Significados de hsd en inglés

No additional inner ear tissue region expressed 11 beta-HSD enzyme during the observed period.

Data were analyzed using linear model procedure including Tukey HSD test and Pearson's correlation coefficient.

Here, we test whether depleting intracellular ATP serves as a possible mechanism for HSD genesis.

Decreased placental 11β-HSD activity increases fetal exposure to maternal glucocorticoids, further increasing fetal oxidative stress.

The enzymatic activity of 3beta-HSD was greatest in the cerebrum and lowest in the mesencephalon.

These findings imply that 11 beta-HSD regulates binding of corticoids to their inner ear receptors.

Therefore, we characterized 11beta-HSD profiles for a wide range of steroids often used in clinical practice.

This study suggests that HSD is not be mediated by depletion of intracellular ATP during hyperthermia.

Inhibition of 11 beta-HSD with glycyrrhetinic acid allowed cortisol to gain direct access to the fetal circulation.

Placental 11 beta HSD has been proposed to protect the fetus from high level of maternal glucocorticoids.

There were no differences in HSD11B1 mRNA levels among adrenal tumor groups.

Cell proliferation was negligible, suggesting that the increase in 3beta-HSD-positive cells is the result of precursor cell differentiation.

AME may involve mutations in a gene for another enzyme with 11HSD activity or perhaps another cortisol-metabolizing enzyme.

We examined whether maternal glucocorticoid administration alters placental 11beta-HSD 2 expression.

Liver fibrosis and serum AFP were significantly increased in DEN + HF-HC-HSD mice compared to controls.

Conclusion: We conclude that human placental 11 beta-HSD plays a crucial role in controlling glucocorticoid access to the fetus.