Evolution of Meteorological Conditions during a Heavy Air Pollution Event under the Influence of Shallow Foehn in Urumqi, China

The air pollution in Urumqi which is located on the northern slope of the Tianshan Mountains in northwestern China,is very serious in winter.Of particular importance is the influence of terrain-induced shallow foehn,known locally as elevated southeasterly gale(ESEG).It usually modulates atmospheric boundary layer structure and wind field patterns and produces favorable meteorological conditions conducive to hazardous air pollution.During 2013-17,Urumqi had an average of 50 d yr-1 of heavy pollution(daily average PM2.5 concentration>150μg m-3),of which 41 days were in winter.The majority(71.4%)of heavy pollution processes were associated with the shallow foehn.Based on microwave radiometer,wind profiler,and surface observations,the surface meteorological fields and boundary layer evolution during the worst pollution episode in Urumqi during 16-23 February 2013 are investigated.The results illustrate the significant role of shallow foehn in the building,strengthening,and collapsing of temperature inversions.There were four wind field patterns corresponding to four different phases during the whole pollution event.The most serious pollution phase featured shallow foehn activity in the south of Urumqi city and the appearance of an intense inversion layer below 600 m.Intense convergence caused by foehn and mountain-valley winds was sustained during most of the phase,resulting in pollutants sinking downward to the lower boundary layer and accumulating around urban area.The key indicators of such events identified in this study are highly correlated to particulate matter concentrations and could be used to predict heavy pollution episodes in the feature.

Multi-omics analyses of G6PD deficiency variants in Chinese population

Glucose-6-phosphate dehydrogenase(G6PD)deficiency is one of the most prevalent hereditary and X-linked enzyme disorders caused by the pathogenetic G6PD(NM_001042351.2)variants(Yang et al.,2016).The clinical manifestations of G6PD deficiency offer a wide spectrum of diverse disease phenotypes(Hecker et al.,2013).Investigations of prevalence and molecular epidemiology demonstrate that G6PD deficiency affects over 400 milion individuals worldwide and leads to thousands of deaths annually(Mortality and Causes of Death,2015).

Adhesion of subsets of human blood mononuclear cells to porcine endothelial cells

Cellular immune response is a major barrier to xenotransplantation, and cell adhesion is the first step in intercellular recognition. Flow-cytometric adhesion assay has been used to investigate the differential adhesions of monocyte (Mo), natural killer celi (NK) and T lymphocyte (T) present within human peripheral blood mononuclear cells (PBMC) to porcine aortic endothelial cells (PAEC), and to demonstrate the effect of human interferon-γ (hIFN-γ) or/and tumor necrosis factor-α (hTNF-α) pretreatment of PAEC on their adhesiveness f or different PBMC subsets. The preferential sequence for PBMC subset binding to resting PAEC is Mo, NK and T cells, among which T cells show the slightest adherence; hTNF- a can act across the species, and augment Mo, NK and T cell adhesion ratios by 40%, 110% and 3 times, respectively. These results confirm at the cell level that host Mo and NK cells are major participants in the cellular xenograft rejection, thereby, providing a prerequisite for further studying the

Genistein inhibits human TNF-α-induced porcine endothelial cell adhesiveness for human monocytes and natural killer cells

Cellular immune response is a major barrier to xenotransplantation. Human tumor necrosis factor-α (hTNF-α) possesses cross-species activity and directly amplifies the immune rejection via the upregulation of adhesion molecules on porcine endothelium. We investigated the role of protein tyrosine phosphorylation in the induction of expression of E-selectin and vascular cell adhesion molecule-1 (VCAM-1), and the augmentation of adhesion of human peripheral blood monocytes (PBMo) and natural killer cells (PBNK), after rhTNF-α-stimulation of porcine aortic endo-thelial cells (PAEC) in vitro. rhTNF-α-increased adhesiveness of PAEC for both PBMo and PBNK was dose-dependently reduced by pretreatment of PAEC with the selective protein tyrosine kinase (PTK) inhibitor genistein. The inhibitory effect occurred at the early time of PAEC activation triggered by rhTNF-α, and was completely reversible. PTK activity assay indicated that genistein also suppressed rhTNF-α stimulated activation of protein tyrosine