Defining Malicious Behavior of a Node and its Defensive Techniques in Ad Hoc Networks

Any node under attack in ad hoc network exhibits an anomalous behavior called the malicious behavior. In this situation, the entire operation of a network gets disturbed and to preclude such malicious behavior several security solutions have been discovered. In this paper, malicious behavior of a node is defined and to defend such behavior, security solutions are presented which are used in furnishing a secure and reliable communication in ad hoc networks

An Approach for Establishing Trust among Nodes in Ad Hoc Network

A node in ad hoc network is accountable for routing the packets to neighboring nodes. This evolves trust factor among nodes which assists in forwarding the packets to other nodes if it is trusted and thereby furnishes a secure & reliable communication. This trust can be defined by several approaches which are based on behavior, monitoring, policies etc. In this paper, an approach is proposed to establish trust among nodes which can be evaluated by monitoring the nodes for their behavior. The values are defined for trust which is dynamic in nature and depends on the behavior of nodes

An Algorithm to Detect Attacks in Mobile Ad Hoc Network

Each node in Mobile Ad Hoc Network (MANETs) communicates with each other for transferring the packet (or data) to destination node. Any anomalous behavior of a node can confine it from executing this operation and even can disturb the whole network process. Therefore, the need of monitoring the nodes arises to keep a check on the behavior of a node. In this paper, an algorithm is proposed to monitor the nodes & to check if a node is any under attack or not. Moreover, a second layer of security is added which is furnished by a testbed to monitor the nodes

Structure-function analysis of ceTIR-1/hSARM1 explains the lack of Wallerian axonal degeneration in C. elegans

Summary: Wallerian axonal degeneration (WD) does not occur in the nematode C. elegans, in contrast to other model animals. However, WD depends on the NADase activity of SARM1, a protein that is also expressed in C. elegans (ceSARM/ceTIR-1). We hypothesized that differences in SARM between species might exist and account for the divergence in WD. We first show that expression of the human (h)SARM1, but not ceTIR-1, in C. elegans neurons is sufficient to confer axon degeneration after nerve injury. Next, we determined the cryoelectron microscopy structure of ceTIR-1 and found that, unlike hSARM1, which exists as an auto-inhibited ring octamer, ceTIR-1 forms a readily active 9-mer. Enzymatically, the NADase activity of ceTIR-1 is substantially weaker (10-fold higher Km) than that of hSARM1, and even when fully active, it falls short of consuming all cellular NAD+. Our experiments provide insight into the molecular mechanisms and evolution of SARM orthologs and WD across species