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Biomedical subjects

R Yamauchi

Publications and source records attributed to R Yamauchi.

At least 37 records · Page 2Linked to original sources

Iron-catalyzed reaction products of alpha-tocopherol with methyl 13(S)-hydroperoxy-9(Z),11(E)-octadecadienoate.

alpha-Tocopherol was reacted with methyl 13(S)-hydroperoxy-9(Z), 11(E)-octadecadienoate in the presence of an iron-chelate, Fe(III)-acetylacetonate, at 37 degrees C in benzene. The reaction was carried out either aerobically or anaerobically. The main products of alpha-tocopherol under air were isolated and identified as two stereoisomers of 4a,5-epoxy-8a-hydroperoxy-alpha-tocopherone, four stereoisomers of methyl 9-(8a-dioxy-alpha-tocopherone)-12, 13-epoxy-10(E)-octadecenoate, four stereoisomers of methyl 11-(8a-dioxy-alpha-tocopherone)-12,13-epoxy-9(Z)-octadecenoa te, two stereoisomers of methyl 13(S)-(8a-dioxy-alpha- tocopherone)-9(Z),11(E)-octadecadienoate, and alpha-tocopherol dimer. Besides the 8a-(lipid-peroxy)-alpha-tocopherones, two stereoisomers of methyl 11-(alpha-tocopheroxy)-12(S),13(S)-epoxy- 9(E)-octadecenoate, two stereoisomers of methyl 9-(alpha-tocopheroxy)-12(S), 13(S)-epoxy-10(E)-octadecenoate, and two isomers of methyl (alpha-tocopheroxy)-octadecadienoate were obtained under nitrogen atmosphere. The results indicate that the peroxyl radicals from lipid hydroperoxides prefer to react with the 8a-carbon radical of alpha-tocopherol and the carbon-centered radicals react with the phenoxyl radical of alpha-tocopherol.

Aerobiosis↗

p53 protein and proliferating cell nuclear antigen in eccrine poroma and porocarcinoma. an immunohistochemical study.

The expression of p53 protein and proliferating cell nuclear antigen (PCNA) in 18 eccrine poromas and four porocarcinomas was examined by immunohistochemistry. Immunoreactivity for p53 in eccrine poromas was negative in five tumors, < 10% of tumor cells in one (low expresser), 10-50% in seven (moderate expressers), and > 50% in five (high expressers). The duration of the presence before excision of p53-negative poromas was shorter, and the size of these tumors was smaller in comparison with those of p53-positive poromas. Moreover, all high expressers showed some atypical cells in limited areas. Of the four porocarcinomas, three were high expressers and one a low expresser of p53 protein. The low-expresser tumor showed clinically more rapid growth and histologically no poromatous foci in contrast to the high expressers. No significant correlation was found between p53 protein expression and PCNA positive staining in either eccrine poromas or porocarcinomas. However, the percentages of PCNA-positive cells in porocarcinomas were significantly higher than those in poromas, with no overlapping values. These results suggest that the PCNA index is useful in differentiating between poroma and porocarcinoma and that p53 gene mutation may occur in long-standing eccrine poromas and correlate with atypical changes in histology as well as subsequent progression to porocarcinoma.

Acrospiroma↗

Structural study on an exocellular polysaccharide produced by Lactobacillus helveticus TY1-2.

Lactobacillus helveticus TY1-2 produced an exocellular polysaccharide when it was cultured in reconstituted skim milk. This polysaccharide is a high molecular weight heteropolymer of D-glucopyranosyl, D-galactopyranosyl, and 2-acetamido-2-deoxy-D-glucopyranosyl residues in the molar ratio 3.0:2.8:0.9. The primary structure of the polysaccharide was shown by glycose analysis, methylation analysis, Smith degradation, and NMR spectroscopy to be composed of branched heptasaccharide repeating units having the following structure: [formula: see text]

Carbohydrate Conformation↗

Isolation and characterization of addition products of alpha-tocopherol with peroxyl radicals of dilinoleoylphosphatidylcholine in liposomes.

alpha-Tocopherol was reacted with peroxyl radicals of phosphatidylcholine at 37 degrees C in liposomes. The phospholipid-peroxyl radicals were generated by the reaction of 1,2-dilinoleoyl-3-sn-phosphatidylcholine with a free radical initiator, 2,2'-azobis(2,4-di-methylvaleronitrile), under air. One peak corresponding to the reaction products of alpha-tocopherol with phosphatidylcholine-peroxyl radicals was isolated by reversed-phase high-performance liquid chromatography. Its structure was identified as a mixture of 8a-(phosphatidylcholine-peroxy)-alpha-tocopherones: 1-[9-(8a-peroxy-alpha-tocopherone)-10,12-octadecadienoyl]-2- linoleoyl-3-sn-phosphatidylcholine,1-[13-(8a-peroxy-alpha-tocopherone )-9,11-octadecadienoyl]-2-linoleoyl-3-sn-phosphatidylcholine, 1-linoleoyl-2-[9-(8a, peroxy-alpha-tocopherone)-10,12-octadecadienoyl]-3-sn-pho sph atidylcholine and 1-linoleoyl-2-[13-(8a-peroxy-alpha-tocopherone)-9,11-octadecadi enoyl]-3-sn- phosphatidylcholine. The results indicate that each alpha-tocopherol can trap two peroxyl radicals during the peroxidation of unsaturated phospholipid in liposomes.

Chromatography, High Pressure Liquid↗

Effects of clentiazem on cerebral ischemia induced by carotid artery occlusion in stroke-prone spontaneously hypertensive rats.

BACKGROUND AND PURPOSE: We examined metabolic and functional changes when forebrain ischemia was induced in stroke-prone spontaneously hypertensive rats by bilateral carotid artery occlusion. In addition, the protective effect of clentiazem was evaluated in this model. METHODS: Rats were anesthetized with urethane. Cerebral blood flow was measured with a laser Doppler flowmeter. Cerebral high-energy phosphates and intracellular pH were measured by phosphorus magnetic resonance spectroscopy. Electroencephalographic activity was evaluated as the summation of its amplitude. These parameters were monitored during a 30-minute period of ischemia and recirculation. Clentiazem was given orally as pretreatment (10 mg/kg twice a day for 3.5 days). RESULTS: Bilateral carotid occlusion caused a decrease in cerebral blood flow to approximately 5% of the preischemic level and the disappearance of electroencephalographic activity. Occlusion also caused a decrease in ATP and phosphocreatine (to 48.7 +/- 4.3% and 23.7 +/- 2.2% of preischemic levels, respectively) as well as intracellular pH (from 7.3 +/- 0.1 to 6.0 +/- 0.1). During recirculation the reversal of these changes was variable: high-energy phosphates were partially restored, but electroencephalographic activity and intracellular pH showed little improvement. Hypoperfusion (55.7 +/- 11.5% of the preischemic flow) developed after reactive hyperemia. Pretreatment with clentiazem lessened the decrease in cerebral blood flow (control, 4.8 +/- 1.4%; clentiazem, 14.1 +/- 4.1% of the preischemic level; P < .05) and prevented the disappearance of electroencephalographic activity in some rats during ischemia. Clentiazem also prevented postischemic hypoperfusion and accelerated the restoration of high-energy phosphates, intracellular pH, and electroencephalographic activity during recirculation. CONCLUSIONS: Carotid artery occlusion induced stable forebrain ischemia in stroke-prone spontaneously hypertensive rats. Clentiazem improved the metabolic and functional disturbances that occurred in this ischemic model, and its beneficial effect appeared to be due mainly to the relative preservation of cerebral blood flow during carotid occlusion.

Adenosine Triphosphate↗

[Permanent pacemaker therapy in a community with many elderly people].

To clarify the utility of permanent pacemakers in a society composed largely of elderly people, clinical characteristics, pacemaker characteristics, outcome, and quality of life in a total of 116 patients in a community with many (19.6%) elderly people were evaluated after permanent pacemaker implantation. Patients above age 65 accounted for 88.8%, while those above 80 years accounted for 24.1%. Syncope was the most common observation before pacemaker implantation and emergency care was needed in 35% of patients. Sick sinus syndrome and complete AV block were seen in a majority, while atrial fibrillation with bradycardia was seen in a minority of patients. Although the physiological pacing and ventricular pacing mode (VVI) were used in about 50% each, recently the physiological pacing mode has markedly increased. During the mean follow-up of 26.1 +/- 16.2 months, only four patients died. NYHA 3 symptom improved to NYHA 1 after pacemaker implantation and 72.5% patients of all cases returned to their jobs. We conclude that the permanent pacemaker is effective in improving symptoms and reducing the death rate in elderly patients.

Aged↗

Reaction of alpha-tocopherol with alkyl and alkylperoxyl radicals of methyl linoleate.

alpha-Tocopherol was reacted with alkyl and alkylperoxyl radicals at 37 degrees C in bulk phase. The lipid-free radicals were generated by the reaction of methyl linoleate with the free radical initiator, 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN) under air-insufficient conditions. The products were isolated by high-performance liquid chromatography. Their structures were identified as 2-(alpha-tocopheroxy)-2,4- dimethylvaleronitrile (1), a mixture of methyl 9-(8a-peroxy-alpha-tocppherone)-10(E),12(Z)-octadecadienoate and methyl 13-(8a-peroxy-alpha-tocopherone)-9(Z),11(E)-octadecadienoate (2), methyl 9-(alpha-tocopheroxy)-10(E),12(Z)-octadecadienoate (3a), methyl 13-(alpha-tocopheroxy)-9(Z),12(E)-octadecadienoate (3b), alpha-tocopherol spirodiene dimer (4) and alpha-tocopherol trimer (5). When methyl linoleate containing alpha-tocopherol was oxidized with AMVN under air-sufficient conditions, the main products were 8a-alkylperoxy-alpha-tocopherones (2). In addition to these compounds, 6-O-alkyl-alpha-tocopherols (1, 3a and 3b) were formed when the reaction was carried out under air-insufficient conditions. The results indicate that alpha-tocopherol can react with both alkyl and alkylperoxyl radicals during the autoxidation of polyunsaturated lipids.

Chromatography, High Pressure Liquid↗

Effect of Ca2+ antagonists on high-K+ evoked increase in [Ca2+]i in rat cerebral synaptosomes and hippocampal neurons.

By fura-2 fluorometry, we investigated the direct effects of Ca2+ antagonists including a new benzothiazepine, clentiazem, on the high-K(+)-evoked increase in the concentration of cytosolic free Ca2+ ([Ca2+]i) in rat cerebral synaptosomes and cultured hippocampal neurons. In both preparations, metal ions inhibited the high-K(+)-induced increase in [Ca2+]i, in the following order: La3+ greater than Cd2+ much greater than Ni2+. Although flunarizine and nicardipine inhibited the K(+)-induced increase in [Ca2+]i in synaptosomes, other Ca2+ antagonists, including clentiazem and nitrendipine, had little effect at 10 microM. In hippocampal neurons, clentiazem inhibited the K(+)-induced increase in [Ca2+]i at 10 microM, as did flunarizine and nicardipine. However, nifedipine and nitrendipine had little effect in either cultured neurons or in synaptosomes.

Animals↗

Sacral nerve root cysts manifesting as localized unilateral perineal pain--case report.

A 62-year-old female presented with multiple sacral nerve root cysts manifesting as localized unilateral perineal pain. Myelography just after contrast material injection revealed multiple cysts at the sacral level. However, perioperative dye injection showed hardly any flow in the reverse direction. Only the S3 nerve was constricted by hyperplasia of the dura mater, and adhered to the cyst wall. Other nerves were not constricted, nor adhered to cyst walls. The S3 nerve constriction and tight adhesion was the cause of the pain. The one-way flow of spinal fluid from the spinal subarachnoid space to the cysts is probably closely correlated with cyst formation.

Cysts↗

Induction of a 31,000-dalton stress protein by prostaglandins D2 and J2 in porcine aortic endothelial cells.

Prostaglandin (PG) D2 and PGJ2 stimulated porcine aortic endothelial cells to synthesize a 31,000-dalton protein (termed p31) in a time- and concentration-dependent manner. The induction of p31 synthesis was specific for PGD2, PGJ2 and PGA1 among the various PGs tested. p31 was also synthesized in response to the thiol-reactive agent diethylmaleate and heavy metal sodium arsenite but not to high temperature treatment, platelet-derived growth factor, and 12-O-tetradecanoylphorbol 13-acetate. Using two-dimensional polyacrylamide gel electrophoresis, p31 induced by PGJ2 had an isoelectric point of 5.4, which overlapped exactly with that induced by by arsenite. These results taken together indicate that p31 represents one of the stress proteins whose expression is regulated primarily by thio-active compounds but not by hyperthermia. Furthermore, it was induced by PGD2 and PGJ2 in rat capillary endothelial cells, rat skin fibroblasts, and rat hepatocytes. The data obtained from this study suggest that p31 induced by PGD2 and PGJ2 may play a role in the metabolic regulation of many mammalian cells.

Animals↗

Malignant fibrous histiocytoma of the hypopharynx.

Malignant fibrous histiocytoma has been the most common soft-tissue sarcoma of late adult life. However, it is relatively uncommon in the head and neck. Furthermore, there has been no report of malignant fibrous histiocytoma of the hypopharynx in the literature. The first case of malignant fibrous histiocytoma of the hypopharynx is presented. The patient, a 70-year-old male, underwent extended laryngectomy and elective neck dissection with primary tracheoesophageal shunt operation and pharyngeal myotomy for voice restoration following total laryngectomy. For more than 2 years, there has been no evidence of the disease or metastasis. He has the satisfactory phonatory and swallowing function.

Aged↗

Reaction products of alpha-tocopherol with a free radical initiator, 2,2'-Azobis(2,4-dimethylvaleronitrile).

alpha-Tocopherol was reacted with an alkylperoxyl radical at 37 degrees C in ethanol. 2,2'-Azobis(2,4-dimethylvaleronitrile) was used to generate the alkylperoxyl radicals. The reaction products of alpha-tocopherol were isolated by reverse-phase and normal-phase high performance liquid chromatography, and their structures were characterized by infrared, ultraviolet, 1H and 13C nuclear magnetic resonances and mass spectrometry. They were 8aS-hydroperoxy-alpha-tocopherone, 8aR-hydroperoxy-alpha-tocopherone, a mixture of 7,8-epoxy-8aS-ethoxy-alpha-tocopherone and 7,8-epoxy-8aR-ethoxy-alpha-tocopherone, 8aS-(1R-cyano-1,3-dimethyl)butylperoxy-alpha-tocopherone+ ++, 8aS-(1S-cyano-1,3-dimethyl)butylperoxy-alpha-tocopherone+ ++, a mixture of 8aR-(1R-cyano-1,3-dimethyl)butylperoxy-alpha-tocopherone+ ++ and 8aR-(1S-cyano-1,3-dimethyl)butyl-peroxy-alpha-tocopherone, 4aS,5R-epoxy-8aR-ethoxy-alpha-tocopherone, 4aR,5S-epoxy-8aS-ethoxy-alpha-tocopherone, 4aS,5R-epoxy-8aS-ethoxy-alpha-tocopherone and 4aR,5S-epoxy-8aR-ethoxy-alpha-tocopherone.

Alkylation↗

Effect of GABA (gamma-aminobutyric acid) on neurotransmission in inferior colliculus slices from the guinea pig.

Inferior colliculus (IC) slices from guinea pigs were prepared by cutting the IC parasagittally and incubating the obtained slices in the standard medium. Postsynaptic field potentials (PSFP) were recorded in the superficial layer of the pericentral nucleus (PN) by stimulating the deep layer of the PN. GABA (gamma-aminobutyric acid) and its agonists (muscimol and baclofen) and antagonist (bicuculline) were applied in the perfusion medium. GABA (1-12.5 mM), muscimol (1-200 microM) and (-)-baclofen (0.1-20 microM) reduced the amplitude of the PSFP in a dose-dependent manner. Bicuculline (1-10 microM) enhanced the amplitude of the PSFP and evoked the epileptiform burst discharge (EBD). The incubation of IC slices with methoxypyridoxin (100 microM) and 3-mercaptopropionic acid (100 microM) for 2 h reduced the GABA level of the slice to about 50% of the initial value, at which point a distinct EBD appeared. The application of GABA (5 mM) to the medium in this condition blocked the EBD completely. The removal of chloride from the medium as well as the application of furosemide (100 microM) enhanced the amplitude of the PSFP and also elicited the EBD; GABA application in this case did not block the EBD. These results indicate that GABA plays an inhibitory role in the IC, and that the reduction of GABA and the blockade of GABA function cause the appearance of EBD in the IC.

Action Potentials↗

Effects of temperature on the oxygen consumption in thin slices from different brain regions.

The oxygen consumption of brain slices from 12 different regions of the guinea pig brain was measured and the effects of temperature on the consumption was investigated. At 37 degrees C the oxygen consumption in cerebral gray matter and inferior colliculus was higher than that of other regions, whilst the consumption in cerebral white matter and brainstem was approximately half of that in cerebral gray matter. In any region lowering the tissue temperature from 37 to 28 degrees C reduced the oxygen consumption by 6-8% of the value obtained at 37 degrees C per one degree. At 21 degrees C the consumption was decreased to 15% of the value obtained at 37 degrees C. It is notable that the consumption in hippocampal slices tested was remarkably increased by raising the temperature up to 50 degrees C and no consumption was observed at 55 degrees C.

Animals↗

Enhancement of the oxygen consumption in the hippocampal slices of the guinea pig induced by glutamate and its related substances.

The effects of glutamate (Glu), kainate (Ka), and N-methyl-D-aspartate (NMDA) on the oxygen consumption of the hippocampal slices of the guinea pig were investigated. The oxygen consumption of slices at resting state was 8.43 mumol/g protein/min. Bath application of Ka (1 x 10(-8) to 1 x 10(-6) M), NMDA (1 x 10(-8) M to 1 x 10(-4) M), and Glu (1 x 10(-5) M to 5 x 10(-4) M) enhanced the oxygen consumption dose-dependently in the similar tendency although the effective doses varied for the different excitants. Subsequently the consumption was maximal at approximately 140% of the resting level. The enhancement of the oxygen consumption due to NMDA and Glu was antagonized by DL-2-amino-5-phosphonovaleric acid (APV) for NMDA and by glutamic acid diethylester (GDEE) and Joro spider toxin (JSTX) for Glu. From these results it was suggested that the increase of the oxygen consumption observed here must reflect the neuronal activation induced by these excitants.

Action Potentials↗