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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]

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]