3 beta,16 alpha,19-Trihydroxy-5-androsten-17-one and 16 alpha,17-dihydroxy-4-androstene-3,17-dione were synthesized from the 5 alpha-bromo-6 beta,19-epoxy-17-ketone derivative 1, using the bromination at C-16 alpha of the 17-ketone 1 and the controlled alkaline hydrolysis of the 16 alpha-bromo-17-ketones 2 and 11 as key reactions. Zinc dust reductive cleavage of the 6 beta,19-epoxy-16 alpha-hydroxy-17-ketones 4 and 12, produced by controlled hydrolysis, gave the corresponding 19-alcohol derivatives 6 and 14, which were rearranged to the 17 beta-hydroxy-16-ketones 7 and 15 when treated with sodium hydroxide. The 3 beta,16 alpha,17 beta,19-tetrol 8 was obtained from the 16 alpha-ketol 6 by reaction with sodium borohydride.

Androstenedione↗

PubMedDate not supplied

Amino acid sequence and function of rubredoxin from Desulfovibrio vulgaris Miyazaki.

Rubredoxin was purified from Desulfovibrio vulgaris Miyazaki. It was sequenced and some of its properties determined. Rubredoxin is composed of 52 amino acids. It is highly homologous to that from D. vulgaris Hildenborough. Its N-terminal methionyl residue is partially formylated. The millimolar absorption coefficients of the rubredoxin at 489 nm and 280 nm are 8.1 and 18.5, respectively, and the standard redox potential is +5 mV, which is slightly higher than those of other rubredoxins. Rubredoxin, as well as cytochrome c-553, was reduced with lactate by the action of lactate dehydrogenase of this organism, and the reaction was stimulated with 2-methyl-1,4-naphthoquinone. It is suggested that rubredoxin, in collaboration with membranous quinone, functions as a natural electron carrier for cytoplasmic lactate dehydrogenase of this organism, whereas cytochrome c-553 plays the same role for periplasmic lactate dehydrogenase.

Amino Acid Sequence↗

PubMedDate not supplied

Immunohistochemical analysis of platelet-derived growth factor-B expression in myocardial tissues in hypertrophic cardiomyopathy.

Intimal and/or medial hyperplasia of intramyocardial small vessels is thought to be one of the causes of myocardial ischemia in hypertrophic cardiomyopathy (HCM). However, the pathogenesis of such vascular lesions in HCM is not yet known. To evaluate the pathogenic role of platelet-derived growth factor (PDGF-B) and basic fibroblast growth factor (b-FGF), which have a potential to induce cellular and molecular changes observed in the vessels in HCM, we examined the expression of these molecules and PDGF receptors in cardiac tissues from six patients with HCM and seven controls using immunohistochemistry. The percentage of PDGF-B positive cells in the myocyte population in HCM was significantly higher than that in controls (52.6 +/- 16.2 (mean +/- SD) vs. 21.6 +/- 9.6, p < 0.01). PDGF-B was also observed in vascular regions in HCM (61.1 +/- 25.5% of arterioles) but not in controls. There were no significant differences in the expression of b-FGF and PDGF receptors in the myocyte and non-myocyte populations and the vascular regions between the HCM and control groups. Our study revealed that the expression of PDGF-B protein was up-regulated in HCM, suggesting the contribution of this molecule to the development of intramyocardial vasculopathy.

Adolescent↗

PubMedDate not supplied

In vitro mercury uptake by human acatalasemic erythrocytes.

Human acatalasemic erythrocytes had only 0.01 to 0.06X the uptake found in normal erythrocytes with hydrogen peroxide, and 0.06 to 0.24X the uptake without hydrogen peroxide in regard to their ability of in vitro mercury uptake from air saturated with mercury vapor. Normal erythrocytes with hydrogen peroxide took up 9.3 to 37.4X more mercury than cells without hydrogen peroxide, whereas acatalesemic cells with hydrogen peroxide took up 2.4 to 5.8X more mercury than cells without hydrogen peroxide. Similar results were obtained from normal and acatalasemic hemolysates. In addition, the concentration of hydrogen peroxide affected the uptake of mercury by both normal and acatalasemic erythrocytes. Data indicate that the catalase-hydrogen peroxide system plays a role in mercury uptake, presumably by mercury oxidation, since oxidation states of the mercury were never determined in these studies.

Acatalasia↗

PubMedDate not supplied

Mercury uptake in vivo by normal and acatalasemic mice exposed to metallic mercury vapor (203Hg degrees) and injected with metallic mercury or mercuric chloride (203HgCl2).

Levels of mercury in the brain and liver of acatalasemic mice immediately following exposure to metallic mercury vapor or injection of metallic mercury were higher than those found in normal mice. Acatalasemic mice had decreased levels of mercury in the blood and kidneys when the levels were compared with those of normal mice, which indicated that catalase plays a role in oxidizing and taking up mercury. Thus, the brain/blood or liver/blood ratio of mercury concentration in acatalasemic mice was significantly higher than that of normal mice. These results suggest that metallic mercury in the blood easily passed through the blood-brain or blood-liver barrier. The levels of mercury distribution to the kidneys of normal and acatalasemic mice, 1 hr after injection of mercuric chloride solution, were higher than that of normal and acatalasemic mice, respectively, 1 hr after injection of metallic mercury.

Animals↗

PubMedDate not supplied

Reduction of mercuric ion and exhalation of mercury in acatalasemic and normal mice.

A significant difference in the amount of exhaled mercury per hour between normal and acatalasemic mice was observed in 7 of 11 experiments for different periods of time. The total amount of mercury exhaled from acatalasemic mice was significantly higher than those of normal mice. The results confirm that the reduction of mercuric ion to metallic mercury occurs by recycling of mercury in the tissues and reoxidized metallic mercury to mercuric ion by catalase. Mercuric ion was reduced to metallic mercury in the presence of superoxide anion in vitro. The reduction rate of mercuric ion to metallic mercury in the presence of both superoxide anion and cytochrome C or nitro blue tetrazolium was higher than that in the presence of superoxide anion alone, and the reduction of mercuric ion by NADPH or NADH was also observed. The reduction of mercuric ion to metallic mercury by liver homogenates of acatalasemic mice was higher than that of normal mice.

Acatalasia↗

PubMedDate not supplied

Facial nerve neuromas: CT findings.

Although neuromas of the facial nerve are rare, they present with uniform clinical and radiological findings. Their pluridirectional tomography findings have been well described; however, the appearance of the intracranial extension of the neuroma which is best visualized by CT has not been emphasized. We report five cases of facial nerve neuromas with particular attention to their intracranial extension. For comparative purposes we also have reviewed 10 cases of acoustic and eight cases of trigeminal neuromas, all involving the cerebellopontine angle (CPA) and the middle cranial fossa. Two of the five facial nerve neuromas affected the second and third segments of the facial canal, and three involved both the CPA and the middle cranial fossa spreading across the midpetrosal bone. This type of tumor extension seems to be characteristic of facial nerve neuromas. In acoustic and trigeminal neuromas the tumor crossing toward the middle fossa takes place via the tentorial hiatus (acoustic) and the petrous apex (trigeminal).

Adult↗

PubMedDate not supplied

Electrolyte and osmolality in alcoholics during experimentally induced intoxication.

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Adult↗

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Adrenal function and alcoholism. I. Serum cortisol.

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Adaptation, Physiological↗