Impact of flexibility on the aggregation of polymeric macromolecules.

Dependence of the dimerization probability and the aggregation behavior of polymeric macromolecules on their flexibility is studied using Langevin dynamics simulations. It is found that the dimerization probability is a non-monotonic function of the polymers persistence length. For a given value of inter-polymer attraction strength, semiflexible polymers have lower dimerization probability relative to flexible and rigid polymers of the same length. The threshold temperature of the formation of aggregates in a many-polymer system and its dependence on the polymers persistence length is also investigated. The simulation results of two- and many-polymer systems are in good agreement and show how the amount of flexibility affects the dimerization and the aggregation behaviors of polymeric macromolecules.

Control of cascading failures using protective measures.

Cascading failures, triggered by a local perturbation, can be catastrophic and cause irreparable damages in a wide area. Hence, blocking the devastating cascades is an important issue in real world networks. One of the ways to control the cascade is to use protective me|asures, so that the agents decide to be protected against failure. Here, we consider a coevolution of the linear threshold mo|del for the spread of cascading failures and a decision-making game based on the perceived risk of failure. Protected agents are less vulnerable to failure and in return the size of the cascade affects the agent's decision to get insured. We find at what range of protection efficiency and cost of failure, the global cascades stop. Also we observe that in some range of protection efficiency, a bistable region emerges for the size of cascade and the prevalence of protected agents. Moreover, we show how savings or the ability of agents to repair can prevent cascades from occurring.

Emergence of oscillations in fixed-energy sandpile models on complex networks.

Fixed-energy sandpile (FES) models, introduced to understand the self-organized criticality, show a continuous phase transition between absorbing and active phases. In this work, we study the dynamics of the deterministic FES models on random networks. We observe that close to absorbing transition the density of active nodes oscillates and nodes topple in synchrony. The deterministic toppling rule and the small-world property of random networks lead to the emergence of sustained oscillations. The amplitude of oscillations becomes larger with increasing the value of network randomness. The bifurcation diagram for the density of active nodes is obtained. We use the activity-dependent rewiring rule and show that the interplay between the network structure and the FES dynamics leads to the emergence of a bistable region with a first-order transition between the absorbing and active states. Furthermore during the rewiring, the ordered activation pattern of the nodes is broken, which causes the oscillations to disappear.

A Novel De Novo Dominant Mutation in GJB2 Gene Associated with a Sporadic Case of Nonsyndromic Sensorineural Hearing Loss.

Mutations in the GJB2 gene are the most common known cause of hereditary congenital hearing loss. Rapid genomic DNA extraction (RGDE) method was used for genomic DNA extraction. After amplification of coding region of CX26 gene with specific primers, expected PCR products with 724bp length were subjected to direct sequencing in both directions. We describe here a novel heterozygous -T to -C transition at codon 202 (TGC→CGC) of the GJB2 gene in a patient, 40-year-old Iranian woman, which replaces a cysteine with an arginine residue (C202R). The dominant mutation C202R associated with non-syndromic sensorineural hearing loss. This mutation has not previously been described in affected or control samples from other populations investigated for GJB2 mutations, indicating that it is a rare substitution. This dominant mutation was recorded in NCBI GenBank with accession number KF 638275.

A novel compound heterozygous mutation (35delG, 363delC) in the Connexin 26 gene causes non-syndromic autosomal recessive hearing loss.

Mutations in the Connexin 26 (Cx26) gene are a common cause of hereditary hearing loss in different populations. In the present study, an Iranian patient with bilateral hearing loss underwent molecular analysis for the causative mutation. DNA studies were performed for the Cx26 gene by PCR and sequencing methods. We describe a novel compound heterozygous mutation (35delG, 363delC) in the Cx26 gene that is strongly associated with congenital non-syndromic hearing loss (NSHL).