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hyperthyroidism/prolina

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ArticoliTest cliniciBrevetti
Pagina 1 a partire dal 23 risultati

Lack of evidence for thyrotropin-releasing hormone deamidation in normal and hyperthyroid human sera.

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Two-hour incubations of human serum with 50 ng TRH or pyroglutamyl-histidyl-proline (TRH-OH) were performed under substrate conditions of 0.2 microgram substrate/ml serum. During incubations with normal serum, 46.3 +/- 1.3 (SEM) ng TRH were degraded while only 14.2 +/- 5.1 ng TRH-OH were degraded (P
Old studies in animals and unblinded studies in a few hyperthyroid patients suggested that L -carnitine is a periferal antagonist of thyroid hormone action at least in some tissues. This conclusion was substantiated by our recent observation that carnitine inhibits thyroid hormone entry into the
In hyperthyroid and hypothyroid rats myocardial infarction was produced by coronary artery ligature. At different times following the ligature the animals were given 3H-thymidine or 3H-proline. The following parameters were determined: the number of DNA- and tropocollagen-synthesizing

Serum levels of fetal antigen 2 in hyperthyroidism and primary hyperparathyroidism.

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Serum concentration of fetal antigen 2 (FA2) in patients with hyperthyroidism (n = 18) (median: 12.9 mAU/l; range: 3.2-22.4 mAU/l) was significantly (p < 0.002) higher than in age- and sex-matched healthy controls (median: 4.1 mAU FA2/l; range: 2.4-10.0 mAU FA2/l). Serum FA2 was positively

Activity of aminoacyl-tRNA synthetases in experimental hyperthyroidism in muscle tissues of the rabbit.

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In cardial and femoral muscles of rabbits specific activities of aminoacyl-tRNA synthetases for twenty amino acids were generally similar, namely the activities towards amino acids and their amides, leucine, isoleucine, histidine, tyrosine, proline and serine were considerably lower than towards the

Sporadic congenital nonautoimmune hyperthyroidism caused by P639S mutation in thyrotropin receptor gene.

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Germline mutations of thyrotropin receptor (TSHR) gene determining a constitutive activation of the receptor were identified as a molecular cause of familial or sporadic congenital nonautoimmune hyperthyroidism (OMIM: 609152) (Nat Genet 7:396-401, 1994; N Engl J Med 332:150-154, 1995; Acta
Cyclo(His-Pro) is believed to be a metabolite of TRH. A specific antiserum directed against cyclo(His-Pro) was used to detect immunoreactive material in human serum. Gel filtration column chromatography was used to establish that cyclo(His-Pro)-like immunoreactivity was found not only in free form
The TSH receptor (TSHR) is the central antigen in Graves' disease. Variant receptor proteins, arising from mutations in the TSHR gene, may play a role in the pathogenesis of the disease. Therefore, we analysed the TSHR from a 38-year-old patient affected with autoimmune hyperthyroidism, diffuse

Determination of serum thyroxine enantiomers in patients by liquid chromatography with a chiral mobile phase.

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A chromatographic method for the separation and determination of D- and L-thyroxine enantiomers (D-, and L-T4) in human serum with a chiral ligand ion-exchange system using a chiral mobile phase additive and a silica column was established. An aqueous eluent containing L-proline (L-pro) sufficiently

L-Arginine metabolism in cardiovascular and renal tissue from hyper- and hypothyroid rats.

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This study assessed the effects of thyroid hormones on the enzymes involved in l-arginine metabolism and the metabolites generated by the different metabolic pathways. Compounds of l-arginine metabolism were measured in the kidney, heart, aorta, and liver of euthyroid, hyperthyroid, and hypothyroid
We herein report the case of a Japanese woman with familial dysalbuminemic hyperthyroxinemia (FDH) who was initially diagnosed with Graves' disease. Direct genomic sequencing revealed a guanine to cytosine transition in the second nucleotide of codon 218 in exon 7 of the albumin gene, which then
An HPLC method was developed with normal HPLC-chiral complex mobile phase for the separation and determination of D- and L-thyroxine enantiomers (D- and L-T4) in human plasma. The method includes extraction of thyroxine from plasma and separation of thyroxine enantiomers on HPLC silica column with

Thyrotropin-releasing hormone and insulin release: in vitro studies with islets of normal and dysthyroid mice.

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Pancreatic islets contain large-quantities of thyrotropin-releasing hormone (TRH) and of its metabolite Histidyl-Proline diketopiperazine (Cyclo His-Pro). The effects of these two putative neurotransmitters on the pancreatic B-cell function have been evaluated in vitro, with islets of normal or
Thyroxine-binding globulin (TBG) is the major thyroid hormone transport protein. Several inherited TBG variants resulting in partial or complete TBG deficiencies have been shown to be caused by either one or two nucleotide substitutions, or one nucleotide deletion in the coding regions of the TBG

Thyroid hormones increase Na+-H+ exchange activity in renal brush border membranes.

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Na+-H+ exchange activity, i.e., amiloride-sensitive Na+ and H+ flux, in renal proximal tubule brush border (luminal) membrane vesicles was increased in the hyperthyroid rat and decreased in the hypothyroid rat, relative to the euthyroid animal. A positive correlation was found between Na+-H+
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