Message Transfer in a Communication Network

We study message transfer in a $2-d$ communication network of regular nodes and randomly distributed hubs. We study both single message transfer and multiple message transfer on the lattice. The average travel time for single messages travelling between source and target pairs of fixed separations shows $q-$exponential behaviour as a function of hub density with a characteristic power-law tail, indicating a rapid drop in the average travel time as a function of hub density. This power-law tail arises as a consequence of the log-normal distribution of travel times seen at high hub densities. When many messages travel on the lattice, a congestion-decongestion transition can be seen. The waiting times of messages in the congested phase show a Gaussian distribution, whereas the decongested phase shows a log-normal distribution. Thus, the congested or decongested behaviour is encrypted in the behaviour of the waiting time distributions.Comment: 7 Pages, 6 figure, to appear in the Proceeding of the conference Perspectives in Nonlinear Dynamics 2007, a special issue of the Journal Praman

Measurement and physical interpretation of the mean motion of turbulent density patterns detected by the BES system on MAST

The mean motion of turbulent patterns detected by a two-dimensional (2D) beam emission spectroscopy (BES) diagnostic on the Mega Amp Spherical Tokamak (MAST) is determined using a cross-correlation time delay (CCTD) method. Statistical reliability of the method is studied by means of synthetic data analysis. The experimental measurements on MAST indicate that the apparent mean poloidal motion of the turbulent density patterns in the lab frame arises because the longest correlation direction of the patterns (parallel to the local background magnetic fields) is not parallel to the direction of the fastest mean plasma flows (usually toroidal when strong neutral beam injection is present). The experimental measurements are consistent with the mean motion of plasma being toroidal. The sum of all other contributions (mean poloidal plasma flow, phase velocity of the density patterns in the plasma frame, non-linear effects, etc.) to the apparent mean poloidal velocity of the density patterns is found to be negligible. These results hold in all investigated L-mode, H-mode and internal transport barrier (ITB) discharges. The one exception is a high-poloidal-beta (the ratio of the plasma pressure to the poloidal magnetic field energy density) discharge, where a large magnetic island exists. In this case BES detects very little motion. This effect is currently theoretically unexplained.Comment: 28 pages, 15 figures, submitted to PPC

Centralized Modularity of N-Linked Glycosylation Pathways in Mammalian Cells

Glycosylation is a highly complex process to produce a diverse repertoire of cellular glycans that are attached to proteins and lipids. Glycans are involved in fundamental biological processes, including protein folding and clearance, cell proliferation and apoptosis, development, immune responses, and pathogenesis. One of the major types of glycans, N-linked glycans, is formed by sequential attachments of monosaccharides to proteins by a limited number of enzymes. Many of these enzymes can accept multiple N-linked glycans as substrates, thereby generating a large number of glycan intermediates and their intermingled pathways. Motivated by the quantitative methods developed in complex network research, we investigated the large-scale organization of such N-linked glycosylation pathways in mammalian cells. The N-linked glycosylation pathways are extremely modular, and are composed of cohesive topological modules that directly branch from a common upstream pathway of glycan synthesis. This unique structural property allows the glycan production between modules to be controlled by the upstream region. Although the enzymes act on multiple glycan substrates, indicating cross-talk between modules, the impact of the cross-talk on the module-specific enhancement of glycan synthesis may be confined within a moderate range by transcription-level control. The findings of the present study provide experimentally-testable predictions for glycosylation processes, and may be applicable to therapeutic glycoprotein engineering

Small anisotropy of the lower critical field and s±s_\pm-wave two-gap feature in single crystal LiFeAs

The in- and out-of-plane lower critical fields and magnetic penetration depths for LiFeAs were examined. The anisotropy ratio $\gamma_{H_{c1}}(0)$ is smaller than the expected theoretical value, and increased slightly with increasing temperature from 0.6$T_c$ to $T_c$. This small degree of anisotropy was numerically confirmed by considering electron correlation effect. The temperature dependence of the penetration depths followed a power law($\sim$$T^n$) below 0.3$T_c$, with $n$$>$3.5 for both $\lambda_{ab}$ and $\lambda_c$. Based on theoretical studies of iron-based superconductors, these results suggest that the superconductivity of LiFeAs can be represented by an extended $s_\pm$-wave due to weak impurity scattering effect. And the magnitudes of the two gaps were also evaluted by fitting the superfluid density for both the in- and out-of-plane to the two-gap model. The estimated values for the two gaps are consistent with the results of angle resolved photoemission spectroscopy and specific heat experiments.Comment: 10 pages, 5 figure

Single crystal growth and superconducting properties of LiFeAs

We report the successful growth of high quality single crystals of LiFeAs with lateral sizes up to 5 x 5 mm2 by the Sn-flux method. Electrical resistivity studies reveal that the superconducting onset temperature is 18.2 K with a transition width less than 1.1 K and the ratio of room temperature to residual resistivity is about 24. Bulk superconductivity is supported by perfect shielding in the magnetic susceptibility and a clear jump in the specific heat Cp, resulting in deltaCp/T ~ 20.0 mJ/mol*K2. Upper critical field slopes of dHc2c/dT ~ -1.39 and dHc2ab/dT ~ -2.99 T/K near Tc predict zero temperature upper critical fields of Hc2c(0) ~ 17.2 and Hc2ab(0) ~ 36.9 T and coherence lengths of Xi_ab = 4.4 and Xi_c = 2.0 nm in a single band model. This result points to a modest superconducting anisotropy about 2.3 in LiFeAs.Comment: 18 pages, 4 figure

Genetic noise control via protein oligomerization

Gene expression in a cell entails random reaction events occurring over disparate time scales. Thus, molecular noise that often results in phenotypic and population-dynamic consequences sets a fundamental limit to biochemical signaling. While there have been numerous studies correlating the architecture of cellular reaction networks with noise tolerance, only a limited effort has been made to understand the dynamic role of protein-protein interactions. Here we have developed a fully stochastic model for the positive feedback control of a single gene, as well as a pair of genes (toggle switch), integrating quantitative results from previous in vivo and in vitro studies. We find that the overall noise-level is reduced and the frequency content of the noise is dramatically shifted to the physiologically irrelevant high-frequency regime in the presence of protein dimerization. This is independent of the choice of monomer or dimer as transcription factor and persists throughout the multiple model topologies considered. For the toggle switch, we additionally find that the presence of a protein dimer, either homodimer or heterodimer, may significantly reduce its random switching rate. Hence, the dimer promotes the robust function of bistable switches by preventing the uninduced (induced) state from randomly being induced (uninduced). The specific binding between regulatory proteins provides a buffer that may prevent the propagation of fluctuations in genetic activity. The capacity of the buffer is a non-monotonic function of association-dissociation rates. Since the protein oligomerization per se does not require extra protein components to be expressed, it provides a basis for the rapid control of intrinsic or extrinsic noise

C1-Ten Is a Protein Tyrosine Phosphatase of Insulin Receptor Substrate 1 (IRS-1), Regulating IRS-1 Stability and Muscle Atrophy

Muscle atrophy occurs under various catabolic conditions, including insulin deficiency, insulin resistance, or increased levels of glucocorticoids. This results from reduced levels of insulin receptor substrate 1 (IRS-1), leading to decreased phosphatidylinositol 3-kinase activity and thereby activation of FoxO transcription factors. However, the precise mechanism of reduced IRS-1 under a catabolic condition is unknown. Here, we report that C1-Ten is a novel protein tyrosine phosphatase (PTPase) of IRS-1 that acts as a mediator to reduce IRS-1 under a catabolic condition, resulting in muscle atrophy. C1-Ten preferentially dephosphorylated Y612 of IRS-1, which accelerated IRS-1 degradation. These findings suggest a novel type of IRS-1 degradation mechanism which is dependent on C1-Ten and extends our understanding of the molecular mechanism of muscle atrophy under catabolic conditions. C1-Ten expression is increased by catabolic glucocorticoid and decreased by anabolic insulin. Reflecting these hormonal regulations, the muscle C1-Ten is upregulated in atrophy but downregulated in hypertrophy. This reveals a previously unidentified role of C1-Ten as a relevant PTPase contributing to skeletal muscle atrophy.open2

Intestinal Epithelial Cell-Specific Deletion of PLD2 Alleviates DSS-Induced Colitis by Regulating Occludin

Ulcerative colitis is a multi-factorial disease involving a dysregulated immune response. Disruptions to the intestinal epithelial barrier and translocation of bacteria, resulting in inflammation, are common in colitis. The mechanisms underlying epithelial barrier dysfunction or regulation of tight junction proteins during disease progression of colitis have not been clearly elucidated. Increase in phospholipase D (PLD) activity is associated with disease severity in colitis animal models. However, the role of PLD2 in the maintenance of intestinal barrier integrity remains elusive. We have generated intestinal specific Pld2 knockout mice (Pld2 IEC-KO) to investigate the mechanism of intestinal epithelial PLD2 in colitis. We show that the knockout of Pld2 confers protection against dextran sodium sulphate (DSS)-induced colitis in mice. Treatment with DSS induced the expression of PLD2 and downregulated occludin in colon epithelial cells. PLD2 was shown to mediate phosphorylation of occludin and induce its proteasomal degradation in a c-Src kinase-dependent pathway. Additionally, we have shown that treatment with an inhibitor of PLD2 can rescue mice from DSS-induced colitis. To our knowledge, this is the first report showing that PLD2 is pivotal in the regulation of the integrity of epithelial tight junctions and occludin turn over, thereby implicating it in the pathogenesis of colitis