Abstract: Glaciers are highly sensitive to climate change and are undergoing significant changes in mid-latitudes. In this study, we analyzed the spatiotemporal changes of typical glaciers and their responses to climate change in the period of 1990–2015 in 4 different mountainous sub-regions in Xinjiang Uygur Autonomous Region of Northwest China: the Bogda Peak and Karlik Mountain sub-regions in the Tianshan Mountains; the Yinsugaiti Glacier sub-region in the Karakorum Mountains; and the Youyi Peak sub-region in the Altay Mountains. The standardized snow cover index (NDSI) and correlation analysis were used to reveal the glacier area changes in the 4 sub-regions from 1990 to 2015. Glacial areas in the Bogda Peak, Karlik Mountain, Yinsugaiti Glacier, and Youyi Peak sub-regions in the period of 1990–2015 decreased by 57.7, 369.1, 369.1, and 170.4 km², respectively. Analysis of glacier area center of gravity showed that quadrant changes of glacier areas in the 4 sub-regions moved towards the origin. Glacier area on the south aspect of the Karlik Mountain sub-region was larger than that on the north aspect, while glacier areas on the north aspect of the other 3 sub-regions were larger than those on the south aspect. Increased precipitation in the Karlik Mountain sub-region inhibited the retreat of glaciers to a certain extent. However, glacier area changes in the Bogda Peak and Youyi Peak sub-regions were not sensitive to the increased precipitation. On a seasonal time scale, glacier area changes in the Bogda Peak, Karlik Mountain, Yinsugaiti Glacier, and Youyi Peak sub-regions were mainly caused by accumulated temperature in the wet season; on an annual time scale, the correlation coefficient between glacier area and annual average temperature was –0.72 and passed the significance test at P<0.05 level in the Karlik Mountain sub-region. The findings of this study can provide a scientific basis for water resources management in the arid and semi-arid regions of Northwest China in the context of global warming.
摘要： Doped elements in alloys significantly impact their performance. Conventional methods usually sputter the surface material of the sample, or their performance is limited to the surface of alloys owing to their poor penetration ability. The X-ray K-edge subtraction (KES) method exhibits great potential for the nondestructive in situ detection of element contents in alloys. However, the signal of doped elements usually deteriorates because of the strong absorption of the principal component and scattering of crystal grains. This in turn prevents the extensive application of X-ray KES imaging to alloys. In this study, methods were developed to calibrate the linearity between the grayscale of the KES image and element content. The methods were aimed at the sensitive analysis of elements in alloys. Furthermore, experiments with phantoms and alloys demonstrated that, after elaborate calibration, X-ray KES imaging is capable of nondestructive and sensitive analysis of doped elements in alloys.
摘要：Scavenger receptor class B, member 2 (SCARB2) is essential for endosome biogenesis and reorganization and serves as a receptor for both beta-glucocerebrosidase and enterovirus 71. However, little is known about its function in innate immune cells. In this study, we show that, among human peripheral blood cells, SCARB2 is most highly expressed in plasmacytoid dendritic cells (pDCs), and its expression is further upregulated by CpG oligodeoxynucleotide stimulation. Knockdown of SCARB2 in pDC cell line GEN2.2 dramatically reduces CpG-induced type I IFN production. Detailed studies reveal that SCARB2 localizes in late endosome/lysosome of pDCs, and knockdown of SCARB2 does not affect CpG oligodeoxynucleotide uptake but results in the retention of TLR9 in the endoplasmic reticulum and an impaired nuclear translocation of IFN regulatory factor 7. The IFN-I production by TLR7 ligand stimulation is also impaired by SCARB2 knockdown. However, SCARB2 is not essential for influenza virus or HSV-induced IFN-I production. These findings suggest that SCARB2 regulates TLR9-dependent IFN-I production of pDCs by mediating endosomal translocation of TLR9 and nuclear translocation of IFN regulatory factor 7.