Ab Initio Thermodynamic Results for the Degenerate Electron Gas at Finite Temperature.

The uniform electron gas at finite temperature is of key relevance for many applications in dense plasmas, warm dense matter, laser excited solids, and much more. Accurate thermodynamic data for the uniform electron gas are an essential ingredient for many-body theories, in particular, density-functional theory. Recently, first-principles restricted path integral Monte Carlo results became available, which, however, had to be restricted to moderate degeneracy, i.e., low to moderate densities with r_{s}=r[over ¯]/a_{B}≳1. Here we present novel first-principles configuration path integral Monte Carlo results for electrons for r_{s}≤4. We also present quantum statistical data within the e^{4} approximation that are in good agreement with the simulations at small to moderate r_{s}.

Kappa opioid receptors of human placental villi modulate acetylcholine release.

Human placental villus tissue is non-innervated, yet it contains components of the opiate and cholinergic systems. We investigated whether opioids modulate a calcium dependent acetylcholine release from the villus tissue in a manner similar to that demonstrated by the parasympathetic nerve-smooth muscle junction. We reported that the kappa receptor agonist ethylketocyclazocine (EKC) inhibits acetylcholine release, and that the inhibition is reversed by the selective antagonist, Mr2266. Findings reported here substantiate the role of opioids as modulators of acetylcholine release from villus tissue. The nonselective agonist, morphine, also inhibits acetylcholine release. Inhibition caused by morphine is reversed by low concentrations of non-selective antagonists, naloxone and naltrexone. Naloxone at high concentrations potentiates the inhibition of acetylcholine release caused by morphine. In addition, the calcium channel blocker, diltiazem, was found to inhibit the release of acetylcholine. The combination of morphine and diltiazem resulted in a greater inhibition of acetylcholine release than by either alone. These results suggest that opiate cholinergic interactions occur in non-neural tissue with a mechanism similar to that known to occur at certain cholinergic synapses.