Quantum transport through a DNA wire in a dissipative environment

Electronic transport through DNA wires in the presence of a strong dissipative environment is investigated. We show that new bath-induced electronic states are formed within the bandgap. These states show up in the linear conductance spectrum as a temperature dependent background and lead to a crossover from tunneling to thermal activated behavior with increasing temperature. Depending on the strength of the electron-bath coupling, the conductance at the Fermi level can show a weak exponential or even an algebraic length dependence. Our results suggest a new environmental-induced transport mechanism. This might be relevant for the understanding of molecular conduction experiments in liquid solution, like those recently performed on poly(GC) oligomers in a water buffer (B. Xu et al., Nano Lett 4, 1105 (2004)).Comment: 5 pages, 3 figure

Fluctuation-Facilitated Charge Migration along DNA

We propose a model Hamiltonian for charge transfer along the DNA double helix with temperature driven fluctuations in the base pair positions acting as the rate limiting factor for charge transfer between neighboring base pairs. We compare the predictions of the model with the recent work of J.K. Barton and A.H. Zewail (Proc.Natl.Acad.Sci.USA, {\bf 96}, 6014 (1999)) on the unusual two-stage charge transfer of DNA.Comment: 4 pages, 2 figure

Density of Superfluid Helium Droplets

The classical integral cross sections of large superfluid 4He_N droplets and the number of atoms in the droplets (N=10^3-10^4) have been measured in molecular beam scattering experiments. These measurements are found to be in good agreement with the cross sections predicted from density functional calculations of the radial density distributions with a 10-90 % surface thickness of 5.7\AA. By using a simple model for the density profile of the droplets a thickness of about 6-8\AA is extracted directly from the data.Comment: 27 pages, REVTeX, 5 postscript figure

Phenyl Saligenin Phosphate Induced Caspase-3 and c-Jun N-Terminal Kinase Activation in Cardiomyocyte-Like Cells

At present, little is known about the effect(s) of organophosphorous compounds (OPs) on cardiomyocytes. In this study we have investigated the effects of phenyl saligenin phosphate (PSP), two organophosphorothioate insecticides (diazinon and chlorpyrifos) and their acutely toxic metabolites (diazoxon and chlorpyrifos oxon) on mitotic and differentiated H9c2 cardiomyoblasts. OP-induced cytotoxicity was assessed by monitoring MTT reduction, LDH release and caspase-3 activity. Cytotoxicity was not observed with diazinon, diazoxon or chlorpyrifos oxon (48 h exposure; 200 μM). Chlorpyrifos-induced cytotoxicity was only evident at concentrations >100 μM. In marked contrast, PSP displayed pronounced cytotoxicity towards mitotic and differentiated H9c2 cells. PSP triggered the activation of JNK1/2, but not ERK1/2, p38 MAPK or PKB, suggesting a role for this pro-apoptotic protein kinase in PSP-induced cell death. The JNK1/2 inhibitor SP 600125 attenuated PSP-induced caspase-3 and JNK1/2 activation, confirming the role of JNK1/2 in PSP-induced cytotoxicity. Fluorescently labelled PSP (dansylated PSP) was used to identify novel PSP binding proteins. Dansylated PSP displayed cytotoxicity towards differentiated H9c2 cells. 2D-gel electrophoresis profiles of cells treated with dansylated PSP (25 μM) were used to identify proteins fluorescently labelled with dansylated PSP. Proteomic analysis identified tropomyosin, heat shock protein β-1 and nucleolar protein 58 as novel protein targets for PSP. In summary, PSP triggers cytotoxicity in differentiated H9c2 cardiomyoblasts via JNK1/2-mediated activation of caspase-3. Further studies are required to investigate whether the identified novel protein targets of PSP play a role in the cytotoxicity of this OP, which is usually associated with the development of OP-induced delayed neuropathy

Quantum dynamics in strong fluctuating fields

A large number of multifaceted quantum transport processes in molecular systems and physical nanosystems can be treated in terms of quantum relaxation processes which couple to one or several fluctuating environments. A thermal equilibrium environment can conveniently be modelled by a thermal bath of harmonic oscillators. An archetype situation provides a two-state dissipative quantum dynamics, commonly known under the label of a spin-boson dynamics. An interesting and nontrivial physical situation emerges, however, when the quantum dynamics evolves far away from thermal equilibrium. This occurs, for example, when a charge transferring medium possesses nonequilibrium degrees of freedom, or when a strong time-dependent control field is applied externally. Accordingly, certain parameters of underlying quantum subsystem acquire stochastic character. Herein, we review the general theoretical framework which is based on the method of projector operators, yielding the quantum master equations for systems that are exposed to strong external fields. This allows one to investigate on a common basis the influence of nonequilibrium fluctuations and periodic electrical fields on quantum transport processes. Most importantly, such strong fluctuating fields induce a whole variety of nonlinear and nonequilibrium phenomena. A characteristic feature of such dynamics is the absence of thermal (quantum) detailed balance.Comment: review article, Advances in Physics (2005), in pres

Ab-initio study of model guanine assemblies: The role of pi-pi coupling and band transport

Several assemblies of guanine molecules are investigated by means of first-principle calculations. Such structures include stacked and hydrogen-bonded dimers, as well as vertical columns and planar ribbons, respectively, obtained by periodically replicating the dimers. Our results are in good agreement with experimental data for isolated molecules, isolated dimers, and periodic ribbons. For stacked dimers and columns, the stability is affected by the relative charge distribution of the pi orbitals in adjacent guanine molecules. pi-pi coupling in some stacked columns induces dispersive energy bands, while no dispersion is identified in the planar ribbons along the connections of hydrogen bonds. The implications for different materials comprised of guanine aggregates are discussed. The bandstructure of dispersive configurations may justify a contribution of band transport (Bloch type) in the conduction mechanism of deoxyguanosine fibres, while in DNA-like configurations band transport should be negligible.Comment: 21 pages, 6 figures, 3 tables, to be published in Phys. Rev.

Sparse, decorrelated odor coding in the mushroom body enhances learned odor discrimination

Sparse coding may be a general strategy of neural systems for augmenting memory capacity. In Drosophila melanogaster, sparse odor coding by the Kenyon cells of the mushroom body is thought to generate a large number of precisely addressable locations for the storage of odor-specific memories. However, it remains untested how sparse coding relates to behavioral performance. Here we demonstrate that sparseness is controlled by a negative feedback circuit between Kenyon cells and the GABAergic anterior paired lateral (APL) neuron. Systematic activation and blockade of each leg of this feedback circuit showed that Kenyon cells activated APL and APL inhibited Kenyon cells. Disrupting the Kenyon cell–APL feedback loop decreased the sparseness of Kenyon cell odor responses, increased inter-odor correlations and prevented flies from learning to discriminate similar, but not dissimilar, odors. These results suggest that feedback inhibition suppresses Kenyon cell activity to maintain sparse, decorrelated odor coding and thus the odor specificity of memories

Immune regulation in Chandipura virus infection: characterization of CD4+ T regulatory cells from infected mice

<p>Abstract</p> <p>Back ground</p> <p>Chandipura virus produces acute infection in mice. During infection drastic reduction of CD4+, CD8+ and CD19 + cell was noticed. Depletion of lymphocytes also noticed in spleen. The reduction may be due to the regulatory mechanism of immune system to prevent the bystander host tissue injury. There are several mechanisms like generation of regulatory cells, activation induced cell death (ACID) etc were indicated to control the activation and maintain cellular homeostasis. Role of regulatory cells in homeostasis has been described in several viral diseases. This study was undertaken to characterize CD4+T regulatory cells from the infected mice.</p> <p>Method</p> <p>In this study we purified the CD4+ T cells from Chandipura virus infected susceptible Balb/c mice. CD4+ T regulatory cells were identified by expression of cell surface markers CD25, CD127 and CTLA-4 and intracellular markers Foxp3, IL-10 and TGF-beta. Antigen specificity and ability to suppress the proliferation of other lymphocytes were studied <it>in vitro </it>by purified CD4+CD25+T regulatory cells from infected mice. The proliferation was calculated by proliferation module of Flow Jo software. Expression of death receptors on regulatory cells were studied by flowcytometer.</p> <p>Results</p> <p>The CD4+ T cells isolated from infected mice expressed characteristic markers of regulatory phenotype at all post infective hours tested. The CD4+ T regulatory cells were proliferated when stimulated with Chandipura virus antigen. The regulatory cells did not suppress the proliferation of splenocytes stimulated with anti CD3 antibody when co cultured with them. Interesting observation was, while purification of CD4+ T cells by negative selection, the population of cells negative for CD4 also co purified along with CD4+ T cell. Flow cytometry analysis and light microscopy revealed that CD4 negative cells were of different size and shape (atypical) compared to the normal lymphocytes. Greater percentage of these atypical lymphocytes expressed <it>Fas </it>Ligand and Programmed Death1 (PD-1) receptor.</p> <p>Conclusion</p> <p>From these results we concluded that virus specific CD4+T regulatory cells are generated during Chandipura virus infection in mice and these cells might control the activated lymphocytes during infection by different mechanism.</p