Topographic influences on transient harbor oscillations excited by N-waves

The main objective of this paper is to comprehensively study influences of the variation of the bottom profile inside the harbor on the transient harbor oscillations excited by normally-incident N-waves. The specific physical phenomena investigated consist of wave profile evolution, maximum runup, relative wave energy distribution and total wave energy inside the harbor. A series of numerical experiments are implemented using a fully nonlinear Boussinesq model, FUNWAVE-TVD. Results show that when the harbor is subjected to the leading-elevation N-waves (LEN waves), the evolution of the maximum free surface elevation during the wave shoaling process inside the harbor coincides well with Green's law overall. When the incident wave amplitude is small, the maximum runup inside the harbor is almost only determined by the incident wave amplitude. As the incident wave amplitude increases, effects of the bottom profile on the maximum runup closely depend on both the incident wave type and amplitude. As the mean water depth inside the harbor decreases, the relative wave energy distribution tends to become more uniform, regardless of the incident wave amplitude and type. Finally, the variation trend of the total wave energy with the bottom profile is found to depend on the incident wave amplitude

Knocking down Stard3 decreases adipogenesis with decreased mitochondrial ROS in 3T3-L1 cells

Start domain-containing protein 3 (Stard3) plays roles in intracellular cholesterol distribution, however, the role of Stard3 in the adipogenesis of 3T3-L1 preadipocytes remains unclear. We demonstrated that Stard3 expression was significantly increased during the adipogenesis of 3T3-L1 preadipocytes, accompanied by an increase of mitochondrial Reactive oxygen species (ROS). Stard3 knocking-down inhibited 3T3-L1 preadipocyte adipogenesis with decreased mitochondrial ROS levels, while ROS inducer rescued the stard3 silencing 3T3 cells with increased ROS. Moreover, Stard3 silencing reduced the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein (C/EBP)α in 3T3- L1 cells. In conclusion, Stard3 enhanced the adipogenesis of preadipocytes by enhancement of cholesterol redistribution to the mitochondrial, increasing mitochondrial ROS production. These results suggest that Stard3 is an essential factor for the 3T3-L1 cells' differentiation

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

Photoelectrocatalytic degradation of rhodamine B using mesh Ti/TiO2 electrode

2002-2003 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

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

The Efficacy of Flupentixol-Melitracen in the Adjuvant Therapy of Ulcerative Colitis in the Chinese Population: A Meta-Analysis

OBJECTIVES: Our aim of this study is to compare the efficacy of flupentixol-melitracen in the adjuvant therapy of ulcerative colitis patients in the Chinese population. // METHODS: Both the RevMan 5.2 and the Stata 12.0 software are used in this study for analysis, and a fixed-effect model (the Mantel-Haenszel method) or a random-effect model (the DerSimonian and Laird method) is used to merge or aggregate the risk ratio (RR) and its 95% confidence intervals (CI) of included studies. // RESULTS: Eleven trials involving 654 ulcerative colitis patients (treated group: 328; control group: 326) were analyzed in this study. Significant differences (RR = 1.29, 95% CI = 1.20 to 1.40, P < 0.001) between patients were observed between the two groups. // CONCLUSIONS: Our results suggested that the efficacy of flupentixol-melitracen in the adjuvant therapy of ulcerative colitis is better than traditional drug treatments

Room temperature chiral magnetic skyrmion in ultrathin magnetic nanostructures

Magnetic skyrmions are chiral spin structures with a whirling configuration. Their topological properties, nanometer size and the fact that they can be moved by small current densities have opened a new paradigm for the manipulation of magnetisation at the nanoscale. To date, chiral skyrmion structures have been experimentally demonstrated only in bulk materials and in epitaxial ultrathin films and under external magnetic field or at low temperature. Here, we report on the observation of stable skyrmions in sputtered ultrathin Pt/Co/MgO nanostructures, at room temperature and zero applied magnetic field. We use high lateral resolution X-ray magnetic circular dichroism microscopy to image their chiral N\'eel internal structure which we explain as due to the large strength of the Dzyaloshinskii-Moriya interaction as revealed by spin wave spectroscopy measurements. Our results are substantiated by micromagnetic simulations and numerical models, which allow the identification of the physical mechanisms governing the size and stability of the skyrmions.Comment: Submitted version. Extended version to appear in Nature Nanotechnolog

Basic Amino Acid Mutations in the Nuclear Localization Signal of Hibiscus Chlorotic Ringspot Virus p23 Inhibit Virus Long Distance Movement

10.1371/journal.pone.0074000PLoS ONE89-POLN

New Deformation Twinning Mechanism Generates Zero Macroscopic Strain In Nanocrystalline Metals

Macroscopic strain was hitherto considered a necessary corollary of deformation twinning in coarse-grained metals. Recently, twinning has been found to be a preeminent deformation mechanism in nanocrystalline face-centered-cubic (fcc) metals with medium-to-high stacking fault energies. Here we report a surprising discovery that the vast majority of deformation twins in nanocrystalline Al, Ni, and Cu, contrary to popular belief, yield zero net macroscopic strain. We propose a new twinning mechanism, random activation of partials, to explain this unusual phenomenon. The random activation of partials mechanism appears to be the most plausible mechanism and may be unique to nanocrystalline fcc metals with implications for their deformation behavior and mechanical properties

Inflammatory Stress Sensitizes the Liver to Atorvastatin-Induced Injury in ApoE-/- Mice

Statins, which are revolutionized cholesterol-lowing agents, have been reported to have unfavorable effects on the liver. Inflammatory stress is a susceptibility factor for drug-induced liver injury. This study investigated whether inflammatory stress sensitized the liver to statin-induced toxicity in mice and explored the underlying mechanisms. We used casein injection in ApoE-/- mice to induce inflammatory stress. Half of the mice were orally administered atorvastatin (10mg/kg/d) for 8 weeks. The results showed that casein injection increased the levels of serum pro-inflammatory cytokines (IL-6 and TNFα). Atorvastatin treatment increased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in casein injection mice. Moreover, atorvastatin treatment exacerbated hepatic steatosis, inflammation and fibrosis, as well as increased hepatic reactive oxygen species (ROS) and malondialdehyde in casein injection mice. However, above changes were not observed in atorvastatin treated alone mice. The protein expression of liver nuclear factor erythroid 2-related factor 2 (Nrf2) and the mRNA expressions of Nrf2 target genes were increased, together with the enhancement of activities of hepatic catalase and superoxide dismutase in atorvastatin treated alone mice, but these antioxidant responses were lost in mice treated with atorvastatin under inflammatory stress. This study demonstrates that atorvastatin exacerbates the liver injury under inflammatory stress, which may be associated with the loss of adaptive antioxidant response mediated by Nrf2