Pacemaker dermatitis from titanium.
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Aged↗
Biomedical subjects
R Yamauchi
Publications and source records attributed to R Yamauchi.
Synthesis of 5-hydroxy-2-(beta-D-ribofuranosyl)pyran-4-one from a pyranulose glycoside.
The synthesis of 5-hydroxy-2-(beta-D-ribofuranosyl)pyran-4-one (9) is described. Treatment of pyranulose glycoside with bromine in carbon tetrachloride afforded brompyranulose glycoside in 90% yield. The reaction of (6S)- and (6R)-4-bromo-6-hydroxy-6-(2,3,5-tri-O-benzoyl-beta-D-ribofuranosyl)-6H- pyran-3-one (2) in acidic media was examined with the following results: the reaction of 2 with trifluoroacetic acid (TFA) in dioxane afforded a mixture of 5-hydroxy-2-(2,3,5-tri-O-benzoyl-beta-D-ribofuranosyl)pyran-4-one (3) and its furan derivative 5-hydroxy-2-{5-(benzoyloxy)methyl]furan-2-yl}pyran-4-one (4), but the use of hydrochloric acid formed the bromofurfural, 3-bromo-5-(2,3,5-tri-O-benzoyl-beta-D-ribofuranosyl)-2-furancarboxyal dehyde only. Acetylation of a mixture (3 and 4) with acetic anhydride facilitated product separation to give the corresponding acetates 5-acetoxy-2-(2,3,5-tri-O-benzoyl-beta-D-ribofuranosyl)pyran-4-one (5) and 5-acetoxy-2-{5-[(benzoyloxy)methyl]furan-2-yl}pyran-4-one (6). Treatment of 5 with hydrazine afforded 3-hydroxymethyl-6-(beta-D-ribofuranosyl)-1H-pyridazin-4-one in 43% yield. Debenzoylation of 5 with aq ammonia gave 9 in 50% yield.
Anti-Bacterial Agents↗
Antioxidant activity of a novel vitamin E derivative, 2-(alpha-D glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol.
A novel vitamin E derivative, 2-(alpha-D-glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol (TMG), has excellent water-solubility (> 1 x 10[3] mg/ml). The antioxidant activity of TMG was investigated. Kinetic studies of the inhibition of radical-chain reaction of methyl linoleate in solution demonstrated that the peroxyl radical-scavenging activity was not changed by the replacement of phytiyl side chain of vitamin E to glucosyl group. TMG acted as an effective inhibitor on lipid peroxidation of egg yolk phosphatidylcholine (PC)-liposomal suspension induced by a water-soluble and a lipid-soluble radical generator, 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) and 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN). Its effectiveness was higher than that of ascorbic acid (AsA) when liposomal suspension was exposed to a lipid-soluble radical generator, AMVN. TMG also showed an excellent antioxidant activity on cupric ion-induced lipid peroxidation of PC-liposomal suspension, and suppressed the oxidation of rat brain homogenate which contained trace level of iron ion. On the other hand, AsA acted as a prooxidant on both the cupric ion-induced liposomal peroxidation and the oxidation of rat brain homogenate. When human plasma was exposed to either AAPH or AMVN, the accumulation of cholesteryl ester hydroperoxides was retarded by the addition of TMG.
Adult↗
Reaction of alpha-tocopherol in heated bulk phase in the presence of methyl linoleate (13S)-hydroperoxide or methyl linoleate.
alpha-Tocopherol and methyl (9Z,11E)-(S)-13-hydroperoxy-9,11-octadecadienoate (13-MeLOOH) were allowed to stand at 100 degrees C in bulk phase. The products were isolated and identified as methyl 13-hydroxyoctadecadienoate (1), stereoisomers of methyl 9,11,13-octadecatrienoate (2), methyl 13-oxo-9,11-octadecadienoate (3), epoxy dimers of methyl linoleate with an ether bond (4), a mixture of methyl (E)-12,13-epoxy-9-(alpha-tocopheroxy)-10-octadecenoates and methyl (E)-12,13-epoxy-11-(alpha-tocopheroxy)-9-octadecenoates (5), a mixture of methyl 9-(alpha-tocopheroxy)-10,12-octadecadienoates and methyl 13-(alpha-tocopheroxy)-9,11-octadecadienoates (6), alpha-tocopherol spirodiene dimer (7), and alpha-tocopherol trimer (8). alpha-Tocopherol and 13-MeLOOH were dissolved in methyl myristate, and the thermal decomposition rate and the distributions of reaction products formed from alpha-tocopherol and 13-MeLOOH were analyzed. alpha-Tocopherol disappeared during the first 20 min, and the main products of alpha-tocopherol were 5 and 6 with the accumulation of 1-4 which were the products of 13-MeLOOH. The results indicate that the alkyl and alkoxyl radicals from the thermal decomposition of 13-MeLOOH could be trapped by alpha-tocopherol to produce 5 and 6. The reaction products of alpha-tocopherol during the thermal oxidation of methyl linoleate were compounds 6 and 7. Since the radical flux during the autoxidation might be low, the excess alpha-tocopheroxyl radical reacted with each other to form 7.
Chromatography, High Pressure Liquid↗
Cloning of hamster preproendothelin-1 cDNA and its expression in the heart.
To elucidate the pathophysiologic roles of endothelin-1 (ET-1) in the heart, we first cloned and sequenced a part of hamster preproET-1 cDNA from the heart of the CHF146 hamsters. The amino acid sequence has 89% homology to that of rat preproET-1 in the cloned part. The deduced hamster 21-residue mature ET-1 is identical to human, rat, canine, and mouse ET-1. In the next step we investigated the expression of preproET-1 mRNA in the failing heart of CHF146 hamsters. For this purpose, we used 46-week-old CHF146 hamsters and age-matched control healthy hamsters. Left ventricular (LV) + dP/dtmax was significantly lower in CHF146 hamsters than in control hamsters. LV end-diastolic pressure was significantly higher in CHF146 hamsters than in control hamsters, as was central venous pressure. These results suggested that the CHF146 hamsters developed congestive heart failure. The expression of preproET-1 mRNA was greatly enhanced in the LV of the CHF146 hamsters. Because it has been reported that ET-1 induces cardiac hypertrophy and injury to cardiac myocytes in addition to its potent positive inotropic and chronotropic actions, the present findings suggest that endogenous ET-1 plays pathophysiologic roles in the failing heart of CHF146 hamsters.
Amino Acid Sequence↗
Preparation and characterization of 8a-(phosphatidylcholine-dioxy)-alpha-tocopherones and their formation during the peroxidation of phosphatidylcholine in liposomes.
alpha-Tocopherol was reacted with the phosphatidylcholines (PCs), 1-palmitoyl-2-linoleoyl-3-sn-PC (PLPC), 1-palmitoyl-2-linolenoyl-3-sn-PC, 1-palmitoyl-2-arachidonoyl-3-sn-PC (PAPC) and 1-stearoyl-2-arachidonoyl-3-sn-PC, in the presence of the free radical initiator, 2,2'-azobis (2,4-dimethylvaleronitrile), at 37 degrees C. The addition products of alpha-tocopherol with the PC peroxyl radicals were isolated and identified as 8a-(PC-dioxy)-alpha-tocopherones, in which the peroxyl radicals derived from each PC molecule attacked the 8a-position of the alpha-tocopheroxyl radical. The antioxidative efficiency of alpha-tocopherol against the peroxidation of PLPC and PAPC in liposomes was assessed by the formation of the reaction products of alpha-tocopherol. When alpha-tocopherol was oxidized in the presence of the water-soluble free radical initiator, 2,2'-azobis (2-amidinopropane) dihydrochloride, epoxy-alpha-tocopherylquinones were mainly produced together with 8a-(PC-dioxy)-alpha-tocopherones and alpha-tocopherylquinone. The yield of alpha-tocopherylquinone was increased by treating each sample with dilute acid which indicates the presence of tocopherone precursors other than the 8a-(PC-dioxy)-alpha-tocopherones. The same products were also detected from iron-dependent peroxidation, although the yields were very low.
Amidines↗
Pharmacological profile of T-0201, a highly potent and orally active endothelin receptor antagonist.
The authors studied the pharmacological properties of N-(6-(2-(5-bromopyrimidin-4-yl)-4-(2-hydroxy-1, 1-dimethylethyl)benzensulfonamide sodium salt sesquihydrate (T-0201), a new nonpeptide endothelin (ET) receptor antagonist, in vitro and in vivo. In binding studies, T-0201 competitively antagonized the specific binding of [125I]-ET-1 to human cloned ETA receptors (the Ki value was 0.015 +/- 0.004 nM). T-0201 weakly inhibited [125I]-ET-1-binding to human cloned ETB receptors; the Ki value was 41 +/- 21 nM. T-0201 shifted the concentration-response curve of ET-1-induced contraction of the isolated rat aorta (ETA receptors) to the right (pA2 = 9.0 +/- 0.2). In the isolated rat trachea, a selective ETB agonist sarafotoxin S6c-induced contraction was inhibited by T-0201 (pA2 = 6.8 +/- 0.3). T-0201 also caused the inhibition of ET-1-induced contraction of the isolated rabbit pulmonary artery (pA2 = 5.7 +/- 0.3). In anesthetized rats, T-0201 (0.01-1 mg/kg) inhibited the pressor response to exogenous big ET-1 (1 nmol/kg i.v.), after both i.v. and p.o. administration, in a dose-dependent manner. The significant inhibitory effect of orally administered T-0201 on big ET-1-induced pressor response lasted for 4 hr at 0.1 mg/kg and for 8 hr at 1 mg/kg. Thus the present study demonstrates that T-0201 is a highly potent, long-lasting, orally active and selective ETA receptor antagonist.
Animals↗
Synthesis of a novel vitamin E derivative, 2-(alpha-D-glucopyranosyl) methyl-2,5,7,8-tetramethylchroman-6-ol, by alpha-glucosidase-catalyzed transglycosylation.
A novel derivative of vitamin E, vitamin E glucoside, was synthesized from 2-hydroxymethyl-2,5,7,8-tetramethylchroman-6-ol and maltose in a solution containing DMSO by transglycosylation with alpha-glucosidase from Saccharomyces species. The glycosylated product was identified as 2-(alpha-D-glucopyranosyl)methyl-2,5,7,8-tetramethylchroman-6-ol (TMG) by mass spectrometry and nuclear magnetic resonance spectroscopy. The optimal pH of transglycosylation was 5.5, and the yield of TMG increased as the concentration of maltose increased. TMG has high solubility in water (> 1 x 10(3) mg/mL). The 1,1-diphenyl-2-picrylhydrazyl radical scavenging activity of TMG was found to be nearly the same as those of alpha-tocopherol, Trolox (2-carboxy-2,5,7,8-tetramethylchroman-6-ol), and ascorbic acid.
Antioxidants↗
Fixed drug eruption caused by iopamidol, a contrast medium.
We report a patient who developed a fixed drug eruption caused by the contrast medium, Iopamidol. We diagnosed it by her episode pattern and the results of patch tests. This substance has not been previously implicated as a cause of fixed drug eruption. Immunohistochemical studies showed Fas expression in keratinocytes of the lesion, but not in the uninvolved skin. This finding may explain the preferential localization of fixed drug eruption.
Adult↗
Oxidation of alpha-tocopherol during the peroxidation of dilinoleoylphosphatidylcholine in liposomes.
Liposomal suspensions of dilinoleoylphosphatidylcholine (DLPC) containing alpha-tocopherol (0.1 mol%, based on DLPC were oxidized at 37 degrees C. The oxidation was initiated by a lipid-soluble or water-soluble free radical initiator, or by the addition of CuSO4 and fructose. In all the oxidation systems, alpha-tocopherol suppressed the formation of DLPC hydroperoxides until all the alpha-tocopherol had been depleted. The oxidation products of alpha-tocopherol were 8a-alkyldioxy-alpha-tocopherones, 5,6-epoxy-alpha-tocopherylquinone, 2,3-epoxy-alpha-tocopherylquinone, and alpha-tocopherylquinone. The 8a-alkyldioxy-alpha-tocopherones were decomposed in the liposomes primarily by being hydrolyzed to produce alpha-tocopherylquinone. The results indicate that alpha-tocopherol can trap peroxyl radical to form 8a-alkyldioxy-alpha-tocopherones which are hydrolyzed to alpha-tocopherylquinone in phospholipid bilayers. In another oxidation pathway, alpha-tocopherol may be oxidized by peroxyl radicals to form isomeric epoxy-alpha-tocopherylquinones.
Amidines↗
Structure of an exocellular polysaccharide of Lactobacillus helveticus TN-4, a spontaneous mutant strain of Lactobacillus helveticus TY1-2.
Lactobacillus helveticus strain TN-4, a spontaneous mutant strain of Lactobacillus helveticus TY1-2, produced an exocellular polysaccharide from reconstituted skim milk. On the basis of the results of methylation analysis, enzymatic digestion, mild Smith degradation, mild acid hydrolysis, acetolysis, and 1D and 2D 1H-NMR spectroscopy, it was concluded that the polysaccharide has a D-galactofuranose containing hexasaccharide repeating unit with the following structure: [formula see text]
Animals↗
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↗
Successful treatment of systemic sclerosis with topical PUVA.
Treatment of a 43-year-old woman with systemic sclerosis with 8-methoxypsoralen and ultraviolet. A radiation (PUVA) resulted in the significant clinical and histological improvement of skin lesions without side effects.
Adult↗
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↗
Areolar sebaceous hyperplasia with a Fordyce's spot-like lesion.
Fordyce's spot-like lesions were observed in both areolae of a 43-year-old female. The histology of the lesions showed sebaceous hyperplasia.
Adult↗
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↗