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The problem of stabilization for wireless networked control system (NCS) with packet dropout and time delay is studied in this article. The impulsive control law for the NCS is defined with time delay and impulse. Using a switching model, the network-induced imperfections can be treated as three switching subsystems. Therein, in the case of packet dropout, the control law use the previous state via the first-order hold. The impulsive control law is designed using the switched system approach and the average dwell time method. The obtained sufficient conditions which can guarantee the exponential stability of switched system are in the form of linear matrix inequalities. Finally, a numerical example is used to demonstrate the merits and applicabilities of the proposed method. © 2015 Wiley Periodicals, Inc. Complexity 21: 291-299, 2016 [ABSTRACT FROM AUTHOR]

In this paper, the problem of H ∞ filtering for impulsive networked control systems with random packet dropouts and randomly occurring nonlinearities is investigated. By utilizing an impulsive model, the network-induced imperfections including packet dropout and delay are described by the Bernoulli distributed sequence. The delay in the model is assumed to be time varying. Moreover, nonlinearity in the model is assumed to satisfy sector-like nonlinearities. The H ∞ filter is designed by using the linear matrix inequality (LMI) approach and convex optimization technique. The filter gain matrices for the nonlinear networked control systems can be achieved by solving LMIs, which can be easily facilitated by using some standard numerical packages. Finally, a numerical example is presented to demonstrate the effectiveness and applicability of the proposed results. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

This study investigates aperiodic sampled‐data synchronisation of complex dynamical network (CDN) incorporate dynamics of actuators saturation. The sampling intervals considered here are time‐varying which allowed to be variable within the lower and upper bounds. In order to fully captures the sawtooth structure characteristic of the sampled‐data systems, a novel time‐dependent continuous Lyapunov functional is employed to obtain less conservative criteria. Furthermore, the generalised sector bound condition is utilised for the estimate about the basin of the attraction. Based on the local stability condition, the sampled‐data controller is constructed to guarantee the synchronisation of CDN in the presence of actuators saturation. The obtained sufficient conditions can be cast in two optimisation cases to maximise the admissible upper bound of sampling instants or enlarge estimate about the domain of attraction for the closed‐loop systems. Subsequently, the validity and applicability of the criteria are verified through numerical examples. [ABSTRACT FROM AUTHOR]

This paper investigates the problem of sampled-data synchronization of chaotic Lur'e systems with time-varying sampling. A novel Lyapunov functional, which is continuous in time and makes full use of the available information about the sampling pattern, is constructed to synchronize the chaotic Lur'e systems. By using a free-weighting matrix approach and solving a set of linear matrix inequalities (LMIs), a sampled-data controller is obtained. The effectiveness and the validity of the proposed theoretical result are illustrated by two numerical examples. [ABSTRACT FROM AUTHOR]

To characterize somatic alterations in colorectal carcinoma, we conducted a genome-scale analysis of 276 samples, analysing exome sequence, DNA copy number, promoter methylation and messenger RNA and microRNA expression. A subset of these samples (97) underwent low-depth-of-coverage whole-genome sequencing. In total, 16% of colorectal carcinomas were found to be hypermutated: three-quarters of these had the expected high microsatellite instability, usually with hypermethylation and MLH1 silencing, and one-quarter had somatic mismatch-repair gene and polymerase ? (POLE) mutations. Excluding the hypermutated cancers, colon and rectum cancers were found to have considerably similar patterns of genomic alteration. Twenty-four genes were significantly mutated, and in addition to the expected APC, TP53, SMAD4, PIK3CA and KRAS mutations, we found frequent mutations in ARID1A, SOX9 and FAM123B. Recurrent copy-number alterations include potentially drug-targetable amplifications of ERBB2 and newly discovered amplification of IGF2. Recurrent chromosomal translocations include the fusion of NAV2 and WNT pathway member TCF7L1. Integrative analyses suggest new markers for aggressive colorectal carcinoma and an important role for MYC-directed transcriptional activation and repression. [ABSTRACT FROM AUTHOR]

Polymicrogyria is a disorder of neuronal development resulting in structurally abnormal cerebral hemispheres characterized by over-folding and abnormal lamination of the cerebral cortex. Polymicrogyria is frequently associated with severe neurologic deficits including intellectual disability, motor problems, and epilepsy. There are acquired and genetic causes of polymicrogyria, but most patients with a presumed genetic etiology lack a specific diagnosis. Here we report using whole-exome sequencing to identify compound heterozygous mutations in the WD repeat domain 62 ( WDR62) gene as the cause of recurrent polymicrogyria in a sibling pair. Sanger sequencing confirmed that the siblings both inherited 1-bp (maternal allele) and 2-bp (paternal allele) frameshift deletions, which predict premature truncation of WDR62, a protein that has a role in early cortical development. The probands are from a non-consanguineous family of Northern European descent, suggesting that autosomal recessive PMG due to compound heterozygous mutation of WDR62 might be a relatively common cause of PMG in the population. Further studies to identify mutation frequency in the population are needed. © 2011 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Summary: Purpose: Clinical features associated with chromosome 1p36 deletion include characteristic craniofacial abnormalities, mental retardation, and epilepsy. The presence and severity of specific phenotypic features are likely to be correlated with loss of a distinct complement of genes in each patient. We hypothesize that hemizygous deletion of one, or a few, critical gene(s) controlling neuronal excitability is associated with the epilepsy phenotype. Because ion channels are important determinants of seizure susceptibility and the voltage-gated K[sup +] channel β-subunit gene, KCNAB2, has been localized to 1p36, we propose that deletion of this gene may be associated with the epilepsy phenotype. Methods: Twenty-four patients were evaluated by fluorescence in situ hybridization with a probe containing KCNAB2. Clinical details were obtained by neurologic examination and EEG. Results: Nine patients are deleted for the KCNAB2 locus, and eight (89%) of these have epilepsy or epileptiform activity on EEG. The majority of patients have a severe seizure phenotype, including infantile spasms. In contrast, of those not deleted for KCNAB2, only 27% have chronic seizures, and none had infantile spasms. Conclusions: Lack of the β subunit would be predicted to reduce K[sup +] channel–mediated membrane repolarization and increase neuronal excitability, suggesting a possible relation between loss of this gene and the development of seizures. Because some patients with seizures were not deleted for KCNAB2, there may be additional genes within 1p36 that contribute to epilepsy in this syndrome. Hemizygosity of this gene in a majority of monosomy 1p36 syndrome patients with epilepsy suggests that haploinsufficiency for KCNAB2 is a significant risk factor for epilepsy. [ABSTRACT FROM AUTHOR]

The deletion of chromosome 1p36 is a newly recognized, relatively common contiguous gene deletion syndrome with a variable phenotype. The clinical features have recently been delineated and molecular analysis indicates that the prevalence of certain phenotypic features appears to correlate with deletion size. Phenotype/genotype comparisons have allowed the assignment of certain clinical features to specific deletion intervals, significantly narrowing the regions within which to search for candidate genes. We have extensively characterized the deletion regions in 30 cases using microsatellite markers and fluorescence in situ hybridization analyses. The map order of 28 microsatellite markers spanning the deletion region was obtained by a combination of genotypic analysis and physical mapping. The deletion region was divided into six intervals and breakpoints were found to cluster in mainly two regions. Molecular analysis of the deletions showed that two patients had complex re-arrangements; these cases shared their distal and proximal breakpoints in the two common breakpoint regions. Of the de novo deletions (n= 28) in whichparental samples were available and the analysis was informative (n = 27), there were significantly morematernally derived deletions (n = 21) than paternally derived deletions (n = 6) (χ[sub 1][sup 2]= 8.35, P < 0.0001). Phenotype/genotype correlations and refinements of critical regions in our naturally occurring deletion panel have delineated specific areas in which to focus the search for the causative genes for the features of this syndrome. [ABSTRACT FROM AUTHOR]