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T Namba

Publications and source records attributed to T Namba.

At least 235 records · Page 13Linked to original sources
PubMed1988

Synthesis and mutagenicity of a ring-A-aromatized bile acid, 3-hydroxy-19-nor-1,3,5(10)-cholatrien-24-oic acid.

It has been presumed that ring-A-aromatized bile acids are produced from biliary bile acids by intestinal flora and the acids thus formed participate in the large bowel carcinogenesis. One of these acids is probably 3-hydroxy-19-nor-1,3,5(10)-cholatrien-24-oic acid, judged from the literatures. Consequently, this acid was synthesized from previously prepared 3-methoxy-19-nor-1,3,5(10)-cholatrien-24-ol. The phenolic ether was successively oxidized with pyridinium chlorochromate and wet silver oxide to give 3-methoxy-19-nor-1,3,5(10)-cholatrien-24-oic acid in high yield, which, after successive treatments with methanol containing a catalytic amount of p-toluenesulfonic acid, a combination of aluminum chloride and ethanethiol, and alkali, gave the desired compound in satisfactory yield. The compound was not mutagenic in Salmonella tester strains TA 98 and TA 100, but it increased the mutagenicity of 2-aminoanthracene when both were applied to plates together. When compared with cholic, deoxycholic, and lithocholic acids, the investigated compound exhibited about two to threefold increase of mutagenicity in the latter assay.

Bile Acids and Salts↗
PubMed1987

Enzymes involved in the formation of 3 beta, 7 beta-dihydroxy-12-oxo-5 beta-cholanic acid from dehydrocholic acid by Ruminococcus sp. obtained from human intestine.

Ruminococcus sp. PO1-3 from human intestinal flora reduced dehydrocholic acid to 3 beta-hydroxy-7,12-dioxo-5 beta-cholanic acid by means of the enzyme 3 beta-hydroxysteroid dehydrogenase (Akao, T., Akao, T., Hattori, M., Namba, T. and Kobashi, K. (1986) J. Biochem. (Tokyo) 99, 1425-1431). This bacterium and its crude extract gave rise to another product, showing a lower RF value on TLC, from dehydrocholic acid. The product was identified as 3 beta, 7 beta-dihydroxy-12-oxo-5 beta-cholanic acid. The crude extract reduced 7-ketolithocholic acid and its methyl ester, but not 6-ketolithocholic acid and 12-ketochenodeoxycholic acid, in the presence of NADPH, and oxidized ursodeoxycholic acid and beta-muricholic acid, but not cholic acid, chenodeoxycholic acid, deoxycholic acid and hydrocholic acid, in the presence of NADP+. Therefore, besides 3 beta-hydroxysteroid dehydrogenase, 7 beta-hydroxysteroid dehydrogenase was shown to be present in this bacterium. The two dehydrogenases were clearly separated from each other by butyl-Toyopearl 650 M column chromatography. From dehydrocholic acid, 7 beta-hydroxy-3,12-dioxo-5 beta-cholanic acid was produced by 7 beta-hydroxysteroid dehydrogenase and 3 beta, 7 beta-dihydroxy-12-oxo-5 beta-cholanic acid was produced by combination of two enzymes, 7 beta- and 3 beta-hydroxysteroid dehydrogenase.

3-Hydroxysteroid Dehydrogenases↗
PubMed1987

Adverse cardiovascular effects of anticholinesterase medications.

Anticholinesterase medications (anti-ChEs) play a significant role in the diagnosis and treatment of myasthenia gravis (MG). The primary effect on the heart produced by a surfeit of ACh is bradyarrhythmias with consequent fall in cardiac output and hypotension; yet, adverse cardiac reactions to these agents have been reported relatively infrequently. The authors describe 12 patients with MG from a pool of more than 1,000 who suffered hypotensive episodes related to use of anti-ChEs. The 12 patients (seven male, five female) had a mean age of 62.6 years; of these, eight adverse reactions occurred after edrophonium, two after neostigmine, and two after pyridostigmine. Seven patients had a recent increase in anti-ChEs and none had a decrease in dosage. Nine patients suffered either from severe sinus bradycardia, (20 beats/min), junctional bradycardia, or complete AV dissociation. Two patients had paradoxic sinus tachycardia and all had syncopal or near-syncopal episodes. Evidence for cholinergic stimulation of other organs was generally lacking. No recurrence appeared with reduction of the dose of anti-ChEs or discontinuation of the drug. The authors believe that these agents should be given with caution to patients with inflammatory, infiltrative, or degenerative disease of the conduction systems, patients being treated with digitalis, calcium-channel antagonists or beta blockers, patients with myocardial ischemia, and elderly patients. Appropriate resuscitative equipment should be readily available.

Adult↗
PubMed1987

The course of myasthenia gravis and therapies affecting outcome.

The course of 1,487 patients with myasthenia gravis followed between 1940 and 1985 for a mean of 18 years provides further evidence that the distribution, severity, and outcome of the disease are determined during the first 1 to 3 (occasionally 5) years after onset, suggesting that injury to acetylcholine receptors occurs mainly during this time. In 14%, the disease remained clinically localized to the extraocular muscles, and in the remaining 86% became generalized, in 87% within a year, with the disease reaching maximum severity within the first year after onset of symptoms in 55%, during the first 3 years in 70%, and during the first 5 years in 85%. Male patients tended to have more rapid progression of disease, higher mortality, and lower rates of remission and improvement than females. From 1940 to 1957, when management relied on anticholinesterase compounds, endotracheal intubation or tracheostomy and negative pressure assisted ventilation for respiratory failure, and thymectomy in 26% of patients and thymomectomy in 8%, 31% of patients with generalized myasthenia gravis died of the disease (29% of these during the first year after onset, 27% during the second and third years, and 17% during the fourth and fifth years), 32% improved, 23% remained unchanged, 10% went into remission, and only 5% were worse during the last year seen than during the worst of the first 3 years (or 5 years in the minority of patients who reached maximum weakness after 3 years). From 1958 to 1965, during which time the management of respiratory failure was improved by positive pressure and volume controlled ventilation and improved intensive care, mortality fell to 14% (p less than 0.005), and a higher proportion remained unchanged (p less than 0.005). From 1966 to 1985, when over half the patients received adrenal cortical steroids, mortality fell to 7% (p less than 0.005) and the proportion who improved rose to 47% (p less than 0.05). Even though the patients who received steroids usually had more severe myasthenia, they had a higher rate of improvement than those who received no steroid, 54% compared to 39% (p less than 0.005). Thymectomy was performed in one-fourth of patients with generalized myasthenia gravis, more frequently in young females and those with more severe weakness, and less often in older males and those with less severe weakness.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1986

3 beta-Hydroxysteroid dehydrogenase of Ruminococcus sp. from human intestinal bacteria.

Ruminococcus sp. PO1-3 obtained from human intestinal flora is able to reduce dehydrocholate as well as 3-ketoglycyrrhetinate. From this bacterium dehydrocholate- and 3-ketoglycyrrhetinate-reducing activities were purified one thousand-fold together with 3-ketocholanate-reducing and 3-beta-hydroxyglycyrrhetinate (glycyrrhetic acid) oxidizing activities by means of Matrex Red A, Sephadex G-200 and Octyl-Sepharose column chromatography. The purified enzyme catalyzed the reduction of dehydrocholic acid to 3 beta-hydroxy-7,12-diketocholanic acid and of 3-ketocholanic acid to 3 beta-hydroxycholanic acid. Studies on substrate specificity revealed that the enzyme had absolute specificity for the beta-configuration of a hydroxyl group at the 3 position of bile acid and steroids having no double bond in the A/B ring. This enzyme was neither beta-hydroxysteroid dehydrogenase [EC 1.1.1.51] nor 3 beta-hydroxy-delta 5-steroid dehydrogenase [EC 1.1.1.145], but a novel type of enzyme, defined as 3 beta-hydroxysteroid dehydrogenase.

3-Hydroxysteroid Dehydrogenases↗