Plasma remedies in dermatology Mechanisms involving action as well as scientific applications

Until now, a specifically designed functional molecular species has been recognized as an absolute necessity for realizing the diode's behavior in molecular electronic junctions. Here, we suggest a facile approach for the implementation of a tailored diode in a molecular junction based on non-functionalized alkyl and conjugated molecular monolayers. A two-dimensional semiconductor (MoS2 and WSe2) is used as a rectifying designer at the alkyl or conjugated molecule/Au interface. From the adjustment of band alignment at molecules/two-dimensional semiconductor interface that can activate different transport pathways depending on the voltage polarity, the rectifying characteristics can be implemented and controlled. The rectification ratio could be widely tuned from 1.24 to 1.83 × 104 by changing the molecular species and type and the number of layers of the two-dimensional semiconductors in the heterostructure molecular junction. Our work sets a design rule for implementing tailored-diode function in a molecular heterojunction structure with non-functionalized molecular systems.The heat shock protein 90 (Hsp90) is a molecular chaperone that employs the free energy of ATP hydrolysis to control the folding and activation of several client proteins in the eukaryotic cell. To elucidate how the local ATPase reaction in the active site couples to the global conformational dynamics of Hsp90, we integrate here large-scale molecular simulations with biophysical experiments. We show that the conformational switching of conserved ion pairs between the N-terminal domain, harbouring the active site, and the middle domain strongly modulates the catalytic barrier of the ATP-hydrolysis reaction by electrostatic forces. Our combined findings provide a mechanistic model for the coupling between catalysis and protein dynamics in Hsp90, and show how long-range coupling effects can modulate enzymatic activity.The quantum mirage effect is a fascinating phenomenon in fundamental physics. Landmark experiments on quantum mirages reveal atomic-scale transport of information with potential to remotely probe atoms or molecules with minimal perturbation. Previous experimental investigations are Kondo-effect based; the quantum mirages appear only near the Fermi energy. This strongly limits the exploration of the mechanism and potential application. Here we demonstrate a Kondo-free quantum mirage that operates in a wide energy range beyond Fermi energy. Together with an analytical model, our systematic investigations identify that the quantum mirage is the result of quantum interference of the onsite electronic states with those scattered by the adatom at the focus of elliptical quantum corrals, where two kinds of scattering paths are of critical importance. Moreover, we also demonstrate the manipulation of quantum mirages with pseudo basic logic operations, such as NOT, FANOUT and OR gates.Heterogeneous interfaces exhibit the unique phenomena by the redistribution of charged species to equilibrate the chemical potentials. Despite recent studies on the electronic charge accumulation across chemically inert interfaces, the systematic research to investigate massive reconfiguration of charged ions has been limited in heterostructures with chemically reacting interfaces so far. Here, we demonstrate that a chemical potential mismatch controls oxygen ionic transport across TiO2/VO2 interfaces, and that this directional transport unprecedentedly stabilizes high-quality rutile TiO2 epitaxial films at the lowest temperature (≤ 150 °C) ever reported, at which rutile phase is difficult to be crystallized. Comprehensive characterizations reveal that this unconventional low-temperature epitaxy of rutile TiO2 phase is achieved by lowering the activation barrier by increasing the "effective" oxygen pressure through a facile ionic pathway from VO2-δ sacrificial templates. This discovery shows a robust control of defect-induced properties at oxide interfaces by the mismatch of thermodynamic driving force, and also suggests a strategy to overcome a kinetic barrier to phase stabilization at exceptionally low temperature.Treatment options for necrotizing enterocolitis (NEC) remain inadequate. Here we examined if and how prolyl hydroxylase 2 (PHD2) silencing enhances the paracrine effects of bone-marrow-derived mesenchymal stem cells (BM-MSCs) on NEC. In this study, BM-MSCs were transduced with lentiviruses containing GFP (GFP-MSC) or shPHD2-GFP constructs (PHDMSC), followed by intraperitoneal injection of the PHDMSC-conditioned medium (PHDMSC-CM) or the GFP-MSC-conditioned medium (MSC-CM) into a rat pup model of NEC. Our results showed that systemic infusion of PHDMSC-CM, but not MSC-CM, significantly improved intestinal damage and survival of NEC rats. Such benefits may involve the modulation of epithelial regeneration and inflammation, as indicated by the regeneration of intestinal epithelial/stem cells, the regulation of Treg cells function and pro-/anti-inflammatory cytokine balance. The mechanism for the superior paracrine efficacy of PHDMSC is related to a higher release of pivotal factor IGF-1 and TGF-β2. compound library Inhibitor NF-κB activation was induced by PHD2 silencing to induce IGF-1 and TGF-β2 secretion via binding to IGF-1 and TGF-β2 gene promoter. Our work indicated that PHD2 silencing enhanced the paracrine effect of BM-MSCs on NEC via the NF-κB-dependent mechanism which may be a novel strategy for stem cell therapy on NEC.Clustering of functionally similar synapses in dendrites is thought to affect neuronal input-output transformation by triggering local nonlinearities. However, neither the in vivo impact of synaptic clusters on somatic membrane potential (sVm), nor the rules of cluster formation are elucidated. We develop a computational approach to measure the effect of functional synaptic clusters on sVm response of biophysical model CA1 and L2/3 pyramidal neurons to in vivo-like inputs. We demonstrate that small synaptic clusters appearing with random connectivity do not influence sVm. With structured connectivity,  ~10-20 synapses/cluster are optimal for clustering-based tuning via state-dependent mechanisms, but larger selectivity is achieved by 2-fold potentiation of the same synapses. We further show that without nonlinear amplification of the effect of random clusters, action potential-based, global plasticity rules cannot generate functional clustering. Our results suggest that clusters likely form via local synaptic interactions, and have to be moderately large to impact sVm responses.