Microscopic formulation of the Zimm-Bragg model for the helix-coil transition

A microscopic spin model is proposed for the phenomenological Zimm-Bragg model for the helix-coil transition in biopolymers. This model is shown to provide the same thermophysical properties of the original Zimm-Bragg model and it allows a very convenient framework to compute statistical quantities. Physical origins of this spin model are made transparent by an exact mapping into a one-dimensional Ising model with an external field. However, the dependence on temperature of the reduced external field turns out to differ from the standard one-dimensional Ising model and hence it gives rise to different thermophysical properties, despite the exact mapping connecting them. We discuss how this point has been frequently overlooked in the recent literature.Comment: 11 pages, 2 figure

Competition for hydrogen bond formation in the helix-coil transition and protein folding

The problem of the helix-coil transition of biopolymers in explicit solvents, like water, with the ability for hydrogen bonding with solvent is addressed analytically using a suitably modified version of the Generalized Model of Polypeptide Chains. Besides the regular helix-coil transition, an additional coil-helix or reentrant transition is also found at lower temperatures. The reentrant transition arises due to competition between polymer-polymer and polymer-water hydrogen bonds. The balance between the two types of hydrogen bonding can be shifted to either direction through changes not only in temperature, but also by pressure, mechanical force, osmotic stress or other external influences. Both polypeptides and polynucleotides are considered within a unified formalism. Our approach provides an explanation of the experimental difficulty of observing the reentrant transition with pressure; and underscores the advantage of pulling experiments for studies of DNA. Results are discussed and compared with those reported in a number of recent publications with which a significant level of agreement is obtained.Comment: 21 pages, 3 figures, submitted to Phys Rev

Bullying behaviors and victimization experiences among adolescent students: the role of resilience

The role of resilience in the relationship between bullying behaviours, victimisation experiences, and self-efficacy was examined. Three hundred and 93 (191 male, 202 female) adolescents (mean age = 15.88, SD = .64) from schools in Coimbatore, India completed scales to assess bullying behaviours and victimisation experiences, resilience, and self-efficacy. Multigroup SEM, with separate groups created according to participant sex, revealed that resilience mediated the relationship between bullying behaviours and self-efficacy in males. Males engaged in bullying behaviours and experienced victimisation more frequently than females. The findings of the study have implication for designing intervention programs to enhance resilience among adolescents and young adults to enable them to manage bullying behaviours

Methylthioadenosine reprograms macrophage activation through adenosine receptor stimulation

Regulation of inflammation is necessary to balance sufficient pathogen clearance with excessive tissue damage. Central to regulating inflammation is the switch from a pro-inflammatory pathway to an anti-inflammatory pathway. Macrophages are well-positioned to initiate this switch, and as such are the target of multiple therapeutics. One such potential therapeutic is methylthioadenosine (MTA), which inhibits TNFα production following LPS stimulation. We found that MTA could block TNFα production by multiple TLR ligands. Further, it prevented surface expression of CD69 and CD86 and reduced NF-KB signaling. We then determined that the mechanism of this action by MTA is signaling through adenosine A2 receptors. A2 receptors and TLR receptors synergized to promote an anti-inflammatory phenotype, as MTA enhanced LPS tolerance. In contrast, IL-1β production and processing was not affected by MTA exposure. Taken together, these data demonstrate that MTA reprograms TLR activation pathways via adenosine receptors to promote resolution of inflammation. © 2014 Keyel et al