A review on approaches to solving Poisson’s equation in projection-based meshless methods for modelling strongly nonlinear water waves

Three meshless methods, including incompressible smooth particle hydrodynamic (ISPH), moving particle semi-implicit (MPS) and meshless local Petrov–Galerkin method based on Rankine source solution (MLPG_R) methods, are often employed to model nonlinear or violent water waves and their interaction with marine structures. They are all based on the projection procedure, in which solving Poisson’s equation about pressure at each time step is a major task. There are three different approaches to solving Poisson’s equation, i.e. (1) discretizing Laplacian directly by approximating the second-order derivatives, (2) transferring Poisson’s equation into a weak form containing only gradient of pressure and (3) transferring Poisson’s equation into a weak form that does not contain any derivatives of functions to be solved. The first approach is often adopted in ISPH and MPS, while the third one is implemented by the MLPG_R method. This paper attempts to review the most popular, though not all, approaches available in literature for solving the equation

Polypyrrole-Fe2O3 nanohybrid materials for electrochemical storage

We report on the synthesis and electrochemical characterization of nanohybrid polypyrrole (PPy) (PPy/Fe2O3) materials for electrochemical storage applications. We have shown that the incorporation of nanoparticles inside the PPy notably increases the charge storage capability in comparison to the “pure” conducting polymer. Incorporation of large anions, i.e., paratoluenesulfonate, allows a further improvement in the capacity. These charge storage modifications have been attributed to the morphology of the composite in which the particle sizes and the specific surface area are modified with the incorporation of nanoparticles. High capacity and stability have been obtained in PC/NEt4BF4 (at 20 mV/s), i.e., 47 mAh/g, with only a 3% charge loss after one thousand cyles. The kinetics of charge–discharge is also improved by the hybrid nanocomposite morphology modifications, which increase the rate of insertion–expulsion of counter anions in the bulk of the film. A room temperature ionic liquid such as imidazolium trifluoromethanesulfonimide seems to be a promising electrolyte because it further increases the capacity up to 53 mAh/g with a high stability during charge–discharge processes

Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage

<p>Abstract</p> <p>Background</p> <p>Inflammatory injury plays a critical role in intracerebral hemorrhage (ICH)-induced neurological deficits; however, the signaling pathways are not apparent by which the upstream cellular events trigger innate immune and inflammatory responses that contribute to neurological impairments. Toll-like receptor 4 (TLR4) plays a role in inflammatory damage caused by brain disorders.</p> <p>Methods</p> <p>In this study, we investigate the role of TLR4 signaling in ICH-induced inflammation. In the ICH model, a significant upregulation of TLR4 expression in reactive microglia has been demonstrated using real-time RT-PCR. Activation of microglia was detected by immunohistochemistry, cytokines were measured by ELISA, MyD88, TRIF and NF-κB were measured by Western blot and EMSA, animal behavior was evaluated by animal behavioristics.</p> <p>Results</p> <p>Compared to WT mice, TLR4^−/−mice had restrained ICH-induced brain damage showing in reduced cerebral edema and lower neurological deficit scores. Quantification of cytokines including IL-6, TNF-α and IL-1β and assessment of macrophage infiltration in perihematoma tissues from TLR4^−/−, MyD88^−/−and TRIF^−/−mice showed attenuated inflammatory damage after ICH. TLR4^−/−mice also exhibited reduced MyD88 and TRIF expression which was accompanied by decreased NF-κB activity. This suggests that after ICH both MyD88 and TRIF pathways might be involved in TLR4-mediated inflammatory injury possibly via NF-κB activation. Exogenous hemin administration significantly increased TLR4 expression and microglial activation in cultures and also exacerbated brain injury in WT mice but not in TLR4^−/−mice. Anti-TLR4 antibody administration suppressed hemin-induced microglial activation in cultures and in the mice model of ICH.</p> <p>Conclusions</p> <p>Our findings suggest that heme potentiates microglial activation <it>via </it>TLR4, in turn inducing NF-κB activation <it>via </it>the MyD88/TRIF signaling pathway, and ultimately increasing cytokine expression and inflammatory injury in ICH. Targeting TLR4 signaling may be a promising therapeutic strategy for ICH.</p

Observation of a ppb mass threshoud enhancement in \psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p}) decay

The decay channel $\psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p})$ is studied using a sample of $1.06\times 10^8$ $\psi^\prime$ events collected by the BESIII experiment at BEPCII. A strong enhancement at threshold is observed in the $p\bar{p}$ invariant mass spectrum. The enhancement can be fit with an $S$-wave Breit-Wigner resonance function with a resulting peak mass of $M=1861^{+6}_{-13} {\rm (stat)}^{+7}_{-26} {\rm (syst)} {\rm MeV/}c^2$ and a narrow width that is $\Gamma<38 {\rm MeV/}c^2$ at the 90% confidence level. These results are consistent with published BESII results. These mass and width values do not match with those of any known meson resonance.Comment: 5 pages, 3 figures, submitted to Chinese Physics

ER Stress Negatively Modulates the Expression of the miR-199a/214 Cluster to Regulates Tumor Survival and Progression in Human Hepatocellular Cancer

Background: Recent studies have emphasized causative links between microRNAs (miRNAs) deregulation and tumor development. In hepatocellular carcinoma (HCC), more and more miRNAs were identified as diagnostic and prognostic cancer biomarkers, as well as additional therapeutic tools. This study aimed to investigate the functional significance and regulatory mechanism of the miR-199a2/214 cluster in HCC progression. Methods and Findings: In this study, we showed that miR-214, as well as miR-199a-3p and miR-199a-5p levels were significantly reduced in the majority of examined 23 HCC tissues and HepG2 and SMMC-7721 cell lines, compared with their nontumor counterparts. To further explore the role of miR-214 in hepatocarcinogenesis, we disclosed that the ER stressinduced pro-survival factor XBP-1 is a target of miR-214 by using western blot assay and luciferase reporter assay. Reexpression of miR-214 in HCC cell lines (HepG2 and SMMC-7721) inhibited proliferation and induced apoptosis. Furthermore, ectopic expression of miR-214 dramatically suppressed the ability of HCC cells to form colonies in vitro and to develop tumors in a subcutaneous xenotransplantation model of the BALB/c athymic nude mice. Moreover, reintroduction of XBP-1s attenuated miR-214-mediated suppression of HCC cells proliferation, colony and tumor formation. To further understand the mechanism of the miR-199a/214 cluster down-expression in HCC, we found that thapsigargin (TG) and tunicamycin (TM) or hypoxia-induced unfolded protein response (UPR) suppresses the expression of the miR-199a/21

Shell-Controlled Photoluminescence in CdSe/CNT Nanohybrids

A new type of nanohybrids containing carbon nanotubes (CNTs) and CdSe quantum dots (QDs) was prepared using an electrostatic self-assembly method. The CdSe QDs were capped by various mercaptocarboxylic acids, including thioglycolic acid (TGA), dihydrolipoic acid (DHLA) and mercaptoundecanoic acid (MUA), which provide shell thicknesses of ~5.2, 10.6 and 15.2 Å, respectively. The surface-modified CdSe QDs are then self-assembled onto aridine orange-modified CNTs via electrostatic interaction to give CdSe/CNT nanohybrids. The photoluminescence (PL) efficiencies of the obtained nanohybrids increase significantly with the increase of the shell thickness, which is attributed to a distance-dependent photo-induced charge-transfer mechanism. This work demonstrates a simple mean for fine tuning the PL properties of the CdSe/CNT nanohybrids and gains new insights to the photo-induced charge transfer in such nanostructures

Variation in Soil Respiration across Soil and Vegetation Types in an Alpine Valley.

BACKGROUND AND AIMS: Soils of mountain regions and their associated plant communities are highly diverse over short spatial scales due to the heterogeneity of geological substrates and highly dynamic geomorphic processes. The consequences of this heterogeneity for biogeochemical transfers, however, remain poorly documented. The objective of this study was to quantify the variability of soil-surface carbon dioxide efflux, known as soil respiration (Rs), across soil and vegetation types in an Alpine valley. To this aim, we measured Rs rates during the peak and late growing season (July-October) in 48 plots located in pastoral areas of a small valley of the Swiss Alps. FINDINGS: Four herbaceous vegetation types were identified, three corresponding to different stages of primary succession (Petasition paradoxi in pioneer conditions, Seslerion in more advanced stages and Poion alpinae replacing the climactic forests), as well as one (Rumicion alpinae) corresponding to eutrophic grasslands in intensively grazed areas. Soils were developed on calcareous alluvial and colluvial fan deposits and were classified into six types including three Fluvisols grades and three Cambisols grades. Plant and soil types had a high level of co-occurrence. The strongest predictor of Rs was soil temperature, yet we detected additional explanatory power of sampling month, showing that temporal variation was not entirely reducible to variations in temperature. Vegetation and soil types were also major determinants of Rs. During the warmest month (August), Rs rates varied by over a factor three between soil and vegetation types, ranging from 2.5 μmol m-2 s-1 in pioneer environments (Petasition on Very Young Fluvisols) to 8.5 μmol m-2 s-1 in differentiated soils supporting nitrophilous species (Rumicion on Calcaric Cambisols). CONCLUSIONS: Overall, this study provides quantitative estimates of spatial and temporal variability in Rs in the mountain environment, and demonstrates that estimations of soil carbon efflux at the watershed scale in complex geomorphic terrain have to account for soil and vegetation heterogeneity

Endothelial Cells' Activation and Apoptosis Induced by a Subset of Antibodies against Human Cytomegalovirus: Relevance to the Pathogenesis of Atherosclerosis

Human cytomegalovirus (hCMV) is involved in the pathogenesis of atherosclerosis. We have previously shown in patients with atherosclerosis that antibodies directed against the hCMV-derived proteins US28 and UL122 are able to induce endothelial cell damage and apoptosis of non-stressed endothelial cells through cross-rection with normally expressed surface molecules. Our aim was to dissect the molecular basis of such interaction and to investigate mechanisms linking innate immunity to atherosclerosis.We analysed the gene expression profiles in endothelial cells stimulated with antibodies affinity-purified against either the UL122 or the US28 peptides using the microarray technology. Microarray results were validated by quantitative PCR and by detection of proteins in the medium. Supernatant of endothelial cells incubated with antibodies was analysed also for the presence of Heat Shock Protein (HSP)60 and was used to assess stimulation of Toll-Like Receptor-4 (TLR4). Antibodies against UL122 and US28 induced the expression of genes encoding for adhesion molecules, chemokines, growth factors and molecules involved in the apoptotis process together with other genes known to be involved in the initiation and progression of the atherosclerotic process. HSP60 was released in the medium of cells incubated with anti-US28 antibodies and was able to engage TLR4.Antibodies directed against hCMV modulate the expression of genes coding for molecules involved in activation and apoptosis of endothelial cells, processes known to play a pivotal role in the pathogenesis of atherosclerosis. Moreover, endothelial cells exposed to such antibodies express HSP60 on the cell surface and release HSP60 in the medium able to activate TLR4. These data confirm that antibodies directed against hCMV-derived proteins US28 and UL122 purified from patients with coronary artery disease induce endothelial cell damage and support the hypothesis that hCMV infection may play a crucial role in mediating the atherosclerotic process