Topology Control Algorithm considering Antenna Radiation Pattern in Three-Dimensional Wireless Sensor Networks

Topology control is a key issue of wireless sensor network to reduce energy consumption and communication collision. Topology control algorithms in three-dimensional space have been proposed by modifying existing two-dimensional algorithms. These algorithms are based on the theoretical assumption that transmission power is radiated equally to the all directions by using isotropic antenna model. However, isotropic antenna does not exist, which is hypothetical antenna to compare the real antenna performance. In the real network, dipole antenna is applied, and because of the radiation pattern, performance of topology control algorithm is degraded. We proposed local remapping algorithm to solve the problem and applied it to existing topology control algorithms. Simulation results show that our algorithm increases performance of existing algorithms and reduces power consumption

Local Approximation Schemes for Ad Hoc and Sensor Networks

We present two local approaches that yield polynomial-time approximation schemes (PTAS) for the Maximum Independent Set and Minimum Dominating Set problem in unit disk graphs. The algorithms run locally in each node and compute a (1+ε)-approximation to the problems at hand for any given ε > 0. The time complexity of both algorithms is O(TMIS + log*! n/εO(1)), where TMIS is the time required to compute a maximal independent set in the graph, and n denotes the number of nodes. We then extend these results to a more general class of graphs in which the maximum number of pair-wise independent nodes in every r-neighborhood is at most polynomial in r. Such graphs of polynomially bounded growth are introduced as a more realistic model for wireless networks and they generalize existing models, such as unit disk graphs or coverage area graphs

Balancing Energy Dissipation in Data Gathering Wireless Sensor Networks Using Ant Colony Optimization

Abstract. Formulation of energy efficient protocols is of utmost importance for wireless sensor networks because of energy constraints of sensor nodes. When a number of nodes is deployed in a field located away from the base station, the nodes undergo unequal energy dissipation while transmitting information to the base station primarily due to two reasons: i) the difference in the distances of nodes from the base station and ii) the variation in inter-nodal distances. The schemes presented here better network lifetime by taking into account these two issues and try to equalize the energy dissipation by the nodes. While constructing the chain we also use Ant Colony Optimization algorithm instead of greedy approach used in PEGASIS. Application of ACO ensures that the chain formed is of shortest possible length and thus further helps enhance network performances by reducing the inter-nodal transmission distances as much as possible. Extensive simulations performed corroborates that the proposed schemes outperform PEGASIS by a significant margin

Digital technologies, legal design and the future of the legal profession

Legal Technology – or “Legal Tech” – is disrupting the traditional operations and self-understanding of the legal profession. This chapter introduces the central claim of this book, namely that these developments are having and will continue to have a disruptive effect on the work of lawyers and that adapting to this new operating environment is crucial for legal professionals remaining relevant in an increasingly technology-driven world. This introductory chapter outlines some of the main features of this on-going transformation process, introduces some of the pressures it is creating for lawyers, and provides short summaries of the chapters that comprise this collection.fi=vertaisarvioitu|en=peerReviewed

Genotype–Phenotype Correlation in DFNB8/10 Families with TMPRSS3 Mutations

In the present study, genotype–phenotype correlations in eight Dutch DFNB8/10 families with compound heterozygous mutations in TMPRSS3 were addressed. We compared the phenotypes of the families by focusing on the mutation data. The compound heterozygous variants in the TMPRSS3 gene in the present families included one novel variant, p.Val199Met, and four previously described pathogenic variants, p.Ala306Thr, p.Thr70fs, p.Ala138Glu, and p.Cys107Xfs. In addition, the p.Ala426Thr variant, which had previously been reported as a possible polymorphism, was found in one family. All affected family members reported progressive bilateral hearing impairment, with variable onset ages and progression rates. In general, the hearing impairment affected the high frequencies first, and sooner or later, depending on the mutation, the low frequencies started to deteriorate, which eventually resulted in a flat audiogram configuration. The ski-slope audiogram configuration is suggestive for the involvement of TMPRSS3. Our data suggest that not only the protein truncating mutation p.T70fs has a severe effect but also the amino acid substitutions p.Ala306Thr and p.Val199Met. A combination of two of these three mutations causes prelingual profound hearing impairment. However, in combination with the p.Ala426Thr or p.Ala138Glu mutations, a milder phenotype with postlingual onset of the hearing impairment is seen. Therefore, the latter mutations are likely to be less detrimental for protein function. Further studies are needed to distinguish possible phenotypic differences between different TMPRSS3 mutations. Evaluation of performance of patients with a cochlear implant indicated that this is a good treatment option for patients with TMPRSS3 mutations as satisfactory speech reception was reached after implantation

Characterization of a new full length TMPRSS3 isoform and identification of mutant alleles responsible for nonsyndromic recessive deafness in Newfoundland and Pakistan

BACKGROUND: Mutant alleles of TMPRSS3 are associated with nonsyndromic recessive deafness (DFNB8/B10). TMPRSS3 encodes a predicted secreted serine protease, although the deduced amino acid sequence has no signal peptide. In this study, we searched for mutant alleles of TMPRSS3 in families from Pakistan and Newfoundland with recessive deafness co-segregating with DFNB8/B10 linked haplotypes and also more thoroughly characterized the genomic structure of TMPRSS3. METHODS: We enrolled families segregating recessive hearing loss from Pakistan and Newfoundland. Microsatellite markers flanking the TMPRSS3 locus were used for linkage analysis. DNA samples from participating individuals were sequenced for TMPRSS3. The structure of TMPRSS3 was characterized bioinformatically and experimentally by sequencing novel cDNA clones of TMPRSS3. RESULTS: We identified mutations in TMPRSS3 in four Pakistani families with recessive, nonsyndromic congenital deafness. We also identified two recessive mutations, one of which is novel, of TMPRSS3 segregating in a six-generation extended family from Newfoundland. The spectrum of TMPRSS3 mutations is reviewed in the context of a genotype-phenotype correlation. Our study also revealed a longer isoform of TMPRSS3 with a hitherto unidentified exon encoding a signal peptide, which is expressed in several tissues. CONCLUSION: Mutations of TMPRSS3 contribute to hearing loss in many communities worldwide and account for 1.8% (8 of 449) of Pakistani families segregating congenital deafness as an autosomal recessive trait. The newly identified TMPRSS3 isoform e will be helpful in the functional characterization of the full length protein

A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction

The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In humans, over 150 non-syndromic loci have been identified, and there are more than 400 human genetic syndromes with a hearing loss component. Over 100 non-syndromic hearing loss genes have been identified in mouse and human, but we remain ignorant of the full extent of the genetic landscape involved in auditory dysfunction. As part of the International Mouse Phenotyping Consortium, we undertook a hearing loss screen in a cohort of 3006 mouse knockout strains. In total, we identify 67 candidate hearing loss genes. We detect known hearing loss genes, but the vast majority, 52, of the candidate genes were novel. Our analysis reveals a large and unexplored genetic landscape involved with auditory function