Synchronization of impulsively coupled complex systems with delay

Author name used in this publication: Francis AustinVersion of RecordPublishe

On spherical twisted conjugacy classes

Let G be a simple algebraic group over an algebraically closed field of good odd characteristic, and let theta be an automorphism of G arising from an involution of its Dynkin diagram. We show that the spherical theta-twisted conjugacy classes are precisely those intersecting only Bruhat cells corresponding to twisted involutions in the Weyl group. We show how the analogue of this statement fails in the triality case. We generalize to good odd characteristic J-H. Lu's dimension formula for spherical twisted conjugacy classes.Comment: proof of Lemma 6.4 polished. The journal version is available at http://www.springerlink.com/content/k573l88256753640

In situ visualization by X-Ray computed tomography on sulfur stabilization and lithium polysulfides immobilization in S@HCS/MnOₓ cathode

The lithium-sulfur (Li-S) batteries have high theoretical energy density, exceeding that of the lithium-ion batteries. However, their practical applications are hindered by the capacity decay due to lithium polysulfide shuttle effect and sulfur volume expansion. Here, we design a S@hollow carbon with porous shell/MnOx (S@HCS/MnOx) cathode to accommodate and immobilize sulfur and polysulfides, and develop a non-destructive technique X-ray computed tomography (X-ray CT) to in situ visualize the volume expansion of Li-S cathode. The designed cathode achieves a specific capacity of ∼1100 mAh g-1 at 0.2 C with a fade rate of 0.18% per cycle over 300 cycles. The X-ray CT shows that only 16% volume expansion and 70% volume fraction of solid sulfur remaining in the S@HCS/MnOx cathode, superior to the commercial cathode with 40% volume expansion and 5% volume remaining of solid sulfur particles. This is the first reported visualization evidence for the effectiveness of hollow carbon structure in accommodating cathode volume expansion and immobilizing sulfur shuttling. X-ray CT can serve as a powerful in situ tool to trace the active materials and then feedback to the structure design, which helps develop efficient and reliable energy storage systems

Ultrasonic Monitoring of Recrystallization Textures in Aluminum

The present paper is an attempt to use ultrasonic velocity measurements to characterize the texture of an aluminum-magnesium alloy (Al 5xxx) and to compare the results with orientation imaging microscopy (OIM) results. The results are characterized in terms of three orientation distribution coefficients (ODC’s), W400, W420, and W440, each of which describes a particular forming anisotropy, and each of which has significant impact on the final products

HMG1A and PPARG are differently expressed in the liver of fat and lean broilers

The expression of nine functional candidates for QT abdominal fat weight and relative abdominal fat content was investigated by real-time polymerase chain reaction (PCR) in the liver, adipose tissue, colon, muscle, pituitary gland and brain of broilers. The high mobility group AT-hook 1 (HMG1A) gene was up-regulated in liver with a ratio of means of 2.90 (P ≤ 0.01) in the «fatty» group (relative abdominal fat content 3.5 ± 0.18%, abdominal fat weight 35.4 ± 6.09 g) relative to the «lean» group (relative abdominal fat content 1.9 ± 0.56%, abdominal fat weight 19.2 ± 5.06 g). Expression of this gene was highly correlated with the relative abdominal fat content (0.70, P ≤ 0.01) and abdominal fat weight (0.70, P ≤ 0.01). The peroxisome proliferator-activated receptor gamma (PPARG) gene was also up-regulated in the liver with a ratio of means of 3.34 (P ≤ 0.01) in the «fatty» group relative to the «lean» group. Correlation of its expression was significant with both the relative abdominal fat content (0.55, P ≤ 0.05) and the abdominal fat weight (0.57, P ≤ 0.01). These data suggest that the HMG1A and PPARG genes were candidate genes for abdominal fat deposition in chickens. Searching of rSNPs in regulatory regions of the HMG1A and PPARG genes could provide a tool for gene-assisted selection

Does the immune reaction cause malignant transformation by disrupting cell-to-cell or cell-to-matrix communications?

Tumor progression: In many (perhaps in all) tumor systems, a malignant cancer is preceded by a benign lesion. Most benign lesions do not transform to malignancy and many regress. The final transformative step to malignancy differs from the preceding steps in, among other things, that it often occurs in the absence of the original carcinogenic stimulus. Mechanism of immunostimulation: Relatively low titers of specific immune reactants are known to stimulate, but cell-to-cell or cell-to-matrix interactions appear to be major inhibitors of tumor-growth. Therefore, it seems reasonable to hypothesize that the mechanism of immunostimulation may be an interference with cell-to-cell or cell-to-matrix communication by a sub-lethal immune-reaction. Discussion: While the above hypothesis remains unproven, some evidence suggests that immunity may have a major facilitating effect on tumor growth especially at the time of malignant transformation. There is even some evidence suggesting that transformation in vivo may seldom occur in the absence of immunostimulation of the premalignant lesion. Positive selection by the immune reaction may be the reason that tumors are immunogenic

Sensitization, energy transfer and infra-red emission decay modulation in Yb3+-doped NaYF4 nanoparticles with visible light through a perfluoroanthraquinone chromophore

The authors thank Dr. R. Wilson for XRD measurements. H.L., Y.P., H.Y., J.H. and H.G. are funded by the China Scholarship Council (CSC) and Queen Mary University of London. H. L. also would like to thank the support from China Postdoctoral Science Foundation Funded Project (2017M611440). I.H. acknowledges funding from the Ministerio de Economía y Competitividad (grant MAT2016-80438-P), the EU FP7 (Marie Curie-CIG-Grant 303535). WPG would like to thank EPSRC for support (EP/K004484/1 and EP/L020114/1) and NSFC (61574095). X.C. was supported by the Centre of Excellence in Medical Engineering funded by the Wellcome Trust and EPSRC under grant number WT088641/Z/09/Z. We are grateful to the EPSRC UK NMSF at Swansea University for mass spectrometry

Varespladib and cardiovascular events in patients with an acute coronary syndrome: the VISTA-16 randomized clinical trial

IMPORTANCE: Secretory phospholipase A2(sPLA2) generates bioactive phospholipid products implicated in atherosclerosis. The sPLA2inhibitor varespladib has favorable effects on lipid and inflammatory markers; however, its effect on cardiovascular outcomes is unknown. OBJECTIVE: To determine the effects of sPLA2inhibition with varespladib on cardiovascular outcomes. DESIGN, SETTING, AND PARTICIPANTS: A double-blind, randomized, multicenter trial at 362 academic and community hospitals in Europe, Australia, New Zealand, India, and North America of 5145 patients randomized within 96 hours of presentation of an acute coronary syndrome (ACS) to either varespladib (n = 2572) or placebo (n = 2573) with enrollment between June 1, 2010, and March 7, 2012 (study termination on March 9, 2012). INTERVENTIONS: Participants were randomized to receive varespladib (500 mg) or placebo daily for 16 weeks, in addition to atorvastatin and other established therapies. MAIN OUTCOMES AND MEASURES: The primary efficacy measurewas a composite of cardiovascular mortality, nonfatal myocardial infarction (MI), nonfatal stroke, or unstable angina with evidence of ischemia requiring hospitalization at 16 weeks. Six-month survival status was also evaluated. RESULTS: At a prespecified interim analysis, including 212 primary end point events, the independent data and safety monitoring board recommended termination of the trial for futility and possible harm. The primary end point occurred in 136 patients (6.1%) treated with varespladib compared with 109 patients (5.1%) treated with placebo (hazard ratio [HR], 1.25; 95%CI, 0.97-1.61; log-rank P = .08). Varespladib was associated with a greater risk of MI (78 [3.4%] vs 47 [2.2%]; HR, 1.66; 95%CI, 1.16-2.39; log-rank P = .005). The composite secondary end point of cardiovascular mortality, MI, and stroke was observed in 107 patients (4.6%) in the varespladib group and 79 patients (3.8%) in the placebo group (HR, 1.36; 95% CI, 1.02-1.82; P = .04). CONCLUSIONS AND RELEVANCE: In patients with recent ACS, varespladib did not reduce the risk of recurrent cardiovascular events and significantly increased the risk of MI. The sPLA2inhibition with varespladib may be harmful and is not a useful strategy to reduce adverse cardiovascular outcomes after ACS. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01130246. Copyright 2014 American Medical Association. All rights reserved