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Highly degenerate n-type CdO with high electron mobility is a promising transparent conducting oxide (TCO) for optoelectronic devices utilizing a spectrum in the Vis-NIR range. In particular, it has been shown that doped CdO thin films can show much superior transparency of >80% in the NIR region compared to conventional transparent conducting oxide (e.g., Sn-doped In2O3) thin films with a similar sheet resistance. However, CdO thin films typically experience rapid degradation in their electron mobilities when exposed to environmental conditions with H2O moisture. Here, we studied the effects of thermal annealing on the environmental stability of In-doped CdO (CdO:In) using a combination of different analytical techniques. CdO:In thin films with different In concentration (0%–8.3%) synthesized by magnetron sputtering were subjected to different post-thermal annealing (PTA) and then aged in different environmental conditions with varying relative humidity (RH) in the range of 0%–85%. Our results reveal that the degradation of CdO:In thin films can be primarily attributed to the oxygen vacancy-related defects at the grain boundaries, which can readily react with the OH− in the moisture. The moisture induced degradation can be mitigated by appropriate PTA at high temperatures (>400 °C) where grain boundary defects, primarily associated with Cd vacancies, can be passivated through hydrogen (H), thus enhancing their environmental stability. The present study provides a comprehensive understanding of the instability mechanisms and defect passivation in transparent conducting CdO:In thin films, which can also be relevant for other wide gap oxides. [ABSTRACT FROM AUTHOR]

In traditional Chinese medicine, Radix Astragali has played a vital role in treating progressive fibrotic diseases. One of its main active components, astragaloside IV, is a promising anti-fibrotic treatment despite its extremely low bioavailability. Our study aimed to optimize sodium astragalosidate (SA) by salt formation to improve solubility and oral absorption for anti-fibrotic therapy in vivo . Isoproterenol-induced myocardial fibrosis rat models and obese BKS-db mice presenting diabetic kidney fibrosis were used in this study. Daily oral administration of SA (20 mg/kg) for 14 days ameliorated cardiac fibrosis by reducing collagen accumulation and fibrosis-related inflammatory signals, including TNF-α, IL-1β, and IL-6. In db/db mice, SA (5,10, and 20 mg/kg per day for 8 weeks) dose-dependently alleviated lipid metabolism impairment and renal dysfunction when administered orally. Furthermore, Western blot and immunohistochemistry analyses demonstrated that SA treatment inhibited renal fibrosis by suppressing TGF-β1/Smads signaling. Taken together, our findings provide the oral-route medication availability of SA, which thus might offer a novel lead compound in preclinical trial-enabling studies for developing a long-term therapy to treat and prevent fibrosis., Competing Interests: The authors declare no competing financial interest., (© 2024 The Authors. Published by American Chemical Society.)

Corticosteroid insensitivity, which is induced by cigarette smoke extract (CSE), is a significant barrier when treating chronic obstructive pulmonary disease (COPD). Erythromycin (EM) has been shown to have an anti-inflammatory role in some chronic airway inflammatory diseases, particularly diffuse panbronchiolitis and cystic fibrosis. Here, we explored whether the combination therapy of EM and dexamethasone (Dex) reverses corticosteroid insensitivity and investigated the molecular mechanism by which this occurs. We demonstrated that the combination of EM and Dex restored corticosteroid sensitivity in peripheral blood mononuclear cells (PBMCs) from COPD patients and U937 cells after CSE exposure. Moreover, pretreatment with 10, 50, or 100 μg/ml EM reversed the HDAC2 protein reduction induced by CSE exposure in a dose-dependent manner. U937 cells exposed to CSE show a reduction in histone deacetylase (HDAC) activity, which was potently reversed by EM or combination treatment. Although 10 and 17.5% CSE increased phosphorylated Akt (PAkt) expression in a concentration-dependent manner, preapplication of EM and the combination treatment in particular blocked this PAkt increase. Total Akt levels were unaffected by CSE or EM treatments. Furthermore, the combination treatment enhanced glucocorticoid receptor (GR)α expression. Our results demonstrate that the combination therapy of EM and Dex can restore corticosteroid sensitivity through inhibition of the PI3K-δ/Akt pathway and enhancing GRα expression., (Copyright © 2015 the American Physiological Society.)

Objective: To examine the expression of matrix metalloproteinases (MMP)-2, -9, tissue inhibitor of matrix metalloproteinase (TIMP)-1 and hs-CRP, and their relationship with coronary artery in children with Kawasaki disease., Methods: One hundred and fifty-one children with Kawasaki disease (111 cases with coronary artery damage and 40 cases without) and 60 healthy children were enrolled. The expression of MMP-2, MMP-9 and TIMP-1 was detected using ELISA, and the hs-CRP concentration was measured using the endpoint nephelometry., Results: There were significant differences in the level of MMP-2, MMP-9 and hs-CRP between the patients with or without coronary artery damage and the healthy children (p<0.05). The levels of MMP-2, MMP-9 and hs-CRP were the highest in the cardiovascular damage group (p<0.05). There were positive correlations between MMP-2, MMP-9 and TIMP-1 in children with Kawasaki disease., Conclusions: MMP-2, MMP-9, TIMP-1 and hs-CRP may play important roles in the development of Kawasaki disease. The combined measurement of MMP-2, MMP-9 and hs-CRP may be useful in the evaluation of the severity in children with Kawasaki disease.