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In this paper, we study several problems related to the theory of randomly forced Burgers equation. Our numerical analysis indicates that despite the localization effects the quenched variance of the endpoint distribution for directed polymers in the strong disorder regime grows as the polymer length t→∞. We also present numerical results in support of the 'one force--one solution' principle. [ABSTRACT FROM AUTHOR]

The present study demonstrates a series of environmentally friendly lanthanum and titanium doped mesoporous bioactive glass with adsorption, photocatalytic and regeneration performance for methylene blue via the sol-gel method. The materials were studied by XRD, XPS, TEM and BET. The influence of the initial dye concentration, contact time, solution pH, temperature, photocatalytic performance and regeneration performance of this glass adsorbed methylene blue were investigated. It is shown that the Freundlich and Langmuir adsorption isotherms can be used to study the equilibrium of methylene blue removal process by bioactive glass. Another test on photocatalytic degradation performance and reproduction performance of the materials by removing methylene blue. This article has its potential in treatment of dyeing waste water as it improves structure and performance by adding La and Ti to mesoporous bioactive glass. [ABSTRACT FROM AUTHOR]

Endothelial cells respond to hypoxia by decreased degradation of hypoxia-inducible factor 1α (HIF-1α), accumulation of which leads to increased transcription of numerous proteins involved in cell growth and survival. Ascorbic acid prevents HIF-1α stabilization in many cell types, but the physiologic relevance of such effects is uncertain. Given their relevance for angiogenesis, endothelial cells in culture were used to evaluate the effects of ascorbate on HIF-1α expression induced by hypoxia and the hypoxia mimic cobalt. Although EA.hy926 cells in culture under oxygenated conditions did not contain ascorbate, HIF-1α expression was very low, showing that the vitamin is not necessary to suppress HIF-1α. On the other hand, hypoxia- or cobalt-induced HIF-1α expression/stabilization was almost completely suppressed by what are likely physiologic intracellular ascorbate concentrations. Increased HIF-1α expression was not associated with significant changes in expression of the SVCT2, the major transporter for ascorbate in these cells. Cobalt at concentrations sufficient to stabilize HIF-1α both oxidized intracellular ascorbate and induced an oxidant stress in the cells that was prevented by ascorbate. Whereas the interaction of ascorbate and cobalt is complex, the presence of physiologic low millimolar concentrations of ascorbate in endothelial cells effectively decreases HIF-1α expression and protects against cobalt-induced oxidant stress. &copy 2009 International Union of Biochemistry and Molecular Biology, Inc. [ABSTRACT FROM AUTHOR]

Mitochondria are the major source of potentially damaging reactive oxygen species in most cells. Since ascorbic acid, or vitamin C, can protect against cellular oxidant stress, we studied the ability of mitochondria prepared from guinea pig skeletal muscle to recycle the vitamin from its oxidized forms. Although ascorbate concentrations in freshly prepared mitochondria were only about 0.2 mM, when provided with 6 mM succinate and 1 mM dehydroascorbate (the two-electron-oxidized form of the vitamin), mitochondria were able to generate and maintain concentrations as high as 4 mM, while releasing most of the ascorbate into the incubation medium. Mitochondrial reduction of dehydroascorbate was strongly inhibited by 1,3-bis(chloroethyl)-1-nitrosourea and by phenylarsine oxide. Despite existing evidence that mitochondrial ascorbate protects the organelle from oxidant damage, ascorbate failed to preserve mitochondrial α-tocopherol during prolonged incubation in oxygenated buffer. Nonetheless, the capacity for mitochondria to recycle ascorbate from its oxidized forms, measured as ascorbate-dependent ferricyanide reduction, was several-fold greater than total steady-state ascorbate concentrations. This, and the finding that more than half of the ascorbate recycled from dehydroascorbate escaped the mitochondrion, suggests that mitochondrial recycling of ascorbate might be an important mechanism for regenerating intracellular ascorbate. [ABSTRACT FROM AUTHOR]

The article studies the fluid-flow characteristics in a two-strand slab tundish with argon bubbling curtain in water modeling experiments. It shows that the argon bubbling curtain can greatly improve the flow characteristics in the tundish with a weir, a dam and a turbulence inhibitor. The article also indicates that the flow characteristics with low gas flow rate and short distance of the argon bubbling curtain from the tundish outlet are better than those with high gas flow rate.

With the development of wireless technology, various emerging mobile applications are attracting significant attention and drastically changing our daily lives. Applications such as augmented reality and object recognition demand stringent delay and powerful processing capability, which exerts enormous pressure on mobile devices with limited resources and energy. In this article, a survey of techniques for mobile device energy optimization is presented in a hierarchy of device design and operation, computation offloading, wireless data transmission, and cloud execution of offloaded computation. Energy management strategies for mobile devices from hardware and software aspects are first discussed, followed by energy-efficient computation offloading frameworks for mobile applications that trade application response time for device energy consumption. Then, techniques for efficient wireless data communication to reduce transmission energy are summarized. Finally, the execution mechanisms of application components or tasks in various clouds are further described to provide energy-saving opportunities for mobile devices. We classify the research works based on key characteristics of devices and applications to emphasize their similarities and differences. We hope that this survey will give insights to researchers into energy management mechanisms on mobile devices, and emphasize the crucial importance of optimizing device energy consumption for more research efforts in this area. [ABSTRACT FROM AUTHOR]

Background: This study investigates the predictive value of the systemic immune-inflammation index (SII), which was calculated as platelet × neutrophil/lymphocyte ratio, for all-cause mortality in patients with hypertrophic cardiomyopathy (HCM). Methods: A total of 360 HCM patients were enrolled. They were divided into three groups based on the tertiles of baseline SII. The association between SII and all-cause mortality was analyzed. Results: There were 53 HCM patients who died during a mean follow-up time of 4.8 years (min: 6 days and max: 10.8 years), and the mortality rate was 3.0 per 100 person years. The cumulative mortality rate was significantly different among the three tertiles of SII (P = 0.004), and the mortality rate in tertile 3 was much higher than that in the first two tertiles. In reference to tertile 1, the fully adjusted hazard ratios of all-cause mortality were 1.02 for the tertile 2 (95% confidence interval [CI]: 0.45-2.31, P = 0.966) and 2.31 for tertile 3 (95% CI: 1.10-4.87, P = 0.027). No significant interactions between SII and other variables were observed during subgroup analysis. The discriminative power was better for mid-term outcome than that for shortterm or long-term outcomes. Sensitivity analyses including patients with normal platelet and white blood cell count have revealed similar results. Conclusion: SII was a significant risk factor for all-cause mortality in HCM patients. However, the discriminative power was poor to moderate. It could be used in combination with other risk factors in mortality risk stratification in HCM. [ABSTRACT FROM AUTHOR]

An increasing number of policy makers in developing countries have made the mass expansion of upper-secondary vocational education and training (VET) a top priority. The goal of this study is to examine whether VET fulfills these objectives of building skills and abilities along multiple dimensions and further identify which school-level factors help vocational students build these skills and abilities. To fulfill this goal, we analyzed representative, longitudinal data that we collected on more than 12,000 students from 118 schools in one province of central China. First, descriptive analysis shows that approximately 90 percent of VET students do not make any gains in vocational or general skills. In addition, negative behaviors (misbehavior in the classroom, antisocial behavior, and other risky behaviors) are highly prevalent among VET students. A nontrivial proportion of student internships also fail to meet minimum government requirements for student safety and well-being. Perhaps as a result of these outcomes, more than 60 percent of students express dissatisfaction with their VET programs, as evidenced by either self-reports or dropping out. Finally, using a multilevel model, we find that school inputs (such as school size, teacher qualifications, and per pupil expenditures) are not correlated with vocational and general skill at the end of the school year, or student dropout in the academic year. [ABSTRACT FROM AUTHOR]

The present study conducted improved delayed detached-eddy simulations of actively controlled flows with a harmonic actuation on a backward-facing step and pulsed blowing on a pitching airfoil for reattachment and separation controls. Spectra analyses based on the unexcited flowfield data were carried out by using dynamic mode decomposition to identify spatial structures corresponding to the different Strouhal frequencies. The characteristic physical modes have been extracted for both cases. With better understanding of unsteady flow features, effective control practices were illustrated. For the backward-facing step case, the optimal excitation frequency was found to be identical with the step-mode frequency of the baseline flow. Such harmonic actuation enhanced the pairing process, forming the largest-scale spanwise coherent structures in the free shear layer, resulting in a 40% maximum reduction of the bubble length. For the airfoil case, with the optimum excitation frequency determined by the vortex-shedding mode of the baseline flow, a 194% increase of the lift-to-drag ratio was obtained; the pulsed blowing with the jet orifices in an antiphased manner was found to be very effective to damp the fluctuations of the lift around its mean value, though it led to a small decrease in mean lift. [ABSTRACT FROM AUTHOR]

Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid produced by sphingosine kinase (SphK1 and 2). We previously showed that S1P receptors (S1P1S1P2, and S1P3) are expressed in hepatic myofibroblasts (hMF), a population of cells that triggers matrix remodeling during liver injury. Here we investigated the function of these receptors in the wound healing response to acute liver injury elicited by carbon tetrachloride, a process that associates hepatocyte proliferation and matrix remodeling. Acute liver injury was associated with the induction of S1P2, S1P3, SphK1, and SphK2 mRNAs and increased SphK activity, with no change in S1P1 expression. Necrosis, inflammation, and hepatocyte regeneration were similar in S1P1-/- and wild-type (WT) mice. However, compared with WT mice, S1P2-/- mice displayed reduced accumulation of hMF, as shown by lower induction of smooth muscle α-actin mRNA and lower induction of TIMP-1, TGF-β1, and PDGF-BB mRNAs, overall reflecting reduced activation of remodeling in response to liver injury. The wound healing response was similar in S1P3-/- and WT mice. In vitro, S1P enhanced proliferation of cultured WT hMF, and PDGF-BB further enhanced the mitogenic effect of S1P. In keeping with these findings, PDGF-BB up-regulated S1P2 and SphK1 mRNAs, increased SphK activity, and S1P2 induced PDGF-BB mRNA. These effects were blunted in S1P2-/- cells, and S1P2-/- hMF exhibited reduced mitogenic and comitogenic responses to S1P. These results unravel a novel major role of S1P2 in the wound healing response to acute liver injury by a mechanism involving enhanced proliferation of hMF. [ABSTRACT FROM AUTHOR]

Background/Aims: Macrophages, the most plastic cells in the haematopoietic system, are found in all tissues and show great functional heterogeneity. Sphingosine 1-phosphate (S1P)/ S1P receptors (S1PRs) system is widely involved in the process of inflammatory disease, whereas little evidence concerning its role in functional macrophage polarization is available. Thus, the present study was designed to evaluate the effects of S1P/S1PRs on functional polarization of macrophage in mouse bone marrow (BM)-derived monocyte/macrophages (BMMs). Methods: For the detection of M1 macrophage markers, such as CD86, tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1/ chemokine (C-C motif) ligand (CCL) 2, nitric oxide synthase (NOS) 2, and macrophage inflammatory protein (MIP)-1β, RT-qPCR and cytometric bead array (CBA) were performed in cultured primary BMMs after the treatment with selective S1PR2/3 antagonists or specific S1PRs siRNA. Western blotting and immunofluorescence were used for the detection of phosphorylation of JNK1/2. Results: BMMs expressed S1PR1-3 and interestingly, S1PR2/3, but not S1PR1, mediates S1P-induced M1 macrophage polarization of BMMs as their siRNA or antagonists reduced M1 genes' expression. We found that PTX (inhibitor of G(α)i/o), LY294002 (inhibitor of PI3K) or SP600125 (inhibitor of JNK1/2) prevented up-regulation of M1 genes expression mediated by S1P/S1PR2/3 signal, and S1P-induced JNK phosphorylation was inhibited by antagonists of S1PR2/3, PTX or LY294002. Conclusion: Collectively, our results demonstrate that S1P/S1PR2/3 plays a key role in regulating M1 type polarization of BMMs and acts by activating G(α)i/o /PI3K/JNK signaling pathway, with potential implications for new approaches to inflammatory liver disease therapy. [ABSTRACT FROM AUTHOR]

Hepatic injury undergoes significant increases in endocannabinoidsand infiltrations of macrophages, yet the concrete mechanisms of changes in endocannabinoids and the functions of macrophage-expressed cannabinoid receptors (CBs) are unclear. Biosynthetic and degradative enzymes of endocannabinoids revealed a significant change in human fibrotic liver. Meanwhile, we showed dynamic changes of these enzymes and CBs (CB1 and CB2) from 1 to 56 d in carbon tetrachloride-induced murine liver injury. Biosynthetic enzymes (N-acylphosphatidyl-ethanolamine selective phospholipase D and diacylglycerol lipase-α) and CBs were markedly increased, whereas degradative enzymes (fatty acid amidohydrolase and monoacylglycerol lipase) were downregulated. Moreover, these enzymes intimately correlated with the fibrosis parameter [procollagen α1(III)]. Bone marrow-derived monocytes/macrophages (BMM) expressed CBs. Interestingly, CB1 but not CB2 mediated BMM migration through a Boyden chambers assay, and the effect depended on the G(α)i/o/RhoA/ROCK signaling pathway. ICR mice were lethally irradiated and received BM transplants from enhanced GFP transgenic mice. Four weeks later, mice of BM reconstruction were subjected to carbon tetrachloride-induced liver injury. In the chimeric murine model, we found that blockade of CB1 by administration of a CB1 antagonist inhibited the recruitment of BMM into injured liver using immunofluorescence staining and FACS, but it did not have effects on migration of T cells and dendritic cells without CB1 expression. Furthermore, activation of CB1 enhanced cytokine expression of BMM. In vivo, inhibition of CB1 attenuated the inflammatory cytokine level through real-time RT-PCR and cytometric bead array, ameliorating hepatic inflammation and fibrosis. In this study, we identify inactivation of BMM-expressed CB1 as a therapeutic strategy for reducing hepatic inflammation and fibrosis. [ABSTRACT FROM AUTHOR]

The microstructures and mechanical properties of coarse grain heat-affected zone (CGHAZ) of domestic X70 pipeline were investigated. The weld CGHAZ thermal cycles having different cooling time Δ t were simulated with the Gleeble-1500 thermal/mechanical simulator. The Charpy impact absorbed energy for toughness was measured, and the corresponding fractographs, optical micrographs, and electron micrographs were systematically investigated to study the effect of cooling time on microstructure, impact toughness, and fracture morphology in the CGHAZ of domestic X70 pipeline steel during in-service welding. The results of simulated experiment show that the microstructure of CGHAZ of domestic X70 pipeline steel during in-service welding mainly consists of granular bainite and lath bainite. Martensite-austenite (M-A) constituents are observed at the lath boundaries. With increase in cooling time, the M-A constituents change from elongated shape to massive shape. The reduction of toughness may be affected by not only the M-A constituents but also the coarse bainite sheaves. Accelerating cooling with cooling time Δ t of 8 s can be chosen in the field in-service welding X70 pipeline to control microstructures and improve toughness. [ABSTRACT FROM AUTHOR]

There are abundant progenitor cells in the developing pancreas, but molecular markers for these cells are lacking. Octamer-binding transcription factor-4 (Oct4) is an important transcription factor for keeping the features of self-renewal and pluripotency of embryonic stem cells. It’s well known that Oct4, as a totipotent stem cells marker, just is expressed in totipotent stem cells. In the present study, we collected ten human fetal pancreases, and found that Oct4 mRNA and protein were expressed in human fetal pancreas samples by RT-PCR, western blot and immunohistochemistry assays. Using double-staining, we demonstrated that Oct4 was not co-expressed with Chromogranin A (a peptide expressed in endocrine cells), but partially co-expressed with Ngn3 (a transcription factor expressed in pancreatic endocrine precursor cells) and Nestin (a intermediate filament, Nestin-positive cells isolated from islets can be induced to express insulin) in human fetal pancreases. Indeed, we prepared Nestin-positive cells from human fetal pancreas by cell selection, and found that these cells expressed Oct4 and Ngn3. The Nestin-positive cells displayed a rapid duplication and could differentiate into osteoblasts, fat and endocrine cells in vitro. These results indicated that the Nestin-positive cells in the fetal age should be pancreatic progenitor cells. Overall, our study suggested that Oct4 was a marker for pancreatic endocrine progenitor. [ABSTRACT FROM AUTHOR]

The role of inflammation in acute coronary syndrome (ACS) and the mechanism by which statin treats ACS is explored. Serum high-sensitivity C-reactive protein (hs-CRP) and interleukin-6 (IL-6) levels were measured in 50 patients with ACS [including 30 cases with unstable angina (UA) and 20 patients with acute myocardial infarction (AMI)], 34 patients with stable angina (SA), and 30 controls. Patients in the ACS group were randomly assigned to a simvastatin group (including a simvastatin AMI subgroup,n= 11 and a simvastatin UA subgroup,n= 14) and a routine group (including a routine AMI subgroup,n= 9 and a routine UA subgroup,n= 16). The simvastatin group was given simvastatin 20?mg/day and the routine group a placebo. After a 3-week follow-up, serum hs-CRP, IL-6 levels, and serum lipid concentrations were measured again. Both serum IL-6 and hs-CRP levels were significantly higher in the ACS group (including the UA and AMI subgroups) than in the SA and control groups (P<0.001). After 3 weeks of treatment with simvastatin, the serum IL-6, hs-CRP, total cholesterol, and low-density lipoprotein cholesterol levels were decreased significantly in the simvastatin group (P<0.001), but no significant changes were observed in the routine group. No relationship was observed between the rate of decrease of serum IL-6 or hs-CRP and serum lipids levels. The hs-CRP level showed a significant correlation with IL-6 by Spearman’s rank correlation analysis (P<0.01). Inflammation plays an important role in the initiation of ACS. Simvastatin possesses an anti-inflammatory effect, independent of its lipid-lowering action, which may play an important role in the early treatment of ACS. [ABSTRACT FROM AUTHOR]