108 research outputs found

    Dense chaos and densely chaotic operators

    Get PDF

    Strict Intuitionistic Fuzzy Distance/Similarity Measures Based on Jensen-Shannon Divergence

    Full text link
    Being a pair of dual concepts, the normalized distance and similarity measures are very important tools for decision-making and pattern recognition under intuitionistic fuzzy sets framework. To be more effective for decision-making and pattern recognition applications, a good normalized distance measure should ensure that its dual similarity measure satisfies the axiomatic definition. In this paper, we first construct some examples to illustrate that the dual similarity measures of two nonlinear distance measures introduced in [A distance measure for intuitionistic fuzzy sets and its application to pattern classification problems, \emph{IEEE Trans. Syst., Man, Cybern., Syst.}, vol.~51, no.~6, pp. 3980--3992, 2021] and [Intuitionistic fuzzy sets: spherical representation and distances, \emph{Int. J. Intell. Syst.}, vol.~24, no.~4, pp. 399--420, 2009] do not meet the axiomatic definition of intuitionistic fuzzy similarity measure. We show that (1) they cannot effectively distinguish some intuitionistic fuzzy values (IFVs) with obvious size relationship; (2) except for the endpoints, there exist infinitely many pairs of IFVs, where the maximum distance 1 can be achieved under these two distances; leading to counter-intuitive results. To overcome these drawbacks, we introduce the concepts of strict intuitionistic fuzzy distance measure (SIFDisM) and strict intuitionistic fuzzy similarity measure (SIFSimM), and propose an improved intuitionistic fuzzy distance measure based on Jensen-Shannon divergence. We prove that (1) it is a SIFDisM; (2) its dual similarity measure is a SIFSimM; (3) its induced entropy is an intuitionistic fuzzy entropy. Comparative analysis and numerical examples demonstrate that our proposed distance measure is completely superior to the existing ones

    Influenza Virus Database (IVDB): an integrated information resource and analysis platform for influenza virus research

    Get PDF
    Frequent outbreaks of highly pathogenic avian influenza and the increasing data available for comparative analysis require a central database specialized in influenza viruses (IVs). We have established the Influenza Virus Database (IVDB) to integrate information and create an analysis platform for genetic, genomic, and phylogenetic studies of the virus. IVDB hosts complete genome sequences of influenza A virus generated by Beijing Institute of Genomics (BIG) and curates all other published IV sequences after expert annotation. Our Q-Filter system classifies and ranks all nucleotide sequences into seven categories according to sequence content and integrity. IVDB provides a series of tools and viewers for comparative analysis of the viral genomes, genes, genetic polymorphisms and phylogenetic relationships. A search system has been developed for users to retrieve a combination of different data types by setting search options. To facilitate analysis of global viral transmission and evolution, the IV Sequence Distribution Tool (IVDT) has been developed to display the worldwide geographic distribution of chosen viral genotypes and to couple genomic data with epidemiological data. The BLAST, multiple sequence alignment and phylogenetic analysis tools were integrated for online data analysis. Furthermore, IVDB offers instant access to pre-computed alignments and polymorphisms of IV genes and proteins, and presents the results as SNP distribution plots and minor allele distributions. IVDB is publicly available a

    Observation of spin-tensor induced topological phase transitions of triply degenerate points with a trapped ion

    Full text link
    Triply degenerate points (TDPs), which correspond to new types of topological semimetals, can support novel quasiparticles possessing effective integer spins while preserving Fermi statistics. Here by mapping the momentum space to the parameter space of a three-level system in a trapped ion, we experimentally explore the transitions between different types of TDPs driven by spin-tensor--momentum couplings. We observe the phase transitions between TDPs with different topological charges by measuring the Berry flux on a loop surrounding the gap-closing lines, and the jump of the Berry flux gives the jump of the topological charge (up to a 2π2\pi factor) across the transitions. For the Berry flux measurement, we employ a new method by examining the geometric rotations of both spin vectors and tensors, which lead to a generalized solid angle equal to the Berry flux. The controllability of multi-level ion offers a versatile platform to study high-spin physics and our work paves the way to explore novel topological phenomena therein.Comment: 9 pages, 10 figure

    MyBASE: a database for genome polymorphism and gene function studies of Mycobacterium

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Mycobacterial pathogens are a major threat to humans. With the increasing availability of functional genomic data, research on mycobacterial pathogenesis and subsequent control strategies will be greatly accelerated. It has been suggested that genome polymorphisms, namely large sequence polymorphisms, can influence the pathogenicity of different mycobacterial strains. However, there is currently no database dedicated to mycobacterial genome polymorphisms with functional interpretations.</p> <p>Description</p> <p>We have developed a <b>my</b>cobacterial data<b>base </b>(MyBASE) housing genome polymorphism data and gene functions to provide the mycobacterial research community with a useful information resource and analysis platform. Whole genome comparison data produced by our lab and the novel genome polymorphisms identified were deposited into MyBASE. Extensive literature review of genome polymorphism data, mainly large sequence polymorphisms (LSPs), operon predictions and curated annotations of virulence and essentiality of mycobacterial genes are unique features of MyBASE. Large-scale genomic data integration from public resources makes MyBASE a comprehensive data warehouse useful for current research. All data is cross-linked and can be graphically viewed via a toolbox in MyBASE.</p> <p>Conclusion</p> <p>As an integrated platform focused on the collection of experimental data from our own lab and published literature, MyBASE will facilitate analysis of genome structure and polymorphisms, which will provide insight into genome evolution. Importantly, the database will also facilitate the comparison of virulence factors among various mycobacterial strains. MyBASE is freely accessible via <url>http://mybase.psych.ac.cn</url>.</p

    The KLF4–p62 axis prevents vascular endothelial cell injury via the mTOR/S6K pathway and autophagy in diabetic kidney disease

    Get PDF
    Introduction: Diabetic kidney disease (DKD) is a complication of systemic diabetic microangiopathy, which has a high risk of developing into end-stage renal disease and death. This study explored the mechanism underlying autophagy in DKD vascular endothelial cell injury. Material and methods: DKD and vascular endothelial cell injury models were established using Sprague Dawley rats and human umbilical vein endothelial cells (HUVECs). HUVECs overexpressing Kruppel-like factor 4 (KLF4) were constructed by transient transfection of plasmids. Biochemical determination of urinary protein and blood urea nitrogen (BUN), superoxide dismutase (SOD), and creatinine (Scr) levels was performed. Renal pathology was observed by periodic acid–Schiff (PAS) staining. Cell Counting Kit-8 (CCK8), terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), and immunocytochemistry (ICC) were used to analyse the growth and apoptosis of HUVECs. Microtubule-associated protein light chain 3 (LC3) expression was observed by immunofluorescence (IF). The reactive oxygen species (ROS) levels were measured using flow cytometry. Monocyte chemoattractant protein-1 (MCP-1), KLF4, and tumour necrosis factor alpha (TNF-α) levels were detected using enzyme-linked immunosorbent assay (ELISA). The expression of KLF4, p62 protein, and LC3 was analysed using reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). S6 kinase (S6K), p70 ribosomal S6 kinase (p-S6K), Beclin1, ATG5, LC3, p62, Caspase-3, mammalian target of rapamycine (mTOR), and phsophorylated mTOR (p-mTOR) expressions were detected by western blotting. Results: PAS-positive substances (polysaccharide and glycogen) and S6K protein levels increased, and LC3 protein expression decreased in DKD rats. The levels of urinary protein, BUN, and Scr increased, and KLF4 decreased in DKD rats. High glucose (HG) levels decreased the proliferation and increased the apoptosis rate of HUVECs. The expression of ROS, TNF-α, MCP-1, and p62 increased, while the expression of SOD, KLF4, Beclin1, ATG5, and LC3 decreased in HG-induced HUVECs. KLF4 overexpression significantly increased Beclin1, ATG5, and LC3 protein expression and decreased p62 protein expression compared to the oe-NC group in HG-induced HUVECs. KLF4 overexpression inhibits the expression of Caspase-3, p-mTOR, and p-S6K in HG-induced HUVECs. Conclusions: KLF4–p62 axis improved vascular endothelial cell injury by regulating inflammation and the mTOR/S6K pathway in DKD

    High Density Lipoprotein Protects Mesenchymal Stem Cells from Oxidative Stress-Induced Apoptosis via Activation of the PI3K/Akt Pathway and Suppression of Reactive Oxygen Species

    Get PDF
    The therapeutic effect of transplantation of mesenchymal stem cells (MSCs) in myocardial infarction (MI) appears to be limited by poor cell viability in the injured tissue, which is a consequence of oxidative stress and pro-apoptotic factors. High density lipoprotein (HDL) reverses cholesterol transport and has anti-oxidative and anti-apoptotic properties. We, therefore, investigated whether HDL could protect MSCs from oxidative stress-induced apoptosis. MSCs derived from the bone marrow of rats were pre-incubated with or without HDL, and then were exposed to hydrogen peroxide (H2O2) in vitro, or were transplanted into experimentally infarcted hearts of rats in vivo. Pre-incubation of MSCs with HDL increased cell viability, reduced apoptotic indices and resulted in parallel decreases in reactive oxygen species (ROS) in comparison with control MSCs. Each of the beneficial effects of HDL on MSCs was attenuated by inhibiting the PI3K/Akt pathway. Preconditioning with HDL resulted in higher MSC survival rates, improved cardiac remodeling and better myocardial function than in the MSC control group. Collectively, these results suggest that HDL may protect against H2O2-induced apoptosis in MSCs through activation of a PI3K/Akt pathway, and by suppressing the production of ROS
    corecore