Event-Triggered Consensus for Discrete-Time Multi-agent Systems with Parameter Uncertainties Based on a Predictive Control Scheme

In this paper, the event-triggered consensus for linear discrete-time multi-agent systems with parameter uncertainties is investigated. The parameter uncertainty is assumed to be normbounded. An event-triggered consensus protocol based on the predictive control method is proposed to make the multi-agent system achieve consensus. And for the design of the consensus protocol, the problem of estimating the control input is transformed into the problem of estimating state differences between agents. Furthermore, the event-triggered consensus protocol proposed in this paper only demands each agent to mornitor its state to determine its event-triggered instants. A sufficient existence condition for the consensus protocol is proposed based on the linear matrix inequality. And a sufficient condition for the nonexistence of the Zeno-like behaviour is also derived. Finally, a numerical example is given to illustrate that the event-triggered consensus protocol proposed in this paper can make the multi-agent system with parameter uncertainties achieve consensus effectively.     

Shotgun sequence assembly and recent segmental duplications within the human genome

Complex eukaryotic genomes are now being sequenced at an accelerated pace primarily using whole-genome shotgun (WGS) sequence assembly approaches. WGS assembly was initially criticized because of its perceived inability to resolve repeat structures within genomes. Here, we quantify the effect of WGS sequence assembly on large, highly similar repeats by comparison of the segmental duplication content of two different human genome assemblies. Our analysis shows that large (> 15 kilobases) and highly identical (> 97%) duplications are not adequately resolved by WGS assembly. This leads to significant reduction in genome length and the loss of genes embedded within duplications. Comparable analyses of mouse genome assemblies confirm that strict WGS sequence assembly will oversimplify our understanding of mammalian genome structure and evolution; a hybrid strategy using a targeted clone-by-clone approach to resolve duplications is proposed.     

A recurrent 15q13.3 microdeletion syndrome associated with mental retardation and seizures

We report a recurrent microdeletion syndrome causing mental retardation, epilepsy and variable facial and digital dysmorphisms. We describe nine affected individuals, including six probands: two with de novo deletions, two who inherited the deletion from an affected parent and two with unknown inheritance. The proximal breakpoint of the largest deletion is contiguous with breakpoint 3 (BP3) of the Prader-Willi and Angelman syndrome region, extending 3.95 Mb distally to BP5. A smaller 1.5-Mb deletion has a proximal breakpoint within the larger deletion (BP4) and shares the same distal BP5. This recurrent 1.5-Mb deletion contains six genes, including a candidate gene for epilepsy (CHRNA7) that is probably responsible for the observed seizure phenotype. The BP4-BP5 region undergoes frequent inversion, suggesting a possible link between this inversion polymorphism and recurrent deletion. The frequency of these microdeletions in mental retardation cases is approximately 0.3% (6/2,082 tested), a prevalence comparable to that of Williams, Angelman and Prader-Willi syndromes.