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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
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↗
PubMed1995

[Warfarin therapy and chlorella].

Warfarin potassium (warfarin) is one of anticoagulants. Its anticoagulant effect is induced by inhibiting vitamin K in a complex manner. It is used effectively and safely in preventing cerebral embolism of cardiac origin, provided that thrombotest (TT) values is maintained from 10 to 20%. A 75-year-old man with atrial fibrillation and cardiomyopathy had cerebral embolism in the territory of the right middle cerebral artery. Warfarin therapy was started to prevent the recurrence of embolic stroke. TT values had been well controlled until intake of chlorella, but they rose above the therapeutic limit after its intake. There was no evidence of discontinuing warfarin, or taking drugs containing vitamin K or Natto. Chlorella is one of vitamin K-rich foods. Thus, it may inhibit the anticoagulant effect of warfarin.

Aged↗
PubMed1994

Comparative clinicopathological and immunohistochemical study of ras and p53 in flat and polypoid type colorectal tumours.

Mutations in oncogenes and tumour suppressor genes may have an important oncogenic role. Although flat type tumours have been frequently detected in recent years, ras and p53 expressions have not been studied in these tumours. Using a monoclonal and polyclonal antibody to the ras p21 and p53 product, paraffin wax embedded sections of 98 colorectal tumours (43 cases of the flat type colorectal tumour and 55 cases of polypoid type tumour) were stained using the immunoperoxidase technique. Staining was evaluated by light microscopic examination. Positive staining rate of ras p21 for the flat type was 0%; for the polypoid type, it was 60% in cancer with submucosal invasion, 82% in adenoma with high grade dysplasia, and 0% in adenoma with low grade dysplasia. The positive staining rate of p53 for the flat type was 50% in submucosal cancer, 9% in adenoma with high grade dysplasia, and 0% in adenoma with low grade dysplasia. For the polypoid type, it was 40% in submucosal cancer, 12% in adenoma with high grade dysplasia, and 0% in adenoma with low grade dysplasia. The intermediate staining rate of p53 in the polypoid type was 20% in submucosal cancer and 41% in adenoma with high grade dysplasia. It was seen that p53 was commonly expressed in both flat and polypoid lesions, p21 was not expressed in flat lesions, whereas it was commonly expressed in polypoid neoplasms. In the flat type cancer, a genetic change different from that of the polypoid type cancer is suggested.

Adenoma↗