The surface air temperature change over the Tibetan Plateau is determined based on historical observations from 1980 to 2013. In contrast to the cooling trend in the rest of China, and the global warming hiatus post-1990s, an accelerated warming trend has appeared over the Tibetan Plateau during 1998–2013 (0.25 °C decade−1), compared with that during 1980–1997 (0.21 °C decade−1). Further results indicate that, to some degree, such an accelerated warming trend might be attributable to cloud–radiation feedback. The increased nocturnal cloud over the northern Tibetan Plateau would warm the nighttime temperature via enhanced atmospheric back-radiation, while the decreased daytime cloud over the southern Tibetan Plateau would induce the daytime sunshine duration to increase, resulting in surface air temperature warming. Meanwhile, the in situ surface wind speed has recovered gradually since 1998, and thus the energy concentration cannot explain the accelerated warming trend over the Tibetan Plateau after the 1990s. It is suggested that cloud–radiation feedback may play an important role in modulating the recent accelerated warming trend over the Tibetan Plateau.

The relationship between Tibetan Plateau (TP) snow cover and the East Asian summer monsoon (EASM) has long been discussed, but the underlying mechanism remains controversial. In this paper, the snow–albedo and snow–hydrology feedbacks over the TP are investigated based on multiple sources of snow data for the period 1979–2011. The results indicate that winter snow cover plays an important role in cooling local air temperature through the snow–albedo effect; the TP surface net solar radiation in years with above-normal snow cover is approximately 18 W m−2 less than that in below-normal snow cover years. However, data analysis demonstrates that persistent effects of winter snow cover are limited to the period from winter to spring over most parts of the central and eastern TP. Therefore, the preceding snow cover over the central and eastern TP exerts little influence over either the in situ summer atmospheric heat source or the EASM, because of its limited persistence. In contrast, the effects of winter or spring snow cover anomalies over the western TP and the Himalayas can last until summer, and these anomalies further influence the EASM by modulating moisture transport to eastern China and favoring eastward-propagating synoptic disturbances that are generated over the TP. Generally, above-normal snow cover over the western TP and the Himalayas facilitates abundant summer precipitation between the Yangtze and Yellow River basins, which is confirmed by results from a regional Weather Research and Forecasting model simulation.

Endothelial dysfunction is involved in various cardiovascular diseases such as atherosclerosis. Endothelial progenitor cells (EPCs) contribute to re-endothelialization and neo-vascularization, and the increase of EPCs in peripherial circulation benefits the prognosis of cardiovascular disease. However, little is known about the biological stimuli that initiate the proliferation and the maintenance of stem cell phenotype of EPCs. Here we reported that human umbilical vein blood derived EPCs expressed gene transcripts coding for Toll-like receptor (TLR) 1-6, TLR8-10, TLR4 co-receptor CD14, and myeloid differentiation factor 88 (MyD88), a TLR adaptor molecule. Protein expression of TLR2, 4, CD14, and MyD88 was also detected by FACS or Western blot. The activation of TLR4 by LPS modulated the expression of TLRs, induced the phosphorylation of NF-kappaB, P38, and ERK42/44, and up-regulated the gene expression of cytokines IL-8, IFN-alpha, IFN-beta, and TNF-alpha, suggesting EPCs expressed functional TLR4. Unexpectedly LPS treatment failed to induce apoptosis in EPCs, but instead promoted cell proliferation of EPCs. Furthermore, the treatment of EPCs with LPS up-regulated stem cell markers AC133 and CD34 in both mRNA and protein levels, and down-regulated the protein expression of differential marker eNOS. These results suggested that TLR4 functions to maintain the stem cell phenotype of EPCs and enlarge its population, which reveals a novel aspect of the multiple-faced TLR biology, and may open new prospects for using TLR4 agonists to promote the production of EPCs for clinical use.

No abstract

No abstract

Temporal variability within the Tibetan Plateau summer monsoon (TPSM) is closely linked to both the East and South Asian summer monsoons over several time scales but has received much less attention than these other systems. In this study, extensive integrations under phase 5 of the Coupled Model Intercomparison Project (CMIP5) historical scenarios from 15 coupled general circulation models (CGCMs) and Atmospheric Model Intercomparison Project (AMIP) runs from eight atmospheric general circulation models (AGCMs) are used to evaluate the performance of these GCMs. Results indicate that all GCMs are able to simulate the climate mean TPSM circulation system. However, the large bias associated with precipitation intensity and patterns remains, despite the higher resolution and inclusion of the indirect effects of sulfate aerosol that have helped to improve the skill of the models to simulate the annual cycle of precipitation in both AGCMs and CGCMs. The interannual variability of the surface heat low and the Tibetan high in most of the AGCMs resembles the observation reasonably because of the prescribed forcing fields. However, only a few models were able to reproduce the observed seesaw pattern associated with the interannual variability of the TPSM and the East Asian summer monsoon (EASM). Regarding long-term trends, most models overestimated the amplitude of the tropospheric warming and the declining trend in the surface heat low between 1979 and 2005. In addition, the observed cooling trend in the upper troposphere and the decline of the Tibetan high were not reproduced by most models. Therefore, there is still significant scope for improving GCM simulations of regional climate change, especially in regions near extensive mountain ranges.

BackgroundCentrosomal protein 55 (CEP55) is an important prognostic biomarker that plays an essential role in the proliferation, migration and invasion of multiple tumors. We aimed to investigate the prognostic value of CEP55 in pN0 esophageal squamous cell carcinoma (ESCC) and explore its biological function in ESCC cells.MethodsWe used immunohistochemistry and Western blot analysis to detect the expression of CEP55 in ESCC. Furthermore, both in vitro and in vivo assays were used to determine the effect of CEP55 on malignant behavior in ESCC cells.ResultsAs expected, we found that CEP55 was overexpressed in ESCC. Univariate and multivariate analyses demonstrated that patients with CEP55 overexpression had a poor prognosis. Additionally, the abilities of proliferation, migration and invasion of cells, as well as the epithelial–mesenchymal transition markers, were all altered with the changed CEP55 expression levels in ESCC cells. Further study elucidated that CEP55 facilitated ESCC via the PI3K/Akt pathway. Blockade of this pathway markedly attenuated CEP55-mediated proliferation, migration, invasion and epithelial–mesenchymal transition of ESCC cells.ConclusionOncogenic CEP55 correlates with a poor prognosis by regulating tumor cell proliferation, migration and invasion via the PI3K/Akt pathway. It can serve as a promising prognostic biomarker and therapeutic target of pN0 ESCC after Ivor-Lewis esophagectomy.

Extracellular ATP mediates a wide range of physiological effects, including cell proliferation, differentiation, maturation, and migration. However, the effect of ATP on cell proliferation has been contradictory, and the mechanism is not fully understood. In the current study, we found that extracellular ATP significantly inhibited the proliferation of human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs). Treatment with ATP did not induce cell apoptosis but instead induced cell cycle arrest in S phase. ATP induced the phosphorylation of ERK1/2, but the ERK inhibitors, U0126 and PD9809, did not regulate the inhibition of cell proliferation induced by ATP. However, ATP-induced inhibition of cell proliferation was blocked by suramin, a nonspecific antagonist of the P2Y receptors, and endothelial cells expressed P2Y11, a P2Y receptor that specifically binds ATP. Moreover, the down-regulation of P2Y11 by RNA interference not only reversed the inhibition of cell proliferation but also ameliorated cell cycle arrest in S phase. In addition, P2Y11 sensitized endothelial cells to cisplatin-induced cell death by down-regulation of the expression of Bcl-2. Taken together, these results suggest that extracellular ATP impairs cell proliferation by triggering signaling to induce cell cycle arrest and sensitizes cell to death via P2Y11 in endothelial cells.