Neurotoxicity of polystyrene containers detected in a closed tissue culture system.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Cochran.
Explore the source record for details and available documents.
The activity of 17 beta-estradiol dehydrogenase (E.C. 1.1.1.62) was measured, and its distribution in the subcellular fractions of bovine placenta was compared. Assay of activity was based on the formation of radioactive estrone from 17 beta[4(-14)C]-estradiol. Either NAD+ or NADP+ can serve as cofactor for the enzyme. The nuclear and microsomal fractions of the placental homogenate exhibited the highest specific enzymatic activities before and after treatment with Triton X-100. Electron micrographs of these two fractions prior to treatment with Triton X-100 showed satisfactory purity. 17 beta-estradiol dehydrogenase from bovine placenta exhibits a pH optimum of about 9.5-10.5, and is activated by 5 x 10(-6)M ZnCl2; comparable concentrations of CaCl2 and MgCl2 inactivate the enzyme. The apparent Michaelis constants, Km, for 17 beta-estradiol and NAD+ are 1.4 x 10(-6)M and 5.5 x 10(-5)M respectively. No 17 alpha-estradiol dehydrogenase activity was demonstrable when using 17 alpha-estradiol as substrate.
Explore the source record for details and available documents.
During a four year period 6 patients from the total of 120 on home dialysis developed pericarditis with effusions. Plasma fibrinolytic activity, measured by euglobulin clot lysis time, was significantly reduced in these patients compared with either normal controls or dialysis patients without pericarditis. These dialysis patients without pericarditis as a group tended to have reduced plasma fibrinolytic activity compared with controls, but the difference was not significant. It is suggested that a reduction in the body's fibrinolytic activity may be a factor in the development of fibrinous pericarditis in chronic renal failure.
Autoradiographs of the kidneys of rachitic rats dosed in vivo with 250 pmoles 25-hydroxycholecaliferol (25-OHD3) and 3H-leucine showed increased grain counts in portions of proximal renal tubules. On incubation of kidney slices the synthesis of only 1 cytosol protein was found to be stimulated by the steroid. On disc gel electrophoresis it had the characteristics of renal calcium binding protein.
The present study describes the response to small oral doses (1--10 microgram/day) of 24,25-DHCC in man. Contrary to expectation, 24,25-DHCC was as potent as 1,25-DHCC in increasing intestinal absorption of calcium both in normal persons and in patients with a variety of disorders of calcium metabolism. Despite this increase in intestinal absorption, plasma and urine calcium did not increase after 24,25-DHCC as they did after 1,25-DHCC. Metabolic balance studies showed calcium balances to increase by 1.6 to 11.5 mmoles/day in 5 of the 6 patients studied. 24,25-DHCC increased intestinal absorption of calcium equally well in anephric patients, suggesting that conversion of 24,25-DHCC to 1,24,25-trihydroxycholecalciferol by the kidney cannot be the sole mechanism by which 24,25-DHCC expresses biological activity, even though in vitamin D deficient rats nephrectomy does abolish the ability of large doses of 24,25-DHCC to increase calcium absorption. It is concluded that 24,25-DHCC may be a calcium-regulating hormone in man. In view of the effects demonstrated here and its relatively high concentration in plasma and slow turnover rate, 24,25-DHCC has the properties that might be ideal for a long-acting stimulator of bone mineralisation. Further work is needed to explain why 24,25-DHCC has effects in man which are not readily seen in other species.
1. In subjects with normal renal function there was a strong positive correlation between serum concentrations of 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol, as measured by competitive protein-binding assay. 2. The 24,25-dihydroxycholecalciferol concentration was about 7% of the prevailing 25-hydroxycholecalciferol concentration. 3. In contrast, sera from anephric patients contained very low or undetectable amounts of 24,25-dihydroxycholecalciferol even after the serum 25-hydroxycholecalciferol concentrations in these patients had been elevated by oral administration of 25-hydroxycholecalciferol. 4. In a further group of anephric patients, all having normal serum 25-hydroxycholecalciferol concentrations, no radioactively labelled 24,25-dihydroxycholecalciferol was formed from an injected pulse dose of [3H,14C]cholecalciferol. 5. These results indicate that in man the kidney is the major site of 24-hydroxylation of 25-hydroxycholecalciferol.
Fundamental questions arising from study of the multiple sclerosis lesion are: (1) why the myelin-forming oligodendrocyte is adversely affected; and (2) what factors might induce the proliferation and differentiation of replacement oligodendrocytes. This paper discusses factors that influence the number and differentiative capacity of myelin-forming cells both in the central nervous system (CNS) and the peripheral nervous system (PNS). New experiments utilizing cultures of fetal rat sensory and autonomic ganglia are also herein reported. It has been found that in cultures free of fibroblasts, normal Schwann cell proliferation and ensheathment of axons require contact with a collagen substrate and may be facilitated by a medium containing chick embryo extract. This demonstration of a connective tissue requirement for normal Schwann cell function raises the question of whether additional factors are necessary for normal oligodendrocyte activity.
Explore the source record for details and available documents.
The acute effect of porcine calcitonin was tested in 17 patients undergoing chronic haemodialysis. In normal adults calcitonin has no effect on plasma calcium or phosphate levels, but in nine patients both concentrations were substantially reduced after calcitonin. This hypocalcaemic and hypophosphataemic effect was a function of the initial plasma phosphate level but was unrelated to the initial plasma calcium level. Plasma hydroxyproline levels were not significantly different in the two groups an were unaffected by calcitonin. In 11 patients fasting plasma calcitonin levels were undetectable with an assay sensitive to 0-1 mug/1. Calcitonin seems to have an acute effect in chronic renal failure which may not operate by arresting bone resorption but is dependent on the plasma phosphate concentration.
Metamorphosis in the flatfish is characterized by the migration of one eye around the dorsal surface of the head to a position adjacent to the other eye on the new top side of the animal. The visual connections of the adult flatfish, Achirus lineatus, were examined. Either the migrating or non-migrating eye was removed and the animal allowed to survive for one to three weeks. Alternate sections of the brain were stained by a modification of the Fink-Heimer technique, or with cresyl violet. The diencephalic visual connections of the flatfish were similar to those of other teleosts with contralateral projections to the nuclei corticalis, dorsomedialis thalami, pretectalis, and the corpus geniculatum laterale. The distribution of the retinal efferents to the optic tectum is unique in the flatfish. In the medial one-third of the tectum, terminal degeneration was found in three bands in the stratum opticum (SO) and the stratum griseum et fibrosum superficiale (sgfs). In the middle part of the tectum, two bands of degeneration remained over the sgfs. The lateral part of the tectum has only a very small amount of degeneration distributed radomly in scattered clusters over the deep SO and superficial sgfs. The Nissl preparations also reflected the differences between the medial and lateral parts of the tectum. Distinct layer was lacking in the medial tectum with a conspicuously absent large cell layer in the stratum griseum centrale (sgc). In contrast, the lateral tectum had a typical tectal stratification. Most notable were the large neurons of the sgc.
Explore the source record for details and available documents.
The role of metabolic acidosis in the genesis of renal osteomalacia was investigated by studying bone mineralisation and resorption rates with a combined isotope and balance technique in six patients, before and after the administration of alkali. Correction of blood pH was achieved in five cases and was associated with a significant rise in the bone mineralisation rates and a significant positive trend in the calcium balances. It is suggested that acidosis contributes to the pathogenesis of osteomalacia in renal failure by slowing skeletal mineralisation, possibly by inhibiting bone alkaline phosphatase.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.