Microstructure of the corneal endothelial transition zone in different laboratory animals.

Purpose: To compare the microstructure of the corneal endothelial transition zone in different laboratory animals. Methods: Flat-mount corneas of rabbits, rats, and mice were stained with Alizarin Red S (ARS) and observed using scanning electron microscopy (SEM). The progenitor cell markers p75 neurotrophin receptor (p75NTR), SRY-box transcription factor 9 (SOX9), leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5), telomerase reverse transcriptase (TERT), and proliferation marker Ki-67 were examined in the flat-mounted corneas of three laboratory animals using immunofluorescence microscopy. Results: On flat mounts, proximity to the trabecular meshwork correlated with weaker ARS staining and greater polymorphism of endothelial cells in the transition zone in all animals. On SEM, distinct and smooth structures of the transition zone were negligibly detected in all animals. The endothelial cells in the transition zone had irregular shapes, with less dense, less wavy intercellular junctions, especially in murine corneas, exhibiting unique intercellular cystic spaces. In the transition zone of the rabbit cornea, progenitor cell markers p75NTR, SOX9, Lgr5, TERT, and proliferation marker Ki-67 were expressed, in contrast to those in other murine corneas. Conclusions: Although the transition zone was not identified clearly, irregular cell morphology and loss of cell-cell contact were observed in all animal corneal endothelial cells. The proliferative capacity and the presence of progenitor cells were confirmed in the transition zone, especially in the rabbit cornea.

Preferential dissolution behaviour of the austenite phase in Fe-27Cr-xC high chromium cast iron.

Preferential dissolution behaviour of the austenite (γ) phase in Fe-27Cr-xC high chromium cast irons (HCCIs) immersed in 0.1 mol dm-3 H2SO4 + 0.05 mol dm-3 HCl was investigated. Potentiodynamic and potentiostatic polarisation revealed that the primary and eutectic γ phases dissolved preferentially at -0.35 and 0.00 VSilver Silverchloride Electrode potential in sat. KCl (SSE), respectively. The immersion of the HCCIs in the solution showed that the dissolution of the primary γ phase dominated for ca. 1 h, while the primary and eutectic γ phases dissolved after ca. 1 h. However, the carbide phases remained undissolved during the dissolution of the γ phases. Furthermore, the corrosion rate of the HCCIs increased with the increasing C content owing to the increase in the contact potential difference values of the γ and carbide phases. The change in electromotive force due to C addition was related to the accelerated corrosion rate of the γ phases.

Passivation of precipitation-hardened UNS N07718 in a shallow sour aqueous solution.

Passivation of precipitation-hardened UNS N07718 in 5 wt% NaCl + 0.5 wt% CH3COOH was investigated. Cyclic potentiodynamic polarisation revealed that the alloy surface was passivated without active-passive transition behaviour. The alloy surface was in a stable passive state during potentiostatic polarisation at 0.5 VSSE for 12 h. Bode and Mott-Schottky plots showed that the passive film became electrically resistive and less defective with n-type semiconductive properties during the polarisation. X-ray photoelectron spectra revealed that Cr- and Fe-enriched hydro/oxide layers were formed on the outer and inner layers of the passive film, respectively. The thickness of the film was almost constant with the increase of the polarisation time. The outer Cr-hydroxide layer changed into a Cr-oxide layer during the polarisation, resulting in a decreased donor density in the passive film. The film's composition change during the polarisation should be related to the corrosion resistance of the alloy in the shallow sour conditions.

Effect of carbon addition on the passivity of hypoeutectic high chromium cast irons.

The effect of adding C on the passivity of hypoeutectic high chromium cast iron (HCCI) was investigated in a pH 8.4 boric-borate buffer solution. The microstructure of HCCI is composed of austenite and carbide phases, whose fractions and chemical compositions are influenced by the amount of C added. Electrochemical and surface analyses revealed that the addition of C in the HCCI increased the defect densities in the n-type and p-type semiconductive oxide layers on the austenite and carbide phases, respectively.

Phytochemicals as Anti-Inflammatory Agents in Animal Models of Prevalent Inflammatory Diseases.

Phytochemicals are known to have anti-inflammatory effects in vitro and in vivo, such as in inflammatory disease model systems. Inflammation is an essential immune response to exogenous stimuli such as infection and injury. Although inflammation is a necessary host-defense mechanism, chronic inflammation is associated with the continuous local or systemic release of inflammatory mediators, non-cytokine mediators, such as ROS and NO, and inflammatory cytokines are strongly implicated in the pathogenesis of various inflammatory disorders. Phytochemicals that exhibit anti-inflammatory mechanisms that reduce sustained inflammation could be therapeutic candidates for various inflammatory diseases. These phytochemicals act by modulating several main inflammatory signaling pathways, including NF-κB, MAPKs, STAT, and Nrf-2 signaling. Here, we discuss the characteristics of phytochemicals that possess anti-inflammatory activities in various chronic inflammatory diseases and review the molecular signaling pathways altered by these anti-inflammatory phytochemicals, with a focus on transcription factor pathways. Furthermore, to evaluate the phytochemicals as drug candidates, we translate the effective doses of phytochemicals in mice or rat disease models into the human-relevant equivalent and compare the human-relevant equivalent doses of several phytochemicals with current anti-inflammatory drugs doses used in different types of chronic inflammatory diseases.

Electrochemical Screening of Tungsten Trioxide-Nickel Oxide Thin Film Combinatorial Library at Low Nickel Concentrations.

The electrochemical behavior of a tungsten trioxide-nickel oxide (WO3-NiO) thin film library was investigated using scanning droplet cell microscopy (SDCM) in 0.1 mol dm-3 sodium perchlorate (NaClO4) solution. The WO3-Ni film library was deposited by thermal coevaporation on an indium tin oxide (ITO)-coated glass substrate in an atomic Ni concentration range from 2.8 to 15.6 at. %. After an oxidation/crystallization heat treatment, the Ni was oxidized and the crystal structure of WO3-NiO was transformed from monoclinic WO3 (3.5 at. % Ni) to cubic WO3 (up to 7.1 at. % Ni) and again to monoclinic WO3 when the Ni amount increased (>11.8 at. %). Proton (H+) intercalation (cathodic reaction) and deintercalation (anodic reaction) into the WO3-NiO mixed phases was induced. Electrochemical impedance spectroscopy (EIS) and Mott-Schottky (M-S) analysis revealed that the WO3-NiO film has n-type bilayer capacitive property, with the outer capacitive layer having a higher defect density than the inner capacitive layer. With a Ni concentration of 7.1 at. %, the WO3-NiO film was the most defective in the library. Introduction of the Ni cation into the WO3 network was associated with changes of the semiconducting properties of the film.

Clinical significance of lncRNA-ATB expression in human hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a worldwide health problem and it is important to understand the mechanistic roles of the biomolecules involved in its pathogenesis. Long non-coding RNAs (lncRNAs) are frequently and aberrantly expressed in various human cancers and are known to play a role in cancer pathogenesis. The aim of this study was to analyze the expression of lncRNA-ATB in HCC and investigate the implications for prognoses. In total, 100 samples of HCC tissues and their corresponding, adjacent, non-cancerous liver tissues were collected. Total RNAs were extracted and the expression levels of lncRNA-ATB were measured by qRT-PCR. The association of lncRNA expression with clinicopathological features and patient survival were then analyzed. LncRNA-ATB was significantly upregulated in HCC tissues compared with the levels in corresponding non-cancerous tissues. Expression of lncRNA-ATB was significantly associated with portal vein thrombosis, intrahepatic or extrahepatic metastases, mUICC stage, and the BCLC stage. Large tumors (> 5 cm, HR = 3.851, 95% CI = 1.431-10.364, p = 0.008) and higher lncRNA-ATB expression (HR = 4.158, 95% CI = 1.226-14.107, p = 0.022) were the significant prognostic factors for overall survival. With this novel evidence of the involvement of lncRNA-ATB in HCC pathogenesis and clinical features, lncRNA-ATB can be concluded to have potential as a biomarker for the prognosis of HCC and as a targeted therapy for afflicted patients.