Delay-dependent stabilization of stochastic interval delay systems with nonlinear disturbances

This is the post print version of the article. The official published version can be obtained from the link below - Copyright 2007 Elsevier Ltd.In this paper, a delay-dependent approach is developed to deal with the robust stabilization problem for a class of stochastic time-delay interval systems with nonlinear disturbances. The system matrices are assumed to be uncertain within given intervals, the time delays appear in both the system states and the nonlinear disturbances, and the stochastic perturbation is in the form of a Brownian motion. The purpose of the addressed stochastic stabilization problem is to design a memoryless state feedback controller such that, for all admissible interval uncertainties and nonlinear disturbances, the closed-loop system is asymptotically stable in the mean square, where the stability criteria are dependent on the length of the time delay and therefore less conservative. By using Itô's differential formula and the Lyapunov stability theory, sufficient conditions are first derived for ensuring the stability of the stochastic interval delay systems. Then, the controller gain is characterized in terms of the solution to a delay-dependent linear matrix inequality (LMI), which can be easily solved by using available software packages. A numerical example is exploited to demonstrate the effectiveness of the proposed design procedure.This work was supported in part by the Engineering and Physical Sciences Research Council (EPSRC) of the UK under Grant GR/S27658/01, the Nuffield Foundation of the UK under Grant NAL/00630/G, and the Alexander von Humboldt Foundation of Germany

Robust stability for stochastic Hopfield neural networks with time delays

This is the post print version of the article. The official published version can be obtained from the link below - Copyright 2006 Elsevier Ltd.In this paper, the asymptotic stability analysis problem is considered for a class of uncertain stochastic neural networks with time delays and parameter uncertainties. The delays are time-invariant, and the uncertainties are norm-bounded that enter into all the network parameters. The aim of this paper is to establish easily verifiable conditions under which the delayed neural network is robustly asymptotically stable in the mean square for all admissible parameter uncertainties. By employing a Lyapunov–Krasovskii functional and conducting the stochastic analysis, a linear matrix inequality (LMI) approach is developed to derive the stability criteria. The proposed criteria can be checked readily by using some standard numerical packages, and no tuning of parameters is required. Examples are provided to demonstrate the effectiveness and applicability of the proposed criteria.This work was supported in part by the Engineering and Physical Sciences Research Council (EPSRC) of the UK under Grant GR/S27658/01, the Nuffield Foundation of the UK under Grant NAL/00630/G, and the Alexander von Humboldt Foundation of German

Effect of Aged Wuyi Rock Tea on Relieving Dextran Sulfate Sodium-Induced Colitis and Regulating the Gut Microbiota in Mice

This research was performed in order to investigate the alleviative effect of aged Wuyi rock tea on dextran sulfate sodium (DSS)-induced colitis in mice. Fifty C57BL/6JGpt female mice were randomly and equally divided into five groups: control, DSS, DSS + infusion of 20-year-old Wuyi rock tea (DSS + OT01), DSS + infusion of 10-year-old Wuyi rock tea (DSS + OT11) and DSS + infusion of fresh Wuyi rock tea (DSS + OT20). The physiological and histopathological conditions of mice after Wuyi rock tea interventions, and the changes of serum inflammatory factors and cecal microbiota were analyzed. The results showed that aged Wuyi rock tea could significantly alleviate the symptoms of body mass loss, diarrhea, bloody stool, and colon length shortening, reduce inflammatory cell infiltration, and significantly inhibit the secretion of pro-inflammatory cytokines. In addition, aged Wuyi rock tea could alleviate the disorder of the gut microbiota, significantly down-regulate the relative abundance of Proteobacteria, Enterobacteriaceae and Escherichia, and up-regulate the relative abundance of Verrucomicrobia and Akkermansia. In summary, aged Wuyi rock tea can alleviate DSS-induced colitis in mice, and the tea produced in 2011 is more effective than that produced in 2001, which may be due to proper oxidation of catechins such as epigallocatechin gallate to produce thearubigins, with better anti-inflammatory and antioxidant properties. In addition, aged Wuyi rock tea is able to maintain intestinal homeostasis by regulating the relative abundance of Escherichia and Akkermansia in the intestine, which in turn alleviates the symptoms of DSS-induced colitis in mice such as body mass loss, diarrhea, bloody stool, colon length shortening, mucosal and crypt damage, inflammatory cell infiltration, and serum inflammatory factor overexpression

The trans-ancestral genomic architecture of glycemic traits

Glycemic traits are used to diagnose and monitor type 2 diabetes and cardiometabolic health. To date, most genetic studies of glycemic traits have focused on individuals of European ancestry. Here we aggregated genome-wide association studies comprising up to 281,416 individuals without diabetes (30% non-European ancestry) for whom fasting glucose, 2-h glucose after an oral glucose challenge, glycated hemoglobin and fasting insulin data were available. Trans-ancestry and single-ancestry meta-analyses identified 242 loci (99 novel; P < 5 x 10(-8)), 80% of which had no significant evidence of between-ancestry heterogeneity. Analyses restricted to individuals of European ancestry with equivalent sample size would have led to 24 fewer new loci. Compared with single-ancestry analyses, equivalent-sized trans-ancestry fine-mapping reduced the number of estimated variants in 99% credible sets by a median of 37.5%. Genomic-feature, gene-expression and gene-set analyses revealed distinct biological signatures for each trait, highlighting different underlying biological pathways. Our results increase our understanding of diabetes pathophysiology by using trans-ancestry studies for improved power and resolution. A trans-ancestry meta-analysis of GWAS of glycemic traits in up to 281,416 individuals identifies 99 novel loci, of which one quarter was found due to the multi-ancestry approach, which also improves fine-mapping of credible variant sets.Peer reviewe

Genetic drivers of heterogeneity in type 2 diabetes pathophysiology

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P &lt; 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care.</p

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services

Long-Term Load Forecasting Based on a Time-Variant Ratio Multiobjective Optimization Fuzzy Time Series Model

Load forecasting problem is a complex nonlinear problem linked with economic and weather factors. Long-term load forecasting provides useful information for maintenance scheduling, adequacy assessment, and limited energy resources for electrical power systems. Fuzzy time series forecasting models can be used for long-term load forecasting. However, the interval length has been chosen arbitrarily in the implementations of known fuzzy time series forecasting models, which has an important impact on the performance of these models. In this paper, a time-variant ratio multiobjective optimization fuzzy time series model (TV-RMOP) is proposed, and its performance is tested on the prediction of enrollment at the University of Alabama. Results clearly promote the forecasting accuracy as compared to the conventional models. A genetic algorithm is used to search for the length of intervals based on the training data while Pareto optimality theory provides the necessary conditions to identify an optimal one. The TV-RMOP model is applied for the long-term load forecasting in Shanghai of China

Differential Evolution for Lifetime Maximization of Heterogeneous Wireless Sensor Networks

Maximizing the lifetime of wireless sensor networks (WSNs) is a hot and significant issue. However, using differential evolution (DE) to research this problem has not appeared so far. This paper proposes a DE-based approach that can maximize the lifetime of WSN through finding the largest number of disjoint sets of sensors, with every set being able to completely cover the target. Different from other methods in the literature, firstly we introduce a common method to generate test data set and then propose an algorithm using differential evolution to solve disjoint set covers (DEDSC) problems. The proposed algorithm includes a recombining operation, which performs after initialization and guarantees at least one critical target’s sensor is divided into different disjoint sets. Moreover, the fitness computation in DEDSC contains both the number of complete cover subsets and the coverage percent of incomplete cover subsets. Applications for sensing a number of target points, named point-coverage, have been used for evaluating the effectiveness of algorithm. Results show that the proposed algorithm DEDSC is promising and simple; its performance outperforms or is similar to other existing excellent approaches in both optimization speed and solution quality