It is highly attractive to construct cost-effective hybrid electrocatalysts with superior activity for the hydrogen evolution reaction (HER) in acids. In this communication, we report a novel structure consisting of a CuP-CoP hybrid nanowire array supported on carbon cloth (CuP-CoP/CC) as a superior HER electrocatalyst in acidic media. Owing to the synergistic effect between CuP and CoP, this CuP-CoP/CC catalyst exhibits superior catalytic HER performance, needing an overpotential of 59 mV to drive a current density of 10 mA cm in 0.5 M HSO, 24 and 130 mV less than that for CoP/CC and CuP/CC, respectively. Moreover, this catalyst also shows high long-term electrochemical durability.

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A series of Cu−Ni/CeO 2 -nanotube catalysts is prepared by an impregnation method for CO 2 hydrogenation to CH 3 OH. Regular CeO 2 nanotubes are perfectly formed with a tube diameter of about 30−50 nm and Cu−Ni alloy is well dispersed on CeO 2 nanotube without nanotube morphology change. There is a synergistic effect between Ni and Cu, promoting the bimetallic Cu−Ni dispersion, reducibility, CO adsorption and hydrogenation. Additionally, a strong interaction is observed between Cu−Ni alloy and CeO 2 , and it contributes to partial reduction of Ce 4+ to Ce 3+ and formation of oxygen vacancies which adsorb and activate CO 2 . It is shown that both CO 2 conversion and CH 3 OH space-time yield increase at first, reach their maximum values at a Ni/ (Cu+Ni) ratio of 2/3, and then decrease with increasing the Ni/(Cu+Ni) ratio. The CeO 2 -nanotube supported CuNi 2 catalyst gives CO 2 conversion of 17.8% and CH 3 OH space-time yield of 18.1 mmol/(g cat •h) after preliminary optimization. Furthermore, it exhibits an excellent catalytic performance within a wide range of space velocity.

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This prospective cross-sectional study aimed to evaluate the agreement of two new biometers for measuring ocular biometric parameters in young healthy eyes. ocular biometric parameters were measured using IOLMaster 700 and OA-2000. Power vector analyses of Cartesian (J0) and oblique (J45) components of corneal astigmatism were performed. The right eyes of 103 healthy volunteers were analyzed. The 95% limits of agreement ranged from −0.03 to 0.03 mm, −0.08 to 0.07 mm, −0.18 to 0.18 diopters (D), −1.09 to 1.16 D, −1.18 to 1.15 D for axial length (AL), anterior chamber depth (ACD), mean keratometry, J0 and J45 respectively, which were all comparable between the two biometers, while significant differences were detected in lens thickness (LT), central corneal thickness (CCT), whiteto-white (WTW) and pupil diameter (PD). Predicted intraocular lens (IOL) powers were comparable between the two biometers by Haigis and Barrett Universal II formulas, while not by SRK/T, Hoffer Q and Holladay 2. Excepting CCT, WTW and PD meaurements, IOLMaster 700 and OA-2000 have excellent agreement on ocular biometric measurements and astigmatism power vectors, which provides more options for ocular biometric measurements and enables constant optimization for IOL power calculation.

The exact mechanism of myocardial hypertrophy has not been completely elucidated. NOD-like receptor protein 3 (NLRP3) and the pyroptotic cascade play a critical role in cardiac hypertrophy and inflammation. The myokine irisin can inhibit NLRP3 activation, although its exact mechanism of action is unknown. In this study, we induced cardiac hypertrophy in a mouse model via aortic constriction (TAC) to further explore the pathological role of NLRP3 inflammasome-mediated pyroptosis and the potential therapeutic effects of irisin. Cardiac hypertrophy significantly increased the percentage of apoptotic cells and upregulated IL-1β, cleaved caspase-1, and GSDMD-N that lie downstream of the NLRP3 inflammasome. Subsequently, irisin was co-administered to the TAC mice or angiotensin II (Ang-II)-treated cardiomyocytes to observe whether it could attenuate pyroptosis and cardiac hypertrophy. We established a direct association between pyroptosis and cardiac hypertrophy and found that pharmacological or genetic inhibition of NLRP3 attenuated cardiac hypertrophy. Furthermore, ectopic overexpression of NLRP3 abrogated the cardioprotective effects of irisin. To summarize, pyroptosis is a pathological factor in cardiac hypertrophy, and irisin is a promising therapeutic agent that inhibits NLRP3-mediated pyroptosis of cardiomyocytes.

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Background and Objectives: Bone marrow mesenchymal stem cells (BMSCs) is an ideal source of stem cells in the treatment of intrauterine adhesion. Exosomes are a type of membrane vesicle and the diameter is 30∼100 nm. Exosomes can take their contents into the target cells, releasing and exerting their functions. In this study, we intend to study the role of human BMSC-derived exosomes (BMSC-Exo) in promoting endometrial damage repair in the treatment of IUA. Methods: We used the magnetic bead affinity method to extract BMSC-Exo and analyzed its biological character. Then we co-cultured the BMSCs-Exo with endometrial cells to detect its effect. We injected BMSCs-Exo into the IUA mouse model. We over-expressed miR-29a in BMSCs-Exo by transient transfection, then used RT-PCR to analyze the expression of the related genes. Results: BMSCs-Exo expressed exosome-specific proteins CD9, CD63, and CD81. BMSCs-Exo could bring the contents into the target cells. BMSCs-Exo can promote endometrial repair in vitro or in vivo. BMSCs-Exo overexpressing miR-29a can reduce αSMA, Collagen I, SMAD2, and SMAD3. Conclusions: In this study, we successfully isolated BMSCs-Exo and proved its character and biological activity. BMSCs-Exo can promote cell proliferation and cell migration in vitro and can repair damaged endometrium in the IUA model. The presence of miR-29a in BMSCs-Exo may be an important factor in its resistance to fibrosis during endometrial repair of IUA. This study provides new ideas for the treatment of patients with IUA and has important clinical research significance.