Thus, in
males, a specific progesterone concentration profile induced by chronic potassium restriction regulates potassium balance.”
“Phthalates, the most abundantly produced plasticizers, leach out from polyvinyl chloride plastics and disrupt androgen action. Male rats that are exposed to phthalates in utero develop symptoms characteristic of the human condition referred to as testicular dysgenesis syndrome (TDS). Environmental influences have been suspected to contribute to the increasing incidence of TDS in humans (Le. cryptorchidism and hypospadias in newborn boys and testicular cancer and reduced sperm quality in adult males). In this review, we discuss the recent findings that prenatal selleck kinase inhibitor Roscovitine solubility dmso exposure to phthalates affects Leydig cell function in the postnatal testis. This review also focuses on the recent progress in our understanding of how Leydig cell factors contribute to phthalate-mediated TDS.”
“Rationale and objective Because of the important role of dopamine in neurotransmission, it would be useful to be able to image brain dopamine receptor-mediated signal transduction in animals and humans. Administering the D-1-D-2 receptor agonist apomorphine may allow
us to do this, as the D-2-like receptor is reported to be coupled to cytosolic phospholipase almost A(2) activation and arachidonic acid (AA) release from membrane phospholipid.
Methods Unanesthetized adult rats were given intraperitoneally apomorphine (0.5 mg/kg) or saline, with or without pretreatment with 6 mg/kg intravenous raclopride, a D-2/D-3 receptor antagonist. [1-C-14]AA was injected intravenously, then AA incorporation coefficients k*-brain radioactivity divided by integrated plasma radioactivity-markers of AA signaling, were measured using quantitative autoradiography in 62 brain regions.
Results Apomorphine significantly elevated k* in 26 brain regions, including the frontal cortex,
motor and somatosensory cortex, caudate-putamen, thalamic nuclei, and nucleus accumbens. Raclopride alone did not change baseline values of k*, but raclopride pretreatment prevented the apomorphine-induced increments in k*.
Conclusions A mixed D-1-D-2 receptor agonist, apomorphine, increased the AA signal by activating only D-2-like receptors in brain circuits containing regions with high D-2-like receptor densities. Thus, apomorphine might be used with positron emission tomography to image brain D-2-like receptor-mediated AA signaling in humans in health and disease.”
“This study develops a system for the efficient valorisation of hemicellulosic hydrolysates of vineshoot trimmings.