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Atlantic-induced pan-tropical climate change over the past three decades
Li, Xichen,Xie, Shang-Ping,Gille, Sarah T.,Yoo, Changhyun Nature Publishing Group 2016 Nature climate change Vol.6 No.3
<P>During the past three decades, tropical sea surface temperature (SST) has shown dipole-like trends, with warming over the tropical Atlantic and Indo-western Pacific but cooling over the eastern Pacific. Competing hypotheses relate this cooling, identified as a driver of the global warming hiatus(1,2), to the warming trends in either the Atlantic(3,4) or Indian Ocean(5). However, the mechanisms, the relative importance and the interactions between these teleconnections remain unclear. Using a state-of-the-art climate model, we show that the Atlantic plays a key role in initiating the tropical-wide teleconnection, and the Atlantic-induced anomalies contribute similar to 55-75% of the tropical SST and circulation changes during the satellite era. The Atlantic warming drives easterly wind anomalies over the Indo-western Pacific as Kelvin waves and westerly anomalies over the eastern Pacific as Rossby waves. The wind changes induce an Indo-western Pacific warming through the wind-evaporation-SST effect(6,7), and this warming intensifies the La Nina-type response in the tropical Pacific by enhancing the easterly trade winds and through the Bjerknes ocean dynamical processes(8). The teleconnection develops into a tropical-wide SST dipole pattern. This mechanism, supported by observations and a hierarchy of climate models, reveals that the tropical ocean basins are more tightly connected than previously thought.</P>
Shi, Hua-Ping,Zhang, Jun,Shang, Xue-Chai,Xie, Xin-You Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.2
Although there have been many studies investigating possible associations between the C1653T mutation and risk of HCC, the results have been inconsistent. We conducted searches of the published literature in Pubmed and Embase databases up to January 2013. Seventeen studies with a total of 1,085 HCC cases and 1,365 healthy controls were retrieved. We found a significant association between the C1653T mutation and HCC risk (OR = 2.01, 95%CI= 1.49-2.70). In the subgroup analysis by ethnicity, a significant association was also found in Asians (OR = 2.07, 95%CI= 1.71-2.51). In subgroup analysis by HBV genotype, B and C were linked with development of HCC (B:OR = 2.21, 95%CI= 1.13-4.34; C:OR = 2.26, 95%CI= 1.61-3.16). However, no significant association was found between the C1653T mutation and HCC risk in HBeAg positive cases. In conclusion, this meta-analysis suggests that the C1653T mutation may be associated with susceptibility to HCC.
Inhibition of Dll4/Notch1 pathway promotes angiogenesis of Masquelet’s induced membrane in rats
Qian Tang,Haimin Jin,Minji Tong,Gang Zheng,Zhongjie Xie,Shangkun Tang,Jialei Jin,Ping Shang,Huazi Xu,Liyan Shen,Yu Zhang,Haixiao Liu 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
The Masquelet’s induced membrane technique for repairing bone defects has been demonstrated to be a promising treatment strategy. Previous studies have shown that the vessel density of induced membrane is decreased in the late stage of membrane formation, which consequently disrupts the bone healing process. However, relatively little is known about certain mechanisms of vessel degeneration in the induced membrane tissue and whether promotion of angiogenesis in induced membranes can improve bone regeneration. Here, we showed that the Delta-like ligand 4/ Notch homolog 1 (Dll4/Notch1) pathway was relatively activated in the late stage of induced membrane, especially at the subcutaneous site. Then, DAPT, a classical γ-secretase inhibitor, was applied to specifically inhibit Notch1 activation, followed by up-regulation of vascular endothelial growth factor receptor 2 (VEGFR2) and CD31 expression. DAPTmodified induced membranes were further confirmed to contribute to bone regeneration after autogenous bone grafting. Finally, in vitro experiments revealed that knocking down Notch1 contributed to the functional improvement of endothelial progenitor cells (EPCs) and that DAPT-treated induced membrane tissue was more favorable for angiogenesis of EPCs compared with the vehicle group. In conclusion, the present findings demonstrate that Dll4/ Notch1 signaling is negatively associated with the vessel density of induced membrane. Pharmacological inhibition of Notch1 attenuated the vessel degeneration of induced membrane both in vitro and in vivo, which consequently improved bone formation at the bone defect site and graft resorption at the subcutaneous site.