A detailed analysis of the dehydrogenation mechanism and reversibility of LiBH₄ doped by active Al* derived from AlH₃ was performed by thermogravimetry (TG), differential scanning calorimetry (DSC), mass spectral analysis (MS), powder X-ray diffraction (XRD), scanning electronic microscopy (SEM) and Fourier transform infrared spectroscopy (FTIR). The results show that the dehydrogenation of LiBH₄/Al* is a five-step reaction: (1) LiBH₄ + Al → LiH + AlB₂ + “Li-Al-B-H” + B₂H₆ + H₂; (2) the decomposition of "Li-Al-B-H" compounds liberating H₂; (3) 2LiBH₄ + Al → 2LiH + AlB₂ + 3H₂; (4) LiBH₄ → LiH + B + 3/2H₂; (5) LiH + Al → LiAl + 1/2H₂. And the reversibility of LiBH₄/Al* composite is based on equation as follows: LiH + LiAl + AlB₂ + 7/2H₂ ↔ 2LiBH₄ + 2Al. The extent of dehydrogenation reaction between LiBH₄ and Al* greatly depends on the precipitation and growth of reaction products (LiH, AlB₂ and LiAl, etc.) on the surface of Al*. A passivation shell of Al* formed by these products is the kinetic barrier to the dehydrogenation of LiBH₄/Al* composite.

Due to the special terrain of Urumqi (in the valley area), which often triggers strong foehn weather, and causes huge losses to local people's lives and social economy. This study uses in-situ surface meteorological variables (including the hourly temperature, pressure, humidity, wind, etc.) from the Urumqi Meteorological Station (downstream station, DS) and the Dabancheng Meteorological Station (upstream station, US) in the Middle Tianshan Valley and NCEP/NCAR reanalysis data from 2008 to 2022. A dataset of the foehn weather process at DS in the past 15 years is established and the variation patterns of each meteorological variable during the process of foehn is analyzed. Based on the physical mechanism of the occurrence of foehn, a three-element identification standard for foehn in Urumqi is established by comparing and analyzing the variation of wind direction (WD), wind speed (WS), and the difference of potential temperature (Δθ) between DS and US during the period of foehn and non-foehn from 2013 to 2022, namely: 94°≤ 2-minute average WD ≤168°, 2-minute average WS ≥2.0 m/s, and Δθ between DS and US ≥ 0.29 K. According to the test and evaluation, the three-element identification standard has an accuracy of 82.96%, and a hit rate of 89.50% for the occurrence of foehn in Urumqi from 2008 to 2012. Moreover, the hit rate of foehn identification is 100% for strong wind or above (i.e., 2-minute average WS ≥10.8 m/s) WS. In addition, combined with two predictors of sea-level pressure difference (ΔP) and Δθ between DS and US, forecasting foehn can be more accurately predicted than a single forecasting factor. When ΔP ≤ -12 hPa and Δθ≥5 K, the probability of the occurrence of foehn is more than 90%. This study provides certain reference and application value for the weather forecasting operation of foehn.

Skeletal muscle atrophy is one of the major side effects of high dose or sustained usage of glucocorticoids. Pyroptosis is a novel form of pro-inflammatory programmed cell death that may contribute to skeletal muscle injury. Trimetazidine, a well-known anti-anginal agent, can also improve skeletal muscle performance both in human and mice. We here showed that dexamethasone induced atrophy, evidenced by the increase of muscle atrophy F-box (Atrogin-1) and muscle ring finger 1 (MuRF1) expression , and the decrease of myotube diameter in C2C12 myotubes. Dexamethasone also induced pyroptosis, indicated by upregulated pyroptosis-related protein NLRP3, Caspase-1 and GSDMD. Knockdown of NLRP3 or GSDMD attenuated dexamethasone-induced myotube pyroptosis and atrophy. Trimetazidine administration ameliorated dexamethasone-induced muscle atrophy both in vivo and in vitro. Moreover, trimetazidine improved exercise tolerance, as evidenced by increased running distance and running time, as well as increased skeletal muscle mass in dexamethasone-treated mice. Mechanically, trimetazidine could reverse dexamethasone-induced activation of pyroptosis both in C2C12 myotubes and in mice. Taken together, our present study demonstrated that NLRP3/GSDMD pathway-mediated pyroptosis was involved in dexamethasone-induced skeletal muscle atrophy. Trimetazidine could partially alleviate dexamethasone-induced skeletal muscle atrophy, and increase the diameter of C2C12 myotubes via inhibiting pyroptosis. Thus, trimetazidine might be a potential therapeutic compound for the prevention of muscle atrophy in glucocorticoid-treated patients.