Publications by authors named "J J Mrotek"

Objectives: To determine the diagnostic accuracy of the sperm penetration assay (SPA) and standard semen parameters for subsequent fertilization in in vitro fertilization-embryo transfer (IVF-ET).

Design: Prospective study.

Setting: Andrology Laboratory, and university research laboratory.

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Objective: Because glucocorticoids stimulate leptin release and, at least in vitro, leptin inhibits cortisol secretion, a feedback system between glucocorticoids and leptin has been proposed. However, in humans and non-human primates there are no in vivo studies to support any role for leptin in the control of the hypothalamic-pituitary-adrenal axis. In this study, we investigated the effect of leptin on (i) ACTH-stimulated secretion of cortisol in six male rhesus monkeys and (ii) basal and forskolin (FSK)-stimulated cortisol secretion by the human adrenal carcinoma cell H295R in vitro.

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In vitro and in vivo cadmium toxicity studies focus almost exclusively on CdCl2 effects. Only a few studies have used adrenocortical cells and tissue to determine cadmium salt effects during stress of adrenocorticotropin stimulation. Because several biologically relevant water-soluble cadmium salts exist, this study extended work with CdCl2 to evaluate the acute adrenocortical cell steroid secretory responses to non-lethal cadmium acetate (CdAc2) and CdSO4 concentrations.

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In previous studies, nonlethal CdCl2 concentrations apparently inhibited basal Y-1 mouse adrenal tumor cell endogenous mitochondrial cholesterol conversion to pregnenolone. In addition, CdCl2 inhibited all agents stimulating both plasma membrane-dependent cAMP synthesis and 20 alpha-hydroxy-4-pregnen-3-one (20DHP) secretion. Bypassing the plasma membrane using dibutyryl-cAMP (dbcAMP) stimulated cytoplasmic cholesterol metabolism and 20DHP secretion in the presence of CdCl2.

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Effects of chronic ethanol exposure on N-methyl-D-aspartate (NMDA) receptor function were examined in hippocampal neurons. Rat hippocampal neurons grown in culture were chronically exposed to 100 mM ethanol to examine mechanisms that could underlie ethanol-induced changes in receptor function and excitotoxicity. NMDA-stimulated, but not kainic acid-stimulated, increases in intracellular calcium were enhanced after 1-, 2- and 7-day exposures to 100 mM ethanol.

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