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Based on the meteorological data (2009–2018) acquired by high-density automatic meteorological stations in the central urban area (CUA) of Beijing, this study adopted an urban-rural ratio method to construct a qr to quantify the impact of urbanization on the spatial and temporal distribution of specific humidity (q). And the urban morphological parameters such as building height (BH), building density (BD), floor area ratio (FAR), sky view factor (SVF), and land surface parameters including vegetation coverage (VC) and impervious coverage (IC) with 500-m spatial resolution in CUA were calculated, and furthermore, the relationships between the six spatial layout parameters and another indicator, urban heat island (UHI) intensity, and qr were studied. The results show that q of CUA is 81~114% of that of the suburbs, and the urban dry island (UDI) effect and urban wet island (UWI) effect coexist throughout the year. The maximum UDI occurs during autumn daytime and the maximum UWI appears at night in winter. The UDI effect is prone to occur in areas with VC < 11%, IC >85%, BH > 15 m, and BD > 24%, while the UWI effect is more likely to appear in areas with VC > 35% and FAR < 0.3. The contributions of the six urbanization parameters to the spatial change of qr in different time periods are 6.2 to 33.5%, and VC is the largest (33.5%), followed by BD (31.9%) and SVF (29.9%), and the main factor affecting the annual average qr is BD with the contribution of 18.9%. Compared with the urbanization parameters, the UHI is more important and the contribution to the change of q can be up to 35.7%. The results show that these spatial layout parameters are not sufficient to explain the main change in q, and more other parameters need to be considered. [ABSTRACT FROM AUTHOR]

Apoptosis occurs frequently in myocardial infarction, oxidative stress injury, and ischemia/reperfusion injury, and plays a pivotal role in the development of heart diseases. Inhibition of apoptosis alone does not necessarily lead to meaningful rescue in terms of either cardiomyocyte survival or function. Activation of the PI3K/Akt signaling pathway induced by insulin not only inhibits cardiomyocyte apoptosis but also substantially preserves and even improves regional and overall cardiac function. Insulin can protect cardiomyocytes from apoptosis by regulating a number of signaling molecules, such as eNOS, FOXOs, Bad, GSK-3β, mTOR, NDRG2, and Nrf2, through activating PI3K and Akt. This review focuses on the protective mechanisms and targets of insulin identified in the prevention and treatment of myocardial injury. [ABSTRACT FROM AUTHOR]