl chains. Based upon the mode of liberation of galactofuranosyl residues from pyridylamino-beta(1-->6)-linked galactofuranoside oligomers, the enzyme can be classified as an endo-beta-galactofuranosidase that randomly hydrolyzes the linkage.

Bacillus↗
PubMed1995

[Asymptomatic atheromatous cerebrovascular diseases in patients with acute myocardial infarction--evaluation by brain magnetic resonance angiography].

To investigate the relationship between atherosclerosis in the cerebral and coronary arteries, we examined the prevalence of asymptomatic atheromatous cerebrovascular lesions in patients with acute myocardial infarction (AMI). The subjects consisted of 33 consecutive AMI patients with angiographically proven coronary artery stenosis/occlusion(s) who had no history of ischemic strokes, and 33 age/sex matched controls without a history of coronary heart diseases or/and cerebrovascular diseases. Asymptomatic cerebrovascular lesions were evaluated by magnetic resonance angiography (MRA) with a 3-dimensional time-of-flight method within 2 months after the AMI onset. The evaluated arteries on MRA included the carotid bifurcation and the intracranial arteries (intracranial portion of the internal carotid artery, horizontal portion of the middle cerebral artery, and the basilar artery). Asymptomatic cerebrovascular stenotic lesions (more than 25% stenosis) on MRA were found in 8 AMI patients (24.2%) at the carotid artery bifurcation and 5 (15.2%) in the intracranial arteries, compared to 1 (3.0%) and 3 (9.1%) respectively in control subjects. The lesions in the carotid bifurcation were significantly frequent in the AMI patients (p < 0.05), while those in the intracranial arteries did not differ between the two groups. The AMI patients with the intracranial artery lesions were significantly older than those without such lesions (p < 0.05). The data obtained indicates that the coexistence of asymptomatic atheromatous cerebrovascular diseases, especially the lesions in the carotid bifurcation, should be considered in treating patients with AMI. The older AMI patients, who may have not only extracranial lesions but also intracranial lesions, should be treated more carefully.

Aged↗
PubMed1995

[Sequential neuroimaging in a patient with delayed post-hypoxic leukoencephalopathy].

We described a patient with delayed cerebral demyelination following a post-operatively hypoxic encephalopathy. A 65-year-old man, with a history of exposure to the atomic bomb at Hiroshima in 1945, suffered from hypoxia, hypotension and respiratory acidosis and became unresponsive 10 hours after a laminectomy for lumbar disc herniation, in December 1993. Following an emergent resuscitation, the patient had gradually recovered and could walk 2 weeks later. Three weeks after the insult, however, the patient developed an apallic state with frontal lobe signs. Except an increased level of myelin basic protein in the CSF, there were no other abnormal laboratory findings. Brain CTs showed a leukoaraiosis. MRI one month post-operation, demonstrated extensive high signal intensity areas in the cerebral white matter on T2-weighted image, and a gadolinium-enhanced spotty lesion in the right globus pallidus on T1-weighted image. Three months after the operation, the high signal intensity on T2-weighted image became more intensive and extensive, while the enhanced spotty lesion in the globus pallidus disappeared. The corpus callosum and cerebellar white matter were spared throughout the observation. The SPECT using 123I-IMP showed a hypoperfusion in the frontal lobe at 1 month. Three months later, the hypoperfusion areas extended to the whole cerebral and cerebellar cortices, relatively less affected in the motor area and basal ganglia. The patient had improved slightly over the next few months. We speculate that subclinical vulnerability in the white matter secondary to exposure to the atomic bomb, in addition to the incomplete prolonged hypoxia, hypotension and acidosis, caused selective cerebral demyelination in this patient.

Aged↗