Pan-African metamorphic and magmatic rocks of the Khanka Massif, NE China: Further evidence regarding their affinity

The Khanka Massif is a crustal block located along the eastern margin of the Central Asian Orogenic Belt (CAOB) and bordered to the east by Late Jurassic-Early Cretaceous circum-Pacific accretionary complexes of the Eastern Asian continental margin. It consists of graphite-, sillimanite- and cordierite-bearing gneisses, carbonates and felsic paragneisses, in association with various orthogneisses. Metamorphic zircons from a sillimanite gneiss from the Hutou complex yield a weighted mean 206Pb/ 238U age of 490 ± 4 Ma, whereas detrital zircons from the same sample give ages from 934-610 Ma. Magmatic zircon cores in two garnet-bearing granite gneiss samples, also collected from the Hutou complex, yield weighted mean 206Pb/ 238U ages of 522 ± 5 Ma and 515 ± 8 Ma, whereas their metamorphic rims record 206Pb/ 238U ages of 510-500 Ma. These data indicate that the Hutou complex in the Khanka Massif records early Palaeozoic magmatic and metamorphic events, identical in age to those in the Mashan Complex of the Jiamusi Massif to the west. The older zircon populations in the sillimanite gneiss indicate derivation from Neoproterozoic sources, as do similar rocks in the Jiamusi Massif. These data confirm that the Khanka Massif has a close affinity with other major components of the CAOB to the west of the Dun-Mi Fault. Based on these results and previously published data, the Khanka Massif is therefore confirmed as having formed a single crustal entity with the Jiamusi (and possibly the Bureya) massif since Neoproterozoic time. Copyright © Cambridge University Press 2010.published_or_final_versio

Study of mechanisms for electric field effects on ethanol oxidation via reactive force field molecular dynamics

Molecular dynamics simulations based on reactive force fields (ReaxFF) were conducted to study the effects of an external electric field with varying electric field strengths on ethanol oxidation reactions. Time evolutions of the reactants and intermediate species indicate that imposition of the electric field has modified the reaction pathways in addition to changing the reaction rate in a non-linear way. Intermediates of ethanol oxidation reactions with and without the electric field are identified and quantified. For the first time, reaction pathways of ethanol oxidation with and without an imposed electric field are scrutinized at the atomic scales. The reaction pathways without the electric field are consistent with previous experimental and numerical studies, which validate the present approach. Reaction pathways under varying electric field strengths, on the other hand, show some common pathways but also unique pathways associated with different strengths of the imposed electric field. The ReaxFF-based molecular dynamics method provides new insight into mechanisms for the effects of an electric field with varying electric field strengths on ethanol oxidation reactions. The present research demonstrates that ReaxFF-based reactive molecular dynamics is a valuable tool for detailed study of reaction mechanisms of hydrocarbon or oxygenated fuels, which complements commonly used experimental and computational techniques

Hyperphosphatemia in chronic kidney disease exacerbates atherosclerosis via a mannosidases-mediated complex-type conversion of SCAP N-glycans

Blood phosphate levels are linked to atherosclerotic cardiovascular disease in patients with chronic kidney disease (CKD), but the molecular mechanisms remain unclear. Emerging studies indicate an involvement of hyperphosphatemia in CKD accelerated atherogenesis through disturbed cholesterol homeostasis. Here, we investigated a potential atherogenic role of high phosphate concentrations acting through aberrant activation of sterol regulatory element-binding protein (SREBP) and cleavage-activating protein (SCAP)-SREBP2 signaling in patients with CKD, hyperphosphatemic apolipoprotein E (ApoE) knockout mice, and cultured vascular smooth muscle cells. Hyperphosphatemia correlated positively with increased atherosclerotic cardiovascular disease risk in Chinese patients with CKD and severe atheromatous lesions in the aortas of ApoE knockout mice. Mice arteries had elevated SCAP levels with aberrantly activated SCAP-SREBP2 signaling. Excess phosphate in vitro raised the activity of α-mannosidase, resulting in delayed SCAP degradation through promoting complex-type conversion of SCAP N-glycans. The retention of SCAP enhanced transactivation of SREBP2 and expression of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase, boosting intracellular cholesterol synthesis. Elevated α-mannosidase II activity was also observed in the aortas of ApoE knockout mice and the radial arteries of patients with uremia and hyperphosphatemia. High phosphate concentration in vitro elevated α-mannosidase II activity in the Golgi, enhanced complex-type conversion of SCAP N-glycans, thereby upregulating intracellular cholesterol synthesis. Thus, our studies explain how hyperphosphatemia independently accelerates atherosclerosis in CKD

Ethanol oxidation with high water content: A reactive molecular dynamics simulation study

Ethanol is a potential alternative to conventional fossil fuels. However, the required dewatering process to produce anhydrous ethanol is extremely energy-intensive and expensive. A promising solution is the direct use of hydrous ethanol for combustion applications, which can dramatically reduce the production cost. Many researchers have undertaken experiments demonstrating the feasibility and advantages of burning hydrous ethanol solely as a fuel. In this study, molecular dynamics (MD) simulation with the reactive force field (ReaxFF) is employed to investigate the fundamental reaction mechanisms of hydrous ethanol oxidation in comparison with the ethanol oxidation under fuel-air condition in order to understand the effects of water addition on ethanol oxidation. The results show that the reaction rate of ethanol oxidation is faster in water than in nitrogen environment and the presence of water advances the ionisation process and accelerates the radical production rate thereby enhancing the oxidation reaction. Additionally, it is suggested that the water content plays a vital role in reactions at low temperatures but that effect can be ignored at high temperatures. The detailed reaction pathways and time evolution of relevant key species indicate that H2O promotes many reactions involving OH generation and these OH radicals also facilitate its reactions with C1& C2intermediates as well as the dehydrogenation of C1& C2intermediates. Similarly, CO production is reduced in hydrous ethanol oxidation as a result of CO reaction with OH converting the CO to CO2ultimately. Therefore, it is the addition of water that promotes the OH production due to the chemical effect of H2O leading to the enhancement of ethanol oxidation and reduction of CO production. In summary, this research provides the scientific base for the direct use of hydrous ethanol as a fuel for combustion systems with a low cost

Al8Mn5 in High-Pressure Die Cast AZ91: Twinning, Morphology and Size Distributions

EPSRC (UK); National Natural Science Foundation of China

The fatty acid receptor CD36 promotes HCC progression through activating Src/PI3K/AKT axis-dependent aerobic glycolysis

Metabolic reprogramming is a new hallmark of cancer but it remains poorly defined in hepatocellular carcinogenesis (HCC). The fatty acid receptor CD36 is associated with both lipid and glucose metabolism in the liver. However, the role of CD36 in metabolic reprogramming in the progression of HCC still remains to be elucidated. In the present study, we found that CD36 is highly expressed in human HCC as compared with non-tumor hepatic tissue. CD36 overexpression promoted the proliferation, migration, invasion, and in vivo tumor growth of HCC cells, whereas silencing CD36 had the opposite effects. By analysis of cell metabolic phenotype, CD36 expression showed a positive association with extracellular acidification rate, a measure of glycolysis, instead of oxygen consumption rate. Further experiments verified that overexpression of CD36 resulted in increased glycolysis flux and lactic acid production. Mechanistically, CD36 induced mTOR-mediated oncogenic glycolysis via activation of Src/PI3K/AKT signaling axis. Pretreatment of HCC cells with PI3K/AKT/mTOR inhibitors largely blocked the tumor-promoting effect of CD36. Our findings suggest that CD36 exerts a stimulatory effect on HCC growth and metastasis, through mediating aerobic glycolysis by the Src/PI3K/AKT/mTOR signaling pathway

CD36 plays a negative role in the regulation of lipophagy in hepatocytes through an AMPK-dependent pathway

Fatty acid translocase CD36 (CD36) is a multifunctional membrane protein that facilitates the uptake of long-chain fatty acid (LCFA). Lipophagy is autophagic degradation of lipid droplets. Accumulating evidence suggests that CD36 is involved in the regulation of intracellular signal transduction that modulates fatty acid storage or usage. However, little is known about the relationship between CD36 and lipophagy. In this study, we found that increasedCD36 expression was coupled with decreasedautophagy in the livers of mice treated with a high-fat diet. Overexpressing CD36 in HepG2 and Huh7 cells inhibited autophagy, while knocking down CD36 expression induced autophagy due to the increased autophagosome formation in autophagic flux. Meanwhile, knockout of CD36 in mice increased autophagy while reconstruction of CD36 expression in CD36-knockout mice reduced autophagy. CD36 knockdown in HepG2 cells increased lipophagy and β-oxidation, which contributed to improving lipid accumulation. In addition, CD36 expression regulated autophagy through the AMPK pathway with phosphorylation of ULK1/Beclin1 also involved in the process. These findings suggest that CD36 is a negative regulator of autophagy and induction of lipophagy by ameliorating CD36 expression can be a potential therapeutic strategy for the treatment of fatty liver diseases through attenuating lipid over-accumulation

Synthesis of MoS2 nanoparticles using MoO3 nanobelts as precursor via a PVP-assisted hydrothermal method

The synthesis of MoS2 nanoparticles from MoO3 with a certain morphology through a surfactant-assisted hydrothermal process is described in this paper. MoO3, which has a nanobelt morphology with a width of 100-500 nm and a length from one to several micrometers, is used as the precursor, and poly(vinylpyrrolidone) (PVP) is used as the surfactant. The morphology of the resulting MoS2 nanomaterial has been characterized by the field-emission scanning electron microscope, which shows that the obtained nanoparticles have diameters ranging from 50 to 100 nm with rough surfaces. Additionally, the composition and crystallinity as well as the phase information of the produced nanoparticles have been characterized by the energy-dispersive X-ray spectrometer and X-ray diffraction. Specifically, in this process, the presence of PVP plays a crucial role for the successful fabrication of the nanoparticle morphology, which may be due to the formation of PVP micelles leading to an oriented aggregation of MoS2 nuclei. In addition, comparative experiments have been conducted and the possible reaction mechanism is proposed. (C) 2016 Elsevier B.V. All rights reserved