Fault Tolerance in DisCSPs: Several Failures Case

International audienceTo solve a distributed problem in presence of a failed entity, we have to find a way to accomplish the failed entity tasks. In this paper, we present an approach which guarantees the resolution of DisCSPs in presence of failed agents. This approach is based on local CSPs replication principle: each failed agent local CSP is replicated in another agent which will support it. Obtained results confirm that our approach can solve a DisCSP in presence of failed agents by giving a solution when it exists

Novel digenic inheritance of PCDH15 and USH1G underlies profound non-syndromic hearing impairment

Abstract Background Digenic inheritance is the simplest model of oligenic disease. It can be observed when there is a strong epistatic interaction between two loci. For both syndromic and non-syndromic hearing impairment, several forms of digenic inheritance have been reported. Methods We performed exome sequencing in a Pakistani family with profound non-syndromic hereditary hearing impairment to identify the genetic cause of disease. Results We found that this family displays digenic inheritance for two trans heterozygous missense mutations, one in PCDH15 [p.(Arg1034His)] and another in USH1G [p.(Asp365Asn)]. Both of these genes are known to cause autosomal recessive non-syndromic hearing impairment and Usher syndrome. The protein products of PCDH15 and USH1G function together at the stereocilia tips in the hair cells and are necessary for proper mechanotransduction. Epistasis between Pcdh15 and Ush1G has been previously reported in digenic heterozygous mice. The digenic mice displayed a significant decrease in hearing compared to age-matched heterozygous animals. Until now no human examples have been reported. Conclusions The discovery of novel digenic inheritance mechanisms in hereditary hearing impairment will aid in understanding the interaction between defective proteins and further define inner ear function and its interactome