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W-(0, 0.1, 0.3, 0.5) wt.% Hf (mass fraction, wt.%) materials were fabricated by the powder metallurgy method and hot rolling. The microstructure, mechanical properties, and high-temperature stability of alloys with varying compositions were systematically studied. The active element Hf can react with the impurity O segregated at the grain boundary to form fine dispersed HfO2 particles, refining the grains and purifies and strengthening the grain boundary. The average size of the sub-grains in the W-0.3 wt.% Hf alloy is 4.32 μm, and the number density of the in situ-formed second phase is 6.4 × 1017 m−3. The W-0.3 wt.% Hf alloy has excellent mechanical properties in all compositions of alloys. The ultimate tensile strength (UTS) is 1048 ± 17.02 MPa at 100 °C, the ductile fracture occurs at 150 °C, and the total elongation (TE) is 5.91 ± 0.41%. The UTS of the tensile test at 500 °C is 614 ± 7.55 MPa, and the elongation is as high as 43.77 ± 1.54%. However, more Hf addition will increase the size of the second-phase particles and reduce the number density of the second-phase particles, resulting in a decrease in the mechanical properties of the tungsten alloy. The isochronal annealing test shows that the recrystallization temperature of W-Hf alloy is 1400 °C, which is 200 °C higher than rolling pure tungsten. [ABSTRACT FROM AUTHOR]

The electrochemical reduction of carbon dioxide (CO2) to value-added multi-carbon products provides a feasible way to achieve carbon neutrality. However, enhancing the faradaic efficiency for a specific multi-carbon product like ethylene at high current densities is still a challenge. Herein, we report a Cu(II)-benzene-1,3,5-tricarboxylate coordination polymer (Cu-BTC-CP) with asymmetric building units, synthesized by a water etching strategy, for highly selective electrochemical CO2-to-C2H4 conversion. The Cu-BTC-CP catalyst achieves an ethylene faradaic efficiency as large as 65.2 ± 3% at a high current density of 350 mA cm−2 in a flow cell. Operando X-ray absorption fine structure analysis uncovers that the Cu-BTC-CP catalyst reconstructs to low-coordinated copper under reaction conditions. Density functional theory calculations further indicate that the low-coordinated Cu sites on metallic Cu surfaces are favorable for *CO intermediate coupling and promote CO2 conversion to ethylene. [ABSTRACT FROM AUTHOR]

Problem: The increased hypothalamic neurokinin B (NKB) level may contribute to the hyperactive LH pulse secretion in Polycystic ovary syndrome (PCOS). However, the expression and role of the neurokinin B‐neurokinin 3 receptor (NKB‐NK3R) system in the local ovarian tissue of PCOS have not been clarified. We constructed in vivo and in vitro models to elucidate the mechanism of the NKB‐NK3R pathway in reproductive endocrine disorders of PCOS. Method of study: The granulosa cell line‐KGN cells were set in palmitic acid (PA) and dihydrotestosterone (DHT) to simulate the PCOS‐like conditions. And we used the high‐fat/high‐glucose diet to build a PCOS‐like mice model and neurokinin 3 receptor antagonist (NK3Ra) was administered to half of the mice. The expression of the NKB‐NK3R system, mitochondrial functions, hormone levels, and inflammatory state was evaluated. Results: The PCOS‐like stimulations induced the NKB‐NK3R system and MAPK‐ERK pathway overexpression in KGN cells, in an approximate dose and time‐dependent manner. The NKB‐NK3R system overactivated the MAPK‐ERK pathway to increase NNT overexpression, disturb NADH/NADPH pools, aggravate the oxidation state, and decrease ATP production. With overexpression of the NKB‐NK3R system in the local ovarian tissue, ovulatory dysfunction, progesterone deficiency, and pro‐inflammatory states were apparent in PCOS‐like mice. Antagonizing the receptor, NK3R, reversed the adverse reproductive endocrine phenotypes via improving mitochondrial dysfunction. Conclusions: In addition to the central regulation, local ovarian overexpression of the NKB‐NK3R system participated in the adverse reproductive endocrine phenotypes, supporting the therapeutic implications of NK3Ra for PCOS. [ABSTRACT FROM AUTHOR]