An evolutionary game based particle swarm optimization algorithm

AbstractParticle swarm optimization (PSO) is an evolutionary algorithm used extensively. This paper presented a new particle swarm optimizer based on evolutionary game (EGPSO). We map particles’ finding optimal solution in PSO algorithm to players’ pursuing maximum utility by choosing strategies in evolutionary games, using replicator dynamics to model the behavior of particles. And in order to overcome premature convergence a multi-start technique was introduced. Experimental results show that EGPSO can overcome premature convergence and has great performance of convergence property over traditional PSO

Detection and characterization of spontaneous internal deletion mutants of Beet Necrotic yellow vein virus RNA3 from systemic host Nicotiana benthamiana

Abstract Background Beet Necrotic Yellow Vein virus (BNYVV) is a member of the genus Benyvirus causing a worldwide sugar beet disease rhizomania. BNYVV contains four or five plus-sense single stranded RNAs. In altered selective conditions, multipartite RNA viruses of plant are prone to undergoing internal deletions, thus turning into Defective RNAs (D RNAs). Although several D RNAs have been reported in BNYVV infection, the spontaneous internal deletion mutants responsible for severe symptom in systemic host Nicotiana benthamiana (N. benthamiana) are not described so far. Results Systemic host N. benthamiana was inoculated by Chinese BNYVV isolates. RT-PCR and Northern blot showed that the D RNAs forms of BNYVV RNA3 were present in the systemic infection of the N. benthamiana. Three distinct D-RNA3s, named as D-RNA 3α, D-RNA 3β and D-RNA 3γ, were made into infectious clones. When inoculated on the N. benthamiana, the in vitro transcripts of D forms exhibited more stable than that of wild-type RNA3 in systemic movement. Among the detected mutant, the p25 protein frame-shift mutant (D-RNA3α) induced obvious necrotic lesions on Tetragonia.expansa (T. expansa) and pronounced systemic symptom on the N. benthamiana. The D-RNA3α was further mutated artificially to pre-terminate the downstream N protein, leading to the abolishment of the pathogenicity, indicating the N protein was responsible for the necrotic symptom. Conclusion Our studies demonstrated the internal deletion mutants of BNYVV-RNA3 were spontaneously generated in the systemic infection on N. benthamiana. The internal deletions didn't affect the efficient replication of D-RNA3s, instead by improving the stability and pathogenicity of RNA3 in the systemic host N. benthamiana. Besides, our results also suggested the downstream N protein of RNA3, but not the upstream p25 protein, may play an important role in the systemic infection on N. benthamiana

Aqua­azido­{3,3′-[o-phenyl­enebis(nitrilo­methyl­idyne)]di-2-naphtholato}manganese(III)

In the title complex, [Mn(C28H18N2O2)(N3)(H2O)], the MnIII ion adopts a distorted fac-MnO3N3 octa­hedral geometry arising from the O,N,N′,O′-tetra­dentate Schiff base ligand, an azide ion and a water mol­ecule. In the crystal, inter­molecular O—H⋯(O,O) and O—H⋯N hydrogen bonds and π–π inter­actions [centroid–centroid separation = 3.5535 (13) Å] link the mol­ecules into chains

CXCR4 Antagonist AMD3100 Modulates Claudin Expression and Intestinal Barrier Function in Experimental Colitis

Ulcerative colitis is a gastrointestinal disorder characterized by local inflammation and impaired epithelial barrier. Previous studies demonstrated that CXC chemokine receptor 4 (CXCR4) antagonists could reduce colonic inflammation and mucosal damage in dextran sulfate sodium (DSS)-induced colitis. Whether CXCR4 antagonist has action on intestinal barrier and the possible mechanism, is largely undefined. In the present study, the experimental colitis was induced by administration of 5% DSS for 7 days, and CXCR4 antagonist AMD3100 was administered intraperitoneally once daily during the study period. For in vitro study, HT-29/B6 colonic cells were treated with cytokines or AMD3100 for 24 h until assay. DSS-induced colitis was characterized by morphologic changes in mice. In AMD3100-treated mice, epithelial destruction, inflammatory infiltration, and submucosal edema were markedly reduced, and the disease activity index was also significantly decreased. Increased intestinal permeability in DSS-induced colitis was also significantly reduced by AMD3100. The expressions of colonic claudin-1, claudin-3, claudin-5, claudin-7 and claudin-8 were markedly decreased after DSS administration, whereas colonic claudin-2 expression was significantly decreased. Treatment with AMD3100 prevented all these changes. However, AMD3100 had no influence on claudin-3, claudin-5, claudin-7 and claudin-8 expression in HT-29/B6 cells. Cytokines as TNF-α, IL-6, and IFN-γ increased apoptosis and monolayer permeability, inhibited the wound-healing and the claudin-3, claudin-7 and claudin-8 expression in HT-29/B6 cells. We suggest that AMD3100 acted on colonic claudin expression and intestinal barrier function, at least partly, in a cytokine-dependent pathway

Proteomic dissection of LPS-inducible, PHF8-dependent secretome reveals novel roles of PHF8 in TLR4-induced acute inflammation and T cell proliferation

Endotoxin (LPS)-induced changes in histone lysine methylation contribute to the gene-specific transcription for control of inflammation. Still unidentified are the chromatin regulators that drive the transition from a transcriptional-repressive to a transcriptional-active chromatin state of pro-inflammatory genes. Here, using combined approaches to analyze LPS-induced changes in both gene-specific transcription and protein secretion to the extracellular compartment, we characterize novel functions of the lysine demethylase PHF8 as a pro-inflammatory, gene-specific chromatin regulator. First, in the LPS-induced, acute-inflamed macrophages, PHF8 knockdown led to both a reduction of pro-inflammatory factors and an increase in a transcriptional-repressive code (H3K9me2) written by the methyltransferase G9a. Through unbiased quantitative secretome screening we discovered that LPS induces the secretion of a cluster of PHF8-dependent, ‘tolerizable’ proteins that are related to diverse extracellular pathways/processes including those for the activation of adaptive immunity. Specifically, we determined that PHF8 promotes T-cell activation and proliferation, thus providing the first link between the epigenetic regulation of inflammation and adaptive immunity. Further, we found that, in the acute-inflamed macrophages, the acute-active PHF8 opposes the H3K9me1/2-writing activity of G9a to activate specific protein secretions that are suppressed by G9a in the endotoxin-tolerant cells, revealing the inflammatory-phenotypic chromatin drivers that regulate the gene-specific chromatin plasticity

AST:Adaptive Self-supervised Transformer for optical remote sensing representation

Due to the variation in spatial resolution and the diversity of object scales, the interpretation of optical remote sensing images is extremely challenging. Deep learning has become the mainstream solution to interpret such complex scenes. However, the explosion of deep learning model architectures has resulted in the need for hundreds of millions of remote sensing images for which labels are very costly or often unavailable publicly. This paper provides an in-depth analysis of the main reasons for this data thirst, i.e., (i) limited representational power for model learning, and (ii) underutilization of unlabeled remote sensing data. To overcome the above difficulties, we present a scalable and adaptive self-supervised Transformer (AST) for optical remote sensing image interpretation. By performing masked image modeling in pre-training, the proposed AST releases the rich supervision signals in massive unlabeled remote sensing data and learns useful multi-scale semantics. Specifically, a cross-scale Transformer architecture is designed to collaboratively learn global dependencies and local details by introducing a pyramid structure, to facilitate multi-granular feature interactions and generate scale-invariant representations. Furthermore, a masking token strategy relying on correlation mapping is proposed to achieve adaptive masking of partial patches without affecting key structures, which enhances the understanding of visually important regions. Extensive experiments on various optical remote sensing interpretation tasks show that AST has good generalization capability and competitiveness.</p

Ten interleukins and risk of prostate cancer

BackgroundInterleukins (ILs) have been reported to be related to prostate cancer. The aims of this study were to estimate the levels for several key interleukins in prostate cancer and the causal effects between them.MethodsWe conducted a bi-directional two-sample Mendelian randomization (MR) study to assess the causal associations between ILs and prostate cancer. Genetic instruments and summary-level data for 10 ILs were obtained from three genome-wide association meta-analyses. Prostate cancer related data were obtained from the PRACTICAL (79,148 cases and 61,106 controls), UK Biobank (7,691 cases and 169,762 controls) and FinnGen consortium (10,414 cases and 124,994 controls), respectively.ResultsThe odds ratio of prostate cancer was 0.92 (95% confidence interval (CI), 0.89, 0.96; P=1.58×10-05) and 1.12 (95% CI, 1.07, 1.17; P=6.61×10-07) for one standard deviation increase in genetically predicted IL-1ra and IL-6 levels, respectively. Genetically predicted levels of IL-1ß, IL-2a, IL-6ra, IL-8, IL-16, IL-17, IL-18, and IL-27 were not associated with the risk of prostate cancer. Reverse MR analysis did not find the associations between genetic liability to prostate cancer and higher levels of IL-1ra (β, -0.005; 95% CI, -0.010, 0.001; P=0.111) and IL-6 (β, 0.002; 95% CI, -0.011, 0.014; P=0.755).ConclusionThis MR study suggests that long-term IL-6 may increase the risk of prostate cancer and IL-1ra may reduce it

3-(5-Methyl-2-fur­yl)-1-(p-tol­yl)-2-propen-1-one

The title compound, C15H14O2, was prepared from 4-methyl­hypnone and 5-methyl­furfural by Clasion–Schmidt condensation. All of the bond lengths and bond angles are in normal ranges. The dihedral angle formed by the benzene ring and furan ring is 5.31 (2)