Dynamic source routing strategy for two-level flows on scale-free networks

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A survey on health-promoting lifestyle among community-dwelling older people with hypertension in Macau

2007-2008 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

SPH study of the evolution of water–water interfaces in dam break flows

The mixing process of upstream and downstream waters in the dam break flow could generate significant ecological impact on the downstream reaches and influence the environmental damages caused by the dam break flood. This is not easily investigated with the analytical and numerical models based on the grid method due to the large deformation of free surface and the water-water interface. In this paper, a weakly compressible Smoothed Particle Hydrodynamics (WCSPH) solver is used to study the advection and mixing process of the water bodies in two-dimensional dam-break flows over a wet bed. The numerical results of the mixing dynamics immediately after the release of the dam water are found to agree satisfactorily with the published experimental and numerical results. Then further investigations are carried out to study the interface development at the later stage of dambreak flows in a long channel. The analyses concentrate on the evolution of the interface at different ratios between the upstream and downstream water depths. The potential capabilities of the mesh-free SPH modelling approach for predicting the detailed development of the water-water interfaces are fully demonstrated.The first author acknowledges the Jafar Studentship during her PhD study at the University of Cambridge. The other authors acknowledge the support of the Major State Basic Research Development Program (973) of China (No. 2013CB036402), Open Fund of the State Key Laboratory of Hydraulics and Mountain River Engineering, Sichuan University (SKHL1404; SKHL1409), Start-up Grant for the Young Teachers of Sichuan University (2014SCU11056) and National Science and Technology Support Plan (2012BAB0513B0).This is the accepted manuscript. The final version is available at http://link.springer.com/article/10.1007%2Fs11069-015-1726-6

Potent Paracrine Effects of human induced Pluripotent Stem Cell-derived Mesenchymal Stem Cells Attenuate Doxorubicin-induced Cardiomyopathy

© 2015, Nature Publishing Group. All rights reserved.Transplantation of bone marrow mesenchymal stem cells (BM-MSCs) can protect cardiomyocytes against anthracycline-induced cardiomyopathy (AIC) through paracrine effects. Nonetheless the paracrine effects of human induced pluripotent stem cell-derived MSCs (iPSC-MSCs) on AIC are poorly understood. In vitro studies reveal that doxorubicin (Dox)-induced reactive oxidative stress (ROS) generation and cell apoptosis in neonatal rat cardiomyocytes (NRCMs) are significantly reduced when treated with conditioned medium harvested from BM-MSCs (BM-MSCs-CdM) or iPSC-MSCs (iPSC-MSCs-CdM). Compared with BM-MSCs-CdM, NRCMs treated with iPSC-MSCs-CdM exhibit significantly less ROS and cell apoptosis in a dose-dependent manner. Transplantation of BM-MSCs-CdM or iPSC-MSCs-CdM into mice with AIC remarkably attenuated left ventricular (LV) dysfunction and dilatation. Compared with BM-MSCs-CdM, iPSC-MSCs-CdM treatment showed better alleviation of heart failure, less cardiomyocyte apoptosis and fibrosis. Analysis of common and distinct cytokines revealed that macrophage migration inhibitory factor (MIF) and growth differentiation factor-15 (GDF-15) were uniquely overpresented in iPSC-MSC-CdM. Immunodepletion of MIF and GDF-15 in iPSC-MSCs-CdM dramatically decreased cardioprotection. Injection of GDF-15/MIF cytokines could partially reverse Dox-induced heart dysfunction. We suggest that the potent paracrine effects of iPSC-MSCs provide novel "cell-free" therapeutic cardioprotection against AIC, and that MIF and GDF-15 in iPSC-MSCs-CdM are critical for these enhanced cardioprotective effects.published_or_final_versio

Activation of Human Stearoyl-Coenzyme A Desaturase 1 Contributes to the Lipogenic Effect of PXR in HepG2 Cells

The pregnane X receptor (PXR) was previously known as a xenobiotic receptor. Several recent studies suggested that PXR also played an important role in lipid homeostasis but the underlying mechanism remains to be clearly defined. In this study, we found that rifampicin, an agonist of human PXR, induced lipid accumulation in HepG2 cells. Lipid analysis showed the total cholesterol level increased. However, the free cholesterol and triglyceride levels were not changed. Treatment of HepG2 cells with rifampicin induced the expression of the free fatty acid transporter CD36 and ABCG1, as well as several lipogenic enzymes, including stearoyl-CoA desaturase-1 (SCD1), long chain free fatty acid elongase (FAE), and lecithin-cholesterol acyltransferase (LCAT), while the expression of acyl:cholesterol acetyltransferase(ACAT1) was not affected. Moreover, in PXR over-expressing HepG2 cells (HepG2-PXR), the SCD1 expression was significantly higher than in HepG2-Vector cells, even in the absence of rifampicin. Down-regulation of PXR by shRNA abolished the rifampicin-induced SCD1 gene expression in HepG2 cells. Promoter analysis showed that the human SCD1 gene promoter is activated by PXR and a novel DR-7 type PXR response element (PXRE) response element was located at -338 bp of the SCD1 gene promoter. Taken together, these results indicated that PXR activation promoted lipid synthesis in HepG2 cells and SCD1 is a novel PXR target gene. © 2013 Zhang et al

Predicting the optoelectronic properties of nanowire films based on control of length polydispersity

We demonstrate that the optoelectronic properties of percolating thin films of silver nanowires (AgNWs) are predominantly dependent upon the length distribution of the constituent AgNWs. A generalized expression is derived to describe the dependence of both sheet resistance and optical transmission on this distribution. We experimentally validate the relationship using ultrasonication to controllably vary the length distribution. These results have major implications where nanowire-based films are a desirable material for transparent conductor applications; in particular when application specific performance criteria must be met. It is of particular interest to have a simple method to generalize the properties of bulk films from an understanding of the base material, as this will speed up the optimisation process. It is anticipated that these results may aid in the adoption of nanowire films in industry, for applications such as touch sensors or photovoltaic electrode structures

Two-Photon Absorption in Monolayer MXenes

Two‐photon absorption (2PA) is a nonlinear optical (NLO) effect that typically occurs in a conventional semiconductor whose bandgap is larger than the energy of one excited photon but smaller than the energy of two photons. In this work, the experimental observation of strong 2PA in gapless MXene monolayers is reported. This phenomenon is verified by a nonlinear transmission method and ultrafast dynamic studies based on a wavelength‐degenerate, non‐collinear pump‐probe technique. The unconventional 2PA is attributed to the structures of the MXene energy bands near the Fermi level, which favors two‐photon transitions and suppresses one‐photon transitions due to parallel band absorption effects. These results, as well as the measured NLO parameters including the 2PA coefficient, absorption cross‐section, excited carrier lifetimes, and third‐order NLO susceptibility, provide a systematic understanding of the unusual NLO effect in MXenes and may be applied in advanced photonic and optoelectronic devices

CLDN3 inhibits cancer aggressiveness via Wnt-EMT signaling and is a potential prognostic biomarker for hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is one of the most common fatal malignancies but the molecular genetic basis of this disease remains unclear. By using genome-wide methylation profiling analysis, we identified CLDN3 as an epigenetically regulated gene in cancer. Here, we investigated its function and clinical relevance in human HCC. CLDN3 downregulation occurred in 87/114 (76.3%) of primary HCCs, where it was correlated significantly with shorter survival of HCC patients (P=0.021). Moreover, multivariate cyclooxygenase regression analysis showed that CLDN3 was an independent prognostic factor for overall survival (P=0.014). Absent expression of CLDN3 was also detected in 67% of HCC cell lines, which was significantly associated with its promoter hypermethylation. Ectopic expression of CLDN3 in HCC cells could inhibit cell motility, cell invasiveness, and tumor formation in nude mice. Mechanistic investigations suggested through downregulation of GSK3B, CTNNB1, SNAI2, and CDH2, CLDN3 could significantly suppress metastasis by inactivating the Wnt/β-catenin-epithelial mesenchymal transition (EMT) axis in HCC cells. Collectively, our findings demonstrated that CLDN3 is an epigenetically silenced metastasis suppressor gene in HCC. A better understanding of the molecular mechanism of CLDN3 in inhibiting liver cancer cell metastasis may lead to a more effective management of HCC patients with the inactivation of CLDN3.published_or_final_versio