Smooth, Chemically Altered Nucleating Platform for Abrupt Performance Enhancement of Ultrathin Cu-Layer-Based Transparent Electrodes.

Rapid advances in flexible optoelectronic devices necessitate the concomitant development of high-performance, cost-efficient, and flexible transparent conductive electrodes (TCEs). This Letter reports an abrupt enhancement in the optoelectronic characteristics of ultrathin Cu-layer-based TCEs via Ar-mediated modulation of the chemical and physical states of a ZnO support surface. This approach strongly regulates the growth mode for the subsequently deposited Cu layer, in addition to marked alteration to the ZnO/Cu interface states, resulting in exceptional TCE performance in the form of ZnO/Cu/ZnO TCEs.

Simultaneous Enhancement in Visible Transparency and Electrical Conductivity via the Physicochemical Alterations of Ultrathin-Silver-Film-Based Transparent Electrodes.

A methodology for the simultaneous modulation of the chemical and physical states of an amorphous TiO layer surface and its impact on the subsequent deposition of a polycrystalline Ag layer are presented. The smoothened TiO layer surface comprising chemically altered, oxygen-deficient states serves as a nucleating platform for Ag deposition, facilitating a marked increase (∼75%) in the nucleation number density, which strongly enhances the wettability of ultrathin Ag layers. The physically smoothened TiO/Ag interface further reduces the optical and electrical losses.

Strategy for Fabricating Ultrathin Au Film Electrodes with Ultralow Optoelectrical Losses and High Stability.

A vital objective in the wetting of Au deposited on chemically heterogeneous oxides is to synthesize a completely continuous, highly crystalline, ultrathin-layered geometry with minimized electrical and optical losses. However, no effective solution has been proposed for synthesizing an ideal Au-layered structure. This study presents evidence for the effectiveness of atomic oxygen-mediated growth of such an ideal Au layer by improving Au wetting on ZnO substrates with a substantial reduction in free energy.

Wip1 regulates Smad4 phosphorylation and inhibits TGF-β signaling.

The tumor suppressor Smad4, a key mediator of the TGF-β/BMP pathways, is essential for development and tissue homeostasis. Phosphorylation of Smad4 in its linker region catalyzed by the mitogen-activated protein kinase (MAPK) plays a pivotal role in regulating its transcriptional activity and stability. In contrast, roles of Smad4 dephosphorylation as a control mechanism of TGF-β/BMP signaling and the phosphatases responsible for its dephosphorylation remain so far elusive.

Role of S100A9 in the development of neutrophilic inflammation in asthmatics and in a murine model.

S100A9 is an endogenous danger signal that promotes and exacerbates the neutrophilic inflammatory response. To investigate the role of S100A9 in neutrophilic asthma, S100A9 levels were measured in sputum from 101 steroid-naïve asthmatics using an ELISA kit and the levels were significantly correlated with percentages of neutrophils in sputum. Intranasal administration of recombinant S100A9 markedly increased neutrophil numbers at 8h and 24h later with concomitant elevation of IL-1β, IL-17, and IFN-γ levels.

Neutrophilic inflammation in asthma: mechanisms and therapeutic considerations.

Neutrophilic airway inflammation represents a pathologically distinct form of asthma and frequently appears in symptomatic adulthood asthmatics. However, clinical impacts and mechanisms of the neutrophilic inflammation have not been thoroughly evaluated up to date. Areas covered: Currently, distinct clinical manifestations, triggers, and molecular mechanisms of the neutrophilic inflammation (namely Toll-like receptor, Th1, Th17, inflammasome) are under investigation in asthma.

Circulating IL-33 level is associated with the progression of lung cancer.

Objectives: Interleukin (IL)-33 protects against infection and inflammation; however, few studies have explored the relevance of IL-33 in lung cancer patients. We evaluated relation of plasma IL-33 levels with development and progression of lung cancer.

Materials And Methods: A total of 160 patients with lung cancer and 160 controls with normal lungs were enrolled.

Role of inflammasome activation in development and exacerbation of asthma.

Human airways contact with pathogen-associated molecular patterns and danger-associated molecular patterns present in many environments. Asthmatic's airways may be more susceptible to these patterns and lead to inflammasome activation; however, the participation of inflammasome in the development and exacerbation of asthma is not fully understood and remains controversial. Asthma is a heterogeneous group composed of different airway inflammation patterns with different underlying immune mechanisms.

Elevation of S100 calcium binding protein A9 in sputum of neutrophilic inflammation in severe uncontrolled asthma.

Background: Neutrophilic airway inflammation is frequently observed in severe uncontrolled asthma (UA) and controlled asthma (CA). However, there is no sputum biomarker to differentiate the 2 conditions.

Objective: To identify biomarkers of severe uncontrolled asthma with neutrophilic airway inflammation.

Quantitative assessment of neurochemical changes in a rat model of long-term alcohol consumption as detected by in vivo and ex vivo proton nuclear magnetic resonance spectroscopy.

The aim of present study was to quantitatively investigate the neurochemical profile of the frontal cortex region in a rat model of long-term alcohol consumption, by using in vivo proton magnetic resonance spectroscopy ((1)H-MRS) at 4.7 T and ex vivo(1)H high-resolution magic angle spinning (HR-MAS) technique at 11.7 T.

Association analysis of formyl peptide receptor 2 (FPR2) polymorphisms and aspirin exacerbated respiratory diseases.

Aspirin-exacerbated respiratory diseases (AERD) are associated with the metabolism of arachidonic acid. FPR2 (formyl peptide receptor2) is a high-affinity ligand receptor for potent anti-inflammatory lipid metabolites: lipoxins. Thus, functional alterations of the FPR2 may contribute to AERD.

Ex vivo detection for chronic ethanol consumption-induced neurochemical changes in rats.

The aim of this study was to quantitatively investigate the chronic ethanol-induced cerebral metabolic changes in various regions of the rat brain, using the proton high resolution magic angle spinning spectroscopy technique. The rats were divided into two groups (control group: N=11, ethanol-treated group: N=11) and fed with the liquid diets for 10 weeks. In each week, the mean intake volumes of liquid diet were measured.

Particle stimulation dephosphorylates glutathione S-transferase π1 of epithelial cells.

Environmental pollutant exposure is associated with adverse respiratory outcomes. The phosphorylation of enzymes activates or deactivates many cellular processes and is related to the development of lung diseases such as asthma and chronic obstructive pulmonary disease. However, little is known about protein phosphorylation of bronchial epithelial cells in response to airborne particulates.

Novel hyaluronate-atelocollagen/beta-TCP-hydroxyapatite biphasic scaffold for the repair of osteochondral defects in rabbits.

The authors devised a novel biphasic scaffold combining hyaluronic acid and atelocollagen for the chondral phase and combining hydroxyapatite (HA) and beta-tricalcium phosphate (beta-TCP) for the osseous phase. The biphasic scaffold was fabricated by placing the freeze-dried chondral phase over the HA/beta-TCP scaffold prewetted with hyaluronate/atelocollagen solution. Chondrocytes were isolated in 28 rabbits, expanded, injected inside the chondral phase of the biphasic scaffold, and then cultured in chondrogenic medium.