The Tienshan Mountains, with its status as “water tower”, is the main water source and ecological barrier in Central Asia. The rapid warming affected precipitation amounts and fraction as well as the original glacier/snowmelt water processes, thereby affecting the runoff and water storage. The ratio of snowfall to precipitation (S/P) experienced a downward trend, along with a shift from snow to rain. Spatially, the snow cover area in Middle Tienshan Mountains decreased significantly, while that in West Tienshan Mountains increased slightly. Approximately 97.52% of glaciers in the Tienshan Mountains showed a retreating trend, which was especially obvious in the North and East Tienshan Mountains. River runoff responds in a complex way to changes in climate and cryosphere. It appears that catchments with a higher fraction of glacierized area showed mainly increasing runoff trends, while river basins with less or no glacierization exhibited large variations in the observed runoff changes. The total water storage in the Tienshan Mountains also experienced a significant decreasing trend in Middle and East Tienshan Mountains, but a slight decreasing trend in West Tienshan Mountains, totally at an average rate of −3.72 mm/a. In future, water storage levels are expected to show deficits for the next half-century.

No abstract

Observations indicate that although average temperatures in Central Asia showed almost no increases from 1997 to 2013, they have been in a state of high variability. Despite the lack of a clear increasing trend, this 15 year period is still the hottest in nearly half a century. Precipitation in Central Asia remained relatively stable from 1960 to 1986 and then showed a sharp increase in 1987. Since the beginning of the 21st century, however, the increasing rate of precipitation has diminished. Dramatic changes in meteorological conditions could potentially have a strong impact on the region's natural ecosystems, as some significant changes have already occurred. Specifically, the normalized difference vegetation index (NDVI) of natural vegetation in Central Asia during 1982–2013 exhibited an increasing trend at a rate of 0.004 per decade prior to 1998, after which the trends reversed, and the NDVI decreased at a rate of 0.003 per decade. Moreover, our results indicate that shrub cover and patch size exhibited a significant increase in 2000–2013 compared to the 1980s–1990s, including shrub encroachment on grasslands. Over the past 10 years, 8% of grassland has converted to shrubland. Precipitation increased in the 1990s, providing favorable conditions for vegetation growth, but precipitation slightly reduced at the end of the 2000s. Meanwhile, warming intensified 0.93°C since 1997 compared to the average value in 1960–1997, causing less moisture to be available for vegetation growth in Central Asia.

No abstract

The endothelial cell protein C receptor (EPCR) is a type 1 transmembrane protein found primarily on endothelium that binds both protein C and activated protein C with similar affinity. EPCR augments the activation of protein C by the thrombin-thrombomodulin complex. To determine the physiological importance of EPCR, we generated EPCR-deficient mice by homologous targeting in embryonic stem cells. Genotyping of progeny obtained from EPCR ؉/؊ interbreeding indicated that EPCR ؊/؊ embryos died on or before embryonic day 10.5 (E10.5). Reverse transcriptase-PCR confirmed the absence of EPCR mRNA in EPCR ؊/؊ embryos. EPCRembryos removed from extra-embryonic membranes and tissues at day E7.5 and cultured in vitro developed beyond E10.5, suggesting a role for EPCR in the normal function of the placenta and/or at the materno-embryonic interface. Immunohistochemistry revealed the lack of EPCR in trophoblast giant cells of EPCR ؊/؊ embryos. These cells, which normally express EPCR, are in direct contact with the maternal circulation and its clotting factors. In EPCR ؊/؊ embryos, greatly increased fibrin deposition was detected around these cells. To prevent this fibrin deposition, EPCR ؉/؊ -crossed female mice received a daily subcutaneous injection of enoxaparin through pregnancy. Although some EPCR ؊/؊ embryos were rescued from midgestational lethality, this regimen yielded no EPCR ؊/؊ pups. We conclude that EPCR is essential for normal embryonic development. Moreover, EPCR plays a key role in preventing thrombosis at the maternal-embryonic interface.

The endothelial cell protein C receptor (EPCR) augments protein C activation by the thrombin-thrombomodulin complex. Deletion of the EPCR gene (Procr) in mice leads to embryonic lethality before embryonic day 10 (E10.0). EPCR is detected in the giant trophoblast cells at the fetomaternal boundary from E7.5 and weakly in embryonic aortic endothelial cells from E13.5, suggesting that extraembryonic EPCR expression may be essential for embryonic viability. Using conditional knock-out strategies, we demonstrate that Procr-deficient embryos with EPCR expression on placenta giant trophoblasts can be carried to term and then develop normally. Conversely, EPCR expression in the embryo, without expression in the giant trophoblast cells, does not rescue the mice. In genetically modified mice with low tissue factor activity, Procr deficiency is not lethal to the embryo. As adults, Procr-deficient mice generate more thrombin and activate less protein C in response to procoagulant stimuli. Spontaneous thrombin formation in the deficient animals increases with age. These findings show that extraembryonic EPCR expression is critical for embryo development. IntroductionThe protein C anticoagulant pathway serves as an "on-demand" anticoagulant system that controls thrombin generation by inhibiting factors Va and VIIIa. 1 Thrombin not only activates platelets and clots fibrinogen, but also binds to thrombomodulin (TM) on the endothelium, at which time these procoagulant activities of thrombin are blocked, while conversion of protein C to the anticoagulant serine proteinase, activated protein C (APC), is augmented. 2 Endothelial cell protein C receptor (EPCR) binds protein C and increases the rate of protein C activation by the thrombin-TM complex in cell culture 3 and in vivo. 4 EPCR overexpression on the endothelial cell surface increases the rate of protein C activation further. 5 Inhibition of EPCR-protein C interaction converts the response to sublethal concentrations of Escherichia coli into a lethal response. These animals exhibit disseminated intravascular coagulation, intense neutrophil influx into the tissues, and elevation of some of the inflammatory cytokines. 6 In adults, EPCR is localized primarily on endothelial cells of large blood vessels and is very low or absent from the microvascular endothelium of most tissues. 7 EPCR is also abundant on the trophoblast giant cells at the feto-maternal boundary from embryonic day 7.5 (E7.5), suggesting a role in the hemostatic regulation of the maternal blood that irrigates these surfaces. Deletion of the EPCR gene (Procr) in mice leads to embryonic lethality before E10.0. (Gene symbols used in this paper are in accordance with the style guidelines of the National Center for Biotechnology Information, National Institutes of Health. Specifically, the gene encoding EPCR is designated Procr; tissue factor, F3; thrombomodulin, Thbd; Tie2, Tek; and Mox2, Meox2.) At this time, excess fibrin deposition is detected around the trophoblast giant cells (derived from the Procr Ϫ/Ϫ embryo...

Over the past two decades, the viewpoint of atherosclerosis has been replaced gradually by a lipiddriven, chronic, low-grade inflammatory disease of the arterial wall. Current treatment of atherosclerosis is focused on limiting its risk factors, such as hyperlipidemia or hypertension. However, treatment targeting the inflammatory nature of atherosclerosis is still very limited and deserves further attention to fight atherosclerosis successfully. Here, we review the current development of inflammation and atherosclerosis to discuss novel insights and potential targets in atherosclerosis, and to address drug discovery based on anti-inflammatory strategy in atherosclerotic disease.

The impacts of climate change and human activities on the surface runoff were analyzed by the Mann-Kendall and trend analysis methods based on the hydrological, meteorological and socioeconomic data over the last 50 years in the Tarim River basin. Results show that the runoff in the headstreams increased but that in the mainstreams decreased significantly during the past 50 years. The former is a response to climate change, and the later is due to human activities. The surface runoff in the mainstreams decreased by 41.59, 63.77 and 75.15% in the 1970s, 1980s and 1990s, respectively, as compared to that without being disturbed by human activities in the same period. The main human activities are the irrigated agriculture combined with population increase in the region. As a consequence, the ecosystem in the lower reaches of Tarim River has degenerated, largely owing to inappropriate allocation of water resources.