PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Transcortin”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1985

Total and unbound cortisol-, progesterone-, oestrone- and transcortin-binding activities in sera from patients with myocardial infarction: evidence for differential responses of good and bad prognostic cases.

Day-of-admission sera from myocardial infarction patients (MI) and patients with cardiopathies other than MI (non-MI) were analysed for total and unbound cortisol (F), progesterone (P4), oestrone (E1), and corticosteroid binding activities (CBG). The MI who survived (n = 28) showed high increases of F, P4 and E1 compared to healthy controls. By contrast, the MI who died within 10 days of admission (n = 6) had unchanged F and less increased P4 and E1 than survivors. The non-MI (n = 6) had higher F and E1 than controls but normal P4. The unbound steroids were increased in all patients: however, the MI who died showed much smaller rises than survivors (P less than 0.001 for unbound F and E1 increases in survivors vs. deceased). The CBG activity was in all MI lower than in normals (P less than 0.001) but unchanged in non-MI. These results are discussed in terms of the potential significance of unbound plasma steroids as predictors of MI severity.

Adult↗
PubMed1987

alpha-Fetoprotein and transcortin behave as acute phase reactants in the maternal and fetal compartments of the inflammatory pregnant mouse.

Immunological and binding methods have been used to demonstrate that acute inflammation induced in the pregnant mouse by a single sc turpentine injection elicits plasma protein responses in the fetal as well as in the maternal compartment. The maternal response involves, along with the classical pattern of positive and negative acute phase reactants seen in the inflammatory nonpregnant animal, a highly specific approximately 2-fold increase of alpha-fetoprotein (AFP) concentrations. In addition, the high pregnancy-associated corticosteroid binding globulin (CBG) levels drop dramatically (2-3 times) in response to inflammation. The fetal response is characterized by small (10-25%) but statistically significant declines of AFP, CBG, and albumin concentrations, without any increase in levels of the positive classical acute phase reactants. The divergent responses of the estrophilic mouse AFP on the two sides of the placental barrier result in a 3- to 4-fold enrichment of the maternal serum vs. an approximately 20% impoverishment of the fetal serum in high affinity estrogen binding sites. The similar decrease in levels of CBG in mother and fetus leads to marked losses of high affinity corticosteroid sites for both. Neither the affinity constants for the estrogen-AFP interactions nor those for the corticosterone-CBG interactions are affected by inflammation. This is the first report of AFP as a positive marker of acute inflammation, of AFP as a pregnancy-specific inflammatory reactant in the mouse, and of a plasma protein response of the fetus in utero to an inflammatory stress undergone by the mother.

Animals↗
PubMed1987

Plasma adrenocorticotropin is more sensitive than transcortin production or thymus weight to inhibition by corticosterone in rats.

After adrenalectomy, ACTH, corticosterone-binding globulin (CBG), and thymus wet weight increase in rats as a consequence of the removal of corticosterone (B) and decrease again in response to replacement with glucocorticoids. We have studied the effect of replacing adrenalectomized male rats with a variety of different concentrations of B. Plasma concentrations of ACTH and CBG and thymus wet weights were related to the measured concentration of free ultrafilterable B in plasma. In other experiments, the clearance of [125I]CBG was determined in adrenalectomized rats with and without B replacement, and the time required for the changes in plasma CBG concentrations after removal and/or replacement of B in adrenalectomized rats was determined. Five to 7 days after adrenalectomy and institution of a relatively constant B replacement signal, plasma CBG concentrations were highly correlated with circulating B concentrations (r2 = 0.745; P less than 0.001). The effect of B was on the CBG production rate, since clearance did not change. Because CBG concentrations decrease as total B concentrations increase, there is an amplification of free B concentrations with increasing total B. The relationships of plasma ACTH and CBG and thymus wet weight to circulating free B levels showed that 50% inhibition of ACTH was achieved at a free B concentration of 0.8 +/- 0.05 nM, whereas 50% inhibition of CBG and thymus wet weight were achieved at free B concentrations of 4.6 +/- 0.9 and 4.4 +/- 0.6 nM, respectively. These inhibition values correlate well with the known Kd values for the high affinity type I B receptor (0.5 nM) and for the lower affinity type II glucocorticoid receptor (2.5-5 nM), respectively, suggesting that ACTH secretion, CBG production, and thymus wet weight are regulated by the association of B with these receptor types.

Adrenalectomy↗