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K Miyal

Publications and source records attributed to K Miyal.

7 recordsLinked to original sources
PubMed1988

Highly specific enzyme immunoassay for the beta-subunit of human thyrotropin with use of monoclonal antibodies.

A highly specific enzyme-linked "sandwich" immunoassay is described for determining free human thyrotropin (hTSH) beta-subunit in serum by using a anti-hTSH beta-subunit monoclonal antibody conjugated with beta-D-galactosidase (EC 3.2.1.23) and a solid phase consisting of silicone rods coated with another monoclonal antibody. We could detect as little as 0.04 ng of beta-subunit per assay. The measurable range of hTSH beta-subunit concentrations in serum was 0.4 to 50 micrograms/L. The assay demonstrated little or no cross reactivity with intact hTSH, hTSH alpha-subunit, or human choriogonadotropin. The mean CVs were 12.2% within assay, 13.9% between assay. The hTSH beta-subunit was not detectable in sera from healthy subjects, patients with hyperthyroidism, or two patients with pituitary tumors producing TSH. It was measurable (at concentrations of 0.65 to 2.70 micrograms/L) in sera from eight of 23 hypothyroid patients. In five of the hypothyroid patients examined, the concentration of hTSH beta-subunit in serum increased after administration of thyroliberin. This method may be useful in elucidating the physiological and pathological significance of the hTSH beta-subunit and in examining the function of the hypothalamus-pituitary-thyroid axis.

Adolescent↗
PubMed1977

Enzyme-labelled immunoassay for plasma cortisol.

An enzyme-labelled immunoassay for plasma cortisol was developed. For this alkaline-phosphatase was conjugated through 21-hemisuccinate of cortisol using water-soluble carbodiimide. An antibody was raised in rabbits against corisol-21-hemisuccinate bovine serum albumin. Before assay 10 mul samples of plasma were mixed with glutamate buffer, pH 3.3, and boiled to denature endogenous cortisol-binding globulin and alkaline-phosphatase. Separation of "bound and free" cortisol was done by the double antibody method. A linear relationship was obtained between the volume of plasma and the amount of cortisol. The minimal detectable level of plasma cortisol was 1 mug/dl and the coefficients of variation were 2.7%-4.4% (within assays) and 4.7%-6.0% (between assays). Cortisol values determined by the present method correlated well with those determined by radioimmunoassay. The present method of enzyme-labelled immunoassay is suitable for routine clinical analysis of plasma cortisol.

Alkaline Phosphatase↗
PubMed1975

Acute cholestasis induced by lithocholic acid in the rat. A freeze-fracture replica and thin section study.

Sodium lithocholate (LCA) was continuously infused intravenously (0.1 or 0.2 mumole per minute per 100 gm. body weight) in Wistar rats with a bile fistula for up to 4 hours. The higher dose induced complete cholestasis within 2 to 3 hours, whereas the low dose reduced the biliary output to less than 10 per cent of the preinfusion level by the 3rd hour. Ultrastructural changes which were primarily localized to the bile canaliculi and the pericanalicular region were seen 30 minutes after the onset of bile acid infusion. Dilation of the bile carnaliculi, loss of canalicular microvilli, prominence of the pericanalicular ectoplasm, and a characteristic lamellar transformation of the canalicular membrane developed, which became more prominent and widespread with progression of time. A freeze-fracture replica study revealed that the canalicular microvilli became transformed through widening and flattening into multilamellar foldings. Intramembranous granules of the canalicular membrane appeared to have become redistributed, being few or absent in the "transformed" regions. In addition, a sharply angulated, crystalline material was seen in occasional bile canaliculi. This material appeared as a negative image in thin sections, indicating its solubility in organic solvents which were used for dehydration. With the lower dose of LCA, subcellular changes were similar to, but less severe and which accompany an acute cholestasis induced by LCA is attributable to the accumulation of this compound in the bile canaliculus and its vicinity. LCA presumably causes an asymmetric perturbation in the molecular organization of the canalicular membrane which results in ultrastructural alterations and failure of fluid transport. In addition, precipitates of LCA appear to form in the bile canaliculi and may contribute to cholestasis.

Animals↗
PubMed1973

Membrane translocation of mannitol in Escherichia coli without phosphorylation.

Galactosyl-mannitol can be transported into cells of Escherichia coli by beta-galactoside permease and can be hydrolyzed rapidly to mannitol and galactose by beta-galactosidase. When a mutant strain lacking enzyme I of the phosphoenolpyruvate phosphotransferase system and constitutive in the lactose system was presented with galactosyl-mannitol in which the mannitol moiety was labeled with (3)H, the liberated mannitol remained inside the cell if the Enzyme II complex of the phosphoenolpyruvate phosphotransferase system for mannitol was uninduced. It is postualted that one of the enzyme II proteins can still catalyze translocation of mannitol across the cell membrane even when phsophorylation is not possible.

Biological Transport, Active↗
PubMed1970

[Cretinism].

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Congenital Hypothyroidism↗