A mechanism design-based secure architecture for mobile ad hoc networks

International audienceTo avoid the single point of failure for the certificate authority (CA) in MANET, a decentralized solution is proposed where nodes are grouped into different clusters. Each cluster should contain at least two confident nodes. One is known as CA and the another as register authority RA. The Dynamic Demilitarized Zone (DDMZ) is proposed as a solution for protecting the CA node against potential attacks. It is formed from one or more RA node. The problems of such a model are: (1) Clusters with one confident node, CA, cannot be created and thus clusters' sizes are increased which negatively affect clusters' services and stability. (2) Clusters with high density of RA can cause channel collision at the CA. (3) Clusters' lifetime are reduced since RA monitors are always launched (i.e., resource consumption). In this paper, we propose a model based on mechanism design that will allow clusters with single trusted node (CA) to be created. Our mechanism will motivate nodes that does not belong to the confident community to participate by giving them incentives in the form of trust, which can be used for cluster's services. To achieve this goal, a RA selection algorithm is proposed that selects nodes based on a predefined selection criteria function. Finally, empirical results are provided to support our solutions

A secure mechanism design-based and game theoretical model for MANETs

International audienceTo avoid the single point of failure for the certificate authority (CA) in MANET, a decentralized solution is proposed where nodes are grouped into different clusters. Each cluster should contain at least two confident nodes. One is known as CA and the another as register authority RA. The Dynamic Demilitarized Zone (DDMZ) is proposed as a solution for protecting the CA node against potential attacks. It is formed from one or more RA node. The problems of such a model are: (1) Clusters with one confident node, CA, cannot be created and thus clusters' sizes are increased which negatively affect clusters' services and stability. (2) Clusters with high density of RA can cause channel collision at the CA. (3) Clusters' lifetime are reduced since RA monitors are always launched (i.e., resource consumption). In this paper, we propose a model based on mechanism design that will allow clusters with single trusted node (CA) to be created. Our mechanism will motivate nodes that do not belong to the confident community to participate by giving them incentives in the form of trust, which can be used for cluster's services. To achieve this goal, a RA selection algorithm is proposed that selects nodes based on a predefined selection criteria function and location (i.e., using directional antenna). Such a model is known as moderate. Based on the security risk, more RA nodes must be added to formalize a robust DDMZ. Here, we consider the tradeoff between security and resource consumption by formulating the problem as a nonzero-sum noncooperative game between the CA and attacker. Finally, empirical results are provided to support our solutions

Study and modeling of the compressive and splitting tensile strengths of polypropylene fiber reinforced concrete containing recycled asphalt pavement

In a context of sustainable development and material recycling, the present study aims to study mechanical properties of a recycled asphalt pavement (RAP) concrete, reinforced with polypropylene fibers (PF). First, five formulations were designed with different RAP content with a maximum of 50% at a water cement ratio (W/C) of 0,50. Experimental results showed that the more RAP content increases in mix, the more mechanical strengths decrease, mainly due to the weak interfacial transition zone (ITZ) between the mortar and the recycled material. Reinforcement of PF at 0.1% and 1% volume fraction was realized on all mixes and the experimental results showed that the compressive strength is increased while the splitting strength is decreased. Then, an experimental linear relationship between the splitting tensile strength and the compressive strength is proposed. In the second part of the study, the mechanical strengths were modeled using a factorial plan 22, giving a quantification of the individual effect of both introduction of the RAP and the reinforcement and the combined effect, on response in terms of compressive strength and splitting tensile strength. Established model predicted the mechanical strength of a hardened concrete, whatever the RAP content and whatever the PF reinforcement content

A 530kb YAC contig tightly linked to the Friedreich ataxia locus contains five CpG clusters and a new highly polymorphic microsatellite

Friedreich ataxia (FA) is a severe autosomal recessive neurodegenerative disease. The defective gene has been previously assigned to chromosome 9q13-q21 by demonstration of tight linkage to the two independent loci D9S15 and D9S5. Linkage data indicate that FRDA is at less than 1 c M from both markers. Previous physical mapping has shown that probes defining D9S15 (MCT112) and D9S5 (26P) are less than 260kb apart and are surrounded by at least six CpG clusters within 450 kb, which might indicate the presence of “candidate” genes for FA. We isolated and characterized a 530 kb YAC (yeast artificial chromosome) contig that contains five of the CpG clusters. The YACs were used to search for new polymorphic markers needed to map FRDA precisely with respect to the cloned segment. In particular, we found a (CA) n microsatellite polymorphism, GS4, that detects 13 alleles with a PIC value of 0.83 and allows the definition of haplotypes extending over 310kb when used in combination with polymorphic markers at D9S5 and D9S15.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47632/1/439_2004_Article_BF00219179.pd

The global burden of cancer attributable to risk factors, 2010-19 : a systematic analysis for the Global Burden of Disease Study 2019

Background Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. Methods The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk-outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. Findings Globally, in 2019, the risk factors included in this analysis accounted for 4.45 million (95% uncertainty interval 4.01-4.94) deaths and 105 million (95.0-116) DALYs for both sexes combined, representing 44.4% (41.3-48.4) of all cancer deaths and 42.0% (39.1-45.6) of all DALYs. There were 2.88 million (2.60-3.18) risk-attributable cancer deaths in males (50.6% [47.8-54.1] of all male cancer deaths) and 1.58 million (1.36-1.84) risk-attributable cancer deaths in females (36.3% [32.5-41.3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20.4% (12.6-28.4) and DALYs by 16.8% (8.8-25.0), with the greatest percentage increase in metabolic risks (34.7% [27.9-42.8] and 33.3% [25.8-42.0]). Interpretation The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license.Peer reviewe

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Convergent Functional Genomics of Oligodendrocyte Differentiation Identifies Multiple Autoinhibitory Signaling Circuits▿ †

Inadequate remyelination of brain white matter lesions has been associated with a failure of oligodendrocyte precursors to differentiate into mature, myelin-producing cells. In order to better understand which genes play a critical role in oligodendrocyte differentiation, we performed time-dependent, genome-wide gene expression studies of mouse Oli-neu cells as they differentiate into process-forming and myelin basic protein-producing cells, following treatment with three different agents. Our data indicate that different inducers activate distinct pathways that ultimately converge into the completely differentiated state, where regulated gene sets overlap maximally. In order to also gain insight into the functional role of genes that are regulated in this process, we silenced 88 of these genes using small interfering RNA and identified multiple repressors of spontaneous differentiation of Oli-neu, most of which were confirmed in rat primary oligodendrocyte precursors cells. Among these repressors were CNP, a well-known myelin constituent, and three phosphatases, each known to negatively control mitogen-activated protein kinase cascades. We show that a novel inhibitor for one of the identified genes, dual-specificity phosphatase DUSP10/MKP5, was also capable of inducing oligodendrocyte differentiation in primary oligodendrocyte precursors. Oligodendrocytic differentiation feedback loops may therefore yield pharmacological targets to treat disease related to dysfunctional myelin deposition