Improved Approximation Algorithm for Minimum-Weight (1,m)(1,m)--Connected Dominating Set

The classical minimum connected dominating set (MinCDS) problem aims to find a minimum-size subset of connected nodes in a network such that every other node has at least one neighbor in the subset. This problem is drawing considerable attention in the field of wireless sensor networks because connected dominating sets can serve as virtual backbones of such networks. Considering fault-tolerance, researchers developed the minimum $k$-connected $m$-fold CDS (Min$(k,m)$CDS) problem. Many studies have been conducted on MinCDSs, especially those in unit disk graphs. However, for the minimum-weight CDS (MinWCDS) problem in general graphs, algorithms with guaranteed approximation ratios are rare. Guha and Khuller designed a $(1.35+\varepsilon)\ln n$-approximation algorithm for MinWCDS, where $n$ is the number of nodes. In this paper, we improved the approximation ratio to $2H(\delta_{\max}+m-1)$ for MinW$(1,m)$CDS, where $\delta_{\max}$ is the maximum degree of the graph

Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway

Purpose: To investigate the protective role of tectorigenin in myocardial ischaemia/reperfusion. Methods: Myocardial cells (H9c2) were treated with different concentrations of tectorigenin and exposed to hypoxia/reoxygenation. Cell viability and apoptosis were determined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) staining, respectively. Oxidative stress and inflammation were evaluated using enzyme-linked immunosorbent assay (ELISA), while autophagy and the underlying mechanisms of action were evaluated by Western blot. Results: Tectorigenin enhanced the proliferative activity of H9c2 under hypoxia/reoxygenation conditions, and significantly reduced the apoptotic activity (p < 0.001) through decrease in Bax and increase in Bcl-2. Tectorigenin also significantly up-regulated SOD (superoxide dismutase) and GSH (glutathione) levels (p < 0.01), and down-regulated MDA (malondialdehyde) and MPO (myeloperoxidase) in hypoxia/reoxygenation-induced H9c2. TNF-α (tumor necrosis factor-α), IL(interleukin)-1β, and IL-6 levels were also inhibited by tectorigenin by down-regulating p-p65. Hypoxia/reoxygenation-induced increase in p62 and decrease in Beclin-1 and LC3-II/LC3-I were reversed by tectorigenin. Protein expressions of p-mTOR, p-AKT, and p-PI3K in hypoxia/reoxygenation-induced H9c2 were elevated by tectorigenin. Conclusion: Tectorigenin exerts anti-oxidant, anti-inflammatory, and anti-autophagic effects on hypoxia/reoxygenation-induced H9c2 through the activation of PI3K/AKT/mTOR pathway, thus suggesting that it is a potential agent for the management of myocardial ischaemia/reperfusion

DSMC Prediction of Particle Behavior in Gas-Particle Two-Phase Impinging Streams

Devices with impinging streams have been employed in various fields of chemical engineering, as a means of intensifying heat and mass transfer processes. The particle behavior in gas-particle two-phase impinging streams (GPISs), which is of essential importance for the research of transfer processes, was simulated by an Eulerian-Lagrangian approach in this paper. Collisional interaction of particles was taken into account by means of a modified direct simulation Monte Carlo (DSMC) method based on a Lagrangian approach and the modified Nanbu method. A quantitative agreement was obtained between the predicted results and the experimental data in the literature. The particle motion behavior and the distributions of particle concentration and particle collision positions were presented reasonably. The results indicate that the particle distribution in GPIS can be divided into three zones: particle-collision zone, particle-jetting zone, and particle-scattering zone. Particle collisions occur mainly in the particle-collision zone, which obviously results in a few particles penetrating into the opposite stream. The interparticle collision rate and the particle concentration reach their maximum values in the particle-collision zone, respectively. The maximum value of the particle concentration increases with the increasing inlet particle concentration according to a logarithmic function. The interparticle collision rate is directly proportional to the square of local particle concentration

Direct and negative regulation of the sycO-ypkA-ypoJ operon by cyclic AMP receptor protein (CRP) in Yersinia pestis

<p>Abstract</p> <p>Background</p> <p>Pathogenic yersiniae, including <it>Y. pestis</it>, share a type III secretion system (T3SS) that is composed of a secretion machinery, a set of translocation proteins, a control system, and six Yop effector proteins including YpkA and YopJ. The cyclic AMP receptor protein (CRP), a global regulator, was recently found to regulate the laterally acquired genes (<it>pla </it>and <it>pst</it>) in <it>Y. pestis</it>. The regulation of T3SS components by CRP is unknown.</p> <p>Results</p> <p>The <it>sycO</it>, <it>ypkA </it>and <it>yopJ </it>genes constitute a single operon in <it>Y. pestis</it>. CRP specifically binds to the promoter-proximate region of <it>sycO</it>, and represses the expression of the <it>sycO-ypkA-yopJ </it>operon. A single CRP-dependent promoter is employed for the <it>sycO-ypkA-yopJ </it>operon, but two CRP binding sites (site 1 and site 2) are detected within the promoter region. A CRP box homologue is found in site 1 other than site 2. The determination of CRP-binding sites, transcription start site and core promoter element (-10 and -35 regions) promotes us to depict the structural organization of CRP-dependent promoter, giving a map of CRP-promoter DNA interaction for <it>sycO-ypkA-yopJ</it>.</p> <p>Conclusion</p> <p>The <it>sycO-ypkA-yopJ </it>operon is under the direct and negative regulation of CRP in <it>Y. pestis</it>. The <it>sycO-ypkA-yopJ </it>promoter-proximate regions are extremely conserved in <it>Y. pestis</it>, <it>Y. pseudotuberculosis </it>and <it>Y. enterocolitica</it>. Therefore, data presented here can be generally applied to the above three pathogenic yersiniae.</p

Overexpression of Class III β-tubulin, Sox2, and nuclear Survivin is predictive of taxane resistance in patients with stage III ovarian epithelial cancer

Failed root canal treatment is best addressed primarily with the provision of repeat endodontic treatment with thorough irrigation under isolation. If a post is present in the root of the tooth it needs to be removed first. This paper is the second in a series of two which provide an overview of techniques for post removal. Specifically designed post removal devices and the removal of fibre posts are described. Post removal device techniques are illustrated with a series of clinical case figures

Paeoniflorin and Albiflorin Attenuate Neuropathic Pain via MAPK Pathway in Chronic Constriction Injury Rats

Neuropathic pain remains as the most frequent cause of suffering and disability around the world. The isomers paeoniflorin (PF) and albiflorin (AF) are major constituents extracted from the roots of Paeonia (P.) lactiflora Pall. Neuroprotective effect of PF has been demonstrated in animal models of neuropathologies. However, only a few studies are related to the biological activities of AF and no report has been published on analgesic properties of AF about neuropathic pain to date. The aim of this study was to compare the effects of AF and PF against CCI-induced neuropathic pain in rat and explore the underlying mechanism. We had found that both PF and AF could inhibit the activation of p38 mitogen-activated protein kinase (p38 MAPK) pathway in spinal microglia and subsequent upregulated proinflammatory cytokines (interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α)). AF further displayed remarkable effects on inhibiting the activation of astrocytes, suppressing the overelevated expression of phosphorylation of c-Jun N-terminal kinases (p-JNK) in astrocytes, and decreasing the content of chemokine CXCL1 in the spinal cord. These results suggest that both PF and AF are potential therapeutic agents for neuropathic pain, which merit further investigation

Characterization of Zur-dependent genes and direct Zur targets in Yersinia pestis

<p>Abstract</p> <p>Background</p> <p>The zinc uptake regulator Zur is a Zn²⁺-sensing metalloregulatory protein involved in the maintenance of bacterial zinc homeostasis. Up to now, regulation of zinc homeostasis by Zur is poorly understood in <it>Y. pestis</it>.</p> <p>Results</p> <p>We constructed a <it>zur </it>null mutant of <it>Y. pestis </it>biovar <it>microtus </it>strain 201. Microarray expression analysis disclosed a set of 154 Zur-dependent genes of <it>Y. pestis </it>upon exposure to zinc rich condition. Real-time reverse transcription (RT)-PCR was subsequently used to validate the microarray data. Based on the 154 Zur-dependent genes, predicted regulatory Zur motifs were used to screen for potential direct Zur targets including three putative operons <it>znuA, znuCB </it>and <it>ykgM</it>-<it>RpmJ2</it>. The LacZ reporter fusion analysis verified that Zur greatly repressed the promoter activity of the above three operons. The subsequent electrophoretic mobility shift assay (EMSA) demonstrated that a purified Zur protein was able to bind to the promoter regions of the above three operons. The DNase I footprinting was used to identify the Zur binding sites for the above three operons, verifying the Zur box sequence as predicted previously in γ-Proteobacteria. The primer extension assay was further used to determine the transcription start sites for the above three operons and to localize the -10 and -35 elements. Zur binding sites overlapped the -10 sequence of its target promoters, which was consistent with the previous observation that Zur binding would block the entry of the RNA polymerase to repress the transcription of its target genes.</p> <p>Conclusion</p> <p>Zur as a repressor directly controls the transcription of <it>znuA, znuCB </it>and <it>ykgM</it>-<it>RpmJ2 </it>in <it>Y. pestis </it>by employing a conserved mechanism of Zur-promoter DNA association as observed in γ-Proteobacteria. Zur contributes to zinc homeostasis in <it>Y. pestis </it>likely through transcriptional repression of the high-affinity zinc uptake system ZnuACB and two alternative ribosomal proteins YkgM and RpmJ2.</p

Discovery and biosynthetic investigation of a new antibacterial dehydrated non‐ribosomal tripeptide

Acknowledgement: QF and HD are grateful to the University of Aberdeen Elphinstone Scholarship and Scottish Funding Council/ScotCHEM (PEER/PERCE) for financial support. HD, ZL and SW thank the financial supports of Biotechnology and Biological Sciences Research Council UK (BBSRC, BB/P00380X/1) and the Royal Society-NSFC Newton Mobility Grant Award (IEC\NSFC\170617 to HD). HD, SAM and CP thank Business Interaction Vouchers (BIV009) from BBSRC funded Natural Products discovery and bioengineering Network (NPRONET). Y.G. thanks NSFC oversea scholarship, Natural Science Foundation of Jiangsu Province (BK20170450), and the Open Research fund of Jiangsu Key Laboratory of Marine Biotechnology (HS2017003).Peer reviewedPostprin

Identification and characterization of PhoP regulon members in Yersinia pestis biovar Microtus

<p>Abstract</p> <p>Background</p> <p>The transcription regulator PhoP has been shown to be important for <it>Y. pestis </it>survival in macrophages and under various <it>in vitro </it>stresses. However, the mechanism by which PhoP promotes bacterial intracellular survival is not fully understood. Our previous microarray analysis suggested that PhoP governed a wide set of cellular pathways in <it>Y. pestis</it>. A series of biochemical experiments were done herein to study members of the PhoP regulon of <it>Y. pestis </it>biovar <it>Microtus</it>.</p> <p>Results</p> <p>By using gel mobility shift assay and quantitative RT-PCR, a total of 30 putative transcription units were characterized as direct PhoP targets. The primer extension assay was further used to determine the transcription start sites of 18 PhoP-dependent promoters and to localize the -10 and -35 elements. The DNase I footprinting was used to identify the PhoP-binding sites within 17 PhoP-dependent promoters, enabling the identification of PhoP box and matrix that both represented the conserved signals for PhoP recognition in <it>Y. pestis</it>. Data presented here providing a good basis for modeling PhoP-promoter DNA interactions that is crucial to the PhoP-mediated transcriptional regulation.</p> <p>Conclusion</p> <p>The proven direct PhoP targets include nine genes encoding regulators and 21 genes or operons with functions of detoxification, protection against DNA damages, resistance to antimicrobial peptides, and adaptation to magnesium limitation. We can presume that PhoP is a global regulator that controls a complex regulatory cascade by a mechanism of not only directly controlling the expression of specific genes, but also indirectly regulating various cellular pathways by acting on a set of dedicated regulators. These results help us gain insights into the PhoP-dependent mechanisms by which <it>Y. pestis </it>survives the antibacterial strategies employed by host macrophages.</p