High photosensitivity few-layered MoSe2 back-gated field-effect phototransistors.

In this paper, we report on the fabrication and optoelectronic properties of high sensitive phototransistors based on few-layered MoSe2 back-gated field-effect transistors, with a mobility of 19.7 cm² V⁻¹ s⁻¹ at room temperature. We obtained an ultrahigh photoresponsivity of 97.1 AW⁻¹ and an external quantum efficiency (EQE) of 22 666% using 532 nm laser excitation at room temperature. The photoresponsivity was improved near the threshold gate voltage; however, the selection of the silicon dioxide as a gate oxide represents a limiting factor in the ultimate performance. Thanks to their high photoresponsivity and external quantum efficiency, the few-layered MoSe2-based devices are promising for photoelectronic applications.

Recovery (passive vs. active) during interval training and plasma catecholamine responses.

The effect of recovery mode (Active [AR] vs. Passive [PR]) on plasma catecholamine (Adrenaline [A] and Noradrenaline [NA]) responses to maximal exercise (Exemax) was studied during interval training (IT). 24 male subjects (21.1±1.1 years) were randomly assigned to a control group (CG, n=6), AR training group (ARG, n=9) or PR group (PRG, n=9). ARG and PRG participated in an IT program 3 times a week for 7 weeks. Before and after training, maximal oxygen uptake (VO2max) and maximal aerobic velocity (MAV) were measured. Plasma A and NA were determined at rest, at the end of Exemax and after 10 and 30 min of recovery. Training induced significant changes only in ARG: an increase of VO2max and MAV along with a significant increase of A and NA at the end of Exemax (2.82±0.15 vs. 1.03±0.15 nmol/l and 7.22±0.36 vs. 6.65±0.57 nmol/l, respectively p<0.05). The ratio A/NA measured at the end of Exemax also increased significantly after training (0.41±0.11 vs. 0.16±0.08, P>0.05). The present results show that IT with AR induces a significant increase of A and NA concentrations in response to maximal exercise. The study furthermore shows that IT program with AR may induce more stress than the same program with PR.

Assessment of bioequivalence of a generic cyclosporine (Equoral) by a prospective randomized controlled trial on allogeneic stem cell transplant recipients.

INTRODUCTION: Bioequivalence of Equoral has been suggested by measurements of pharmacokinetic parameters in healthy volunteers and in stable renal transplant recipients, but not study in allogeneic stem cell transplant (ASCT) recipients. The aim of our study was to compare the pharmacokinetics and safety of Equoral to Neoral solution among ASCT recipients. PATIENTS AND METHODS: Our open-label, two-way crossover, randomized controlled trial compared Equoral versus Neoral solutions in ASCT recipients. The 30 enrolled patients from June 2007 to November 2008 had a 7 to 14-day duration of the test period. A 10-point blood sampling from 0 to 12 hours measured Cmax (extent of absorption), tmax (rate of absorption) and AUC(0-12h) (area under the concentration-time curve) calculated by the linear trapezoid rule. The study protocol was approved by the ethics committee. RESULTS: Median age was 26 years (range = 6-47). The mean pharmacokinetic features were: AUC(0-12h): Equoral 4162 ± 1231 ng·mL/h vs Neoral 4370 ± 1059 ng·mL/h (P = .50); Cmax: Equoral 821 ± 244 ng/mL vs Neoral 834 ± 298 ng/mL (P = .86); and tmax: 105 minutes for both formulations. Comparable toxicities and rates of graft-versus-host disease were recorded in both groups. CONCLUSION: We suggest that Equoral and Neoral solution can be considered interchangeable in ASCT recipients.

Direct activation of K(Ca) channel in airway smooth muscle by nitric oxide: involvement of a nitrothiosylation mechanism?

Clinically, nitric oxide (NO*) is widely used as a pulmonary vaso- and bronchodilator agent. However, the precise molecular mechanisms by which NO. induces smooth muscle relaxation are not well established. It has been suggested that NO. relaxes airway smooth muscle (ASM) via a 3',5'-cyclic guanosine monophosphate (cGMP)-dependent pathway, and our previous work has shown that Ca2+-activated K+ (KCa) channels are susceptible to cGMP-dependent protein kinase (PKG)-dependent phosphorylation (A. Alioua, J. P. Huggins, and E. Rousseau. Am. J. Physiol. 1995;268:L1057-L1063). To assess whether KCa channels are also directly activated by NO. or one of its derivatives such as peroxynitrite, the activity of these channels was measured upon fusion of sarcolemmal vesicles derived from bovine tracheal smooth muscle cells into planar lipid bilayers (PLB). It was found that in the absence of adenosine triphosphate (ATP), cGMP, and cGMP-dependent protein kinase, NO* donors such as 1-propanamine-3-(2-hydroxy-2-nitroso-1-propylhydrazine) (PAPA NONOate) or 3-morpholinosydnonimine hydrochloride (SIN-1) in the presence of superoxide dismutase (SOD), added on either side of the bilayer, caused a concentration- dependent increase in the open probability (Po) of KCa channels without altering their unitary conductance. Release of NO*, which was measured by chemiluminescence analysis in parallel experiments, affected the gating behavior of KCa channels in the presence of SOD and ethyleneglycol-bis-(beta-aminoethyl ether)- N,N'-tetraacetic acid (EGTA) by reducing the mean closed times and increasing the number and duration of short open events. PAPA NONOate, a true NO. donor, had similar effects in the presence of ethylenediaminetetraacetic acid (EDTA), a heavy-metal chelator, and K-urate, a peroxynitrite scavenger. Addition of either 5 mM dithiothreitol (DTT) or 5 mM reduced glutathione (GSH), as well as 5 mM N-ethylmaleimide (NEM)-an alkylating agent-to the trans (intracellular) side of an experimental chamber slightly increased channel Po but prevented further channel activation by NO* donors. However, neither DTT nor GSH was able to reverse the effect of NO*. In contrast to SIN-1, DTT had no effect when added to the cis (extracellular) side of the chamber. This suggests that the effect of NO* is most likely due to a chemical modification (nitrothiosylation) of intracellular sulfhydryl group(s). Neither PAPA NONOate (NO*), nor SIN-1 had any effect on sarcolemmal Cl- channels reconstituted from the same membrane preparations. Pharmacomechanical measurements made on epithelium-denuded rat bronchus showed that 100 nM charybdotoxin decreased the sensitivity of bronchial smooth muscle to SIN-1-induced relaxations. Altogether, our data suggest that NO-induced bronchorelaxation occurs partly via a direct activation of KCa channels, possibly through a covalent interaction with the cytoplasmic side of their alpha subunit.