Dynamic Fluctuation Phenomena in Double Membrane Films

Dynamics of double membrane films is investigated in the long-wavelength limit including the overdamped squeezing mode. We demonstrate that thermal fluctuations essentially modify the character of the mode due to its nonlinear coupling to the transversal shear hydrodynamic mode. The corresponding Green function acquires as a function of the frequency a cut along the imaginary semi-axis. Fluctuations lead to increasing the attenuation of the squeezing mode it becomes larger than the `bare' value.Comment: 7 pages, Revte

Factorised Steady States in Mass Transport Models

We study a class of mass transport models where mass is transported in a preferred direction around a one-dimensional periodic lattice and is globally conserved. The model encompasses both discrete and continuous masses and parallel and random sequential dynamics and includes models such as the Zero-range process and Asymmetric random average process as special cases. We derive a necessary and sufficient condition for the steady state to factorise, which takes a rather simple form.Comment: 6 page

Fluid-membrane tethers: minimal surfaces and elastic boundary layers

Thin cylindrical tethers are common lipid bilayer membrane structures, arising in situations ranging from micromanipulation experiments on artificial vesicles to the dynamic structure of the Golgi apparatus. We study the shape and formation of a tether in terms of the classical soap-film problem, which is applied to the case of a membrane disk under tension subject to a point force. A tether forms from the elastic boundary layer near the point of application of the force, for sufficiently large displacement. Analytic results for various aspects of the membrane shape are given.Comment: 12 page

Processing and Transmission of Information

Contains reports on four research projects.Lincoln Laboratory, Purchase Order DDL B-00306U. S. ArmyU. S. NavyU. S. Air Force under Air Force Contract AF19(604)-520

Regulatory control and the costs and benefits of biochemical noise

Experiments in recent years have vividly demonstrated that gene expression can be highly stochastic. How protein concentration fluctuations affect the growth rate of a population of cells, is, however, a wide open question. We present a mathematical model that makes it possible to quantify the effect of protein concentration fluctuations on the growth rate of a population of genetically identical cells. The model predicts that the population's growth rate depends on how the growth rate of a single cell varies with protein concentration, the variance of the protein concentration fluctuations, and the correlation time of these fluctuations. The model also predicts that when the average concentration of a protein is close to the value that maximizes the growth rate, fluctuations in its concentration always reduce the growth rate. However, when the average protein concentration deviates sufficiently from the optimal level, fluctuations can enhance the growth rate of the population, even when the growth rate of a cell depends linearly on the protein concentration. The model also shows that the ensemble or population average of a quantity, such as the average protein expression level or its variance, is in general not equal to its time average as obtained from tracing a single cell and its descendants. We apply our model to perform a cost-benefit analysis of gene regulatory control. Our analysis predicts that the optimal expression level of a gene regulatory protein is determined by the trade-off between the cost of synthesizing the regulatory protein and the benefit of minimizing the fluctuations in the expression of its target gene. We discuss possible experiments that could test our predictions.Comment: Revised manuscript;35 pages, 4 figures, REVTeX4; to appear in PLoS Computational Biolog

Charge Solitons in 1-D Arrays of Serially Coupled Josephson Junctions

We study a 1-D array of Josephson coupled superconducting grains with kinetic inductance which dominates over the Josephson inductance. In this limit the dynamics of excess Cooper pairs in the array is described in terms of charge solitons, created by polarization of the grains. We analyze the dynamics of these topological excitations, which are dual to the fluxons in a long Josephson junction, using the continuum sine-Gordon model. We find that their classical relativistic motion leads to saturation branches in the I-V characteristic of the array. We then discuss the semi-classical quantization of the charge soliton, and show that it is consistent with the large kinetic inductance of the array. We study the dynamics of a quantum charge soliton in a ring-shaped array biased by an external flux through its center. If the dephasing length of the quantum charge soliton is larger than the circumference of the array, quantum phenomena like persistent current and coherent current oscillations are expected. As the characteristic width of the charge soliton is of the order of 100 microns, it is a macroscopic quantum object. We discuss the dephasing mechanisms which can suppress the quantum behaviour of the charge soliton.Comment: 26 pages, LaTex, 7 Postscript figure

Genetic Variation in CCL5 Signaling Genes and Triple Negative Breast Cancer: Susceptibility and Prognosis Implications

Triple-negative breast cancer (TNBC) accounts for ~15\u201320% of breast cancer (BC) and has a higher rate of early relapse and mortality compared to other subtypes. The Chemokine (C-C motif) ligand 5 (CCL5) and its signaling pathway have been linked to TNBC. We aimed to investigate the susceptibility and prognostic implications of genetic variation in CCL5 signaling genes in TNBC in the present study. We characterized variants in CCL5 and that of six other CCL5 signaling genes (CCND1, ZMIZ1, CASP8, NOTCH2, MAP3K21, and HS6ST3) among 1,082 unrelated Tunisian subjects (544 BC patients, including 196 TNBC, and 538 healthy controls), assessed the association of the variants with BC-specific overall survival (OVS) and progression-free survival (PFS), and correlated CCL5 mRNA and serum levels with CCL5 genotypes. We found a highly significant association between the CCND1 rs614367-TT genotype (OR = 5.14; P = 0.004) and TNBC risk, and identified a significant association between the rs614367-T allele and decreased PFS in TNBC. A decreased risk of lymph node metastasis was associated with the MAP3K21 rs1294255-C allele, particularly in rs1294255-GC (OR = 0.47; P = 0.001). CCL5 variants (rs2107538 and rs2280789) were linked to CCL5 serum and mRNA levels. In the TCGA TNBC/Basal-like cohort the MAP3K21 rs1294255-G allele was associated with a decreased OVS. High expression of CCL5 in breast tumors was significantly associated with an increased OVS in all BC patients, but particularly in TNBC/Basal-like patients. In conclusion, genetic variation in CCL5 signaling genes may predict not only TNBC risk but also disease aggressiveness

Subgraphs in random networks

Understanding the subgraph distribution in random networks is important for modelling complex systems. In classic Erdos networks, which exhibit a Poissonian degree distribution, the number of appearances of a subgraph G with n nodes and g edges scales with network size as \mean{G} ~ N^{n-g}. However, many natural networks have a non-Poissonian degree distribution. Here we present approximate equations for the average number of subgraphs in an ensemble of random sparse directed networks, characterized by an arbitrary degree sequence. We find new scaling rules for the commonly occurring case of directed scale-free networks, in which the outgoing degree distribution scales as P(k) ~ k^{-\gamma}. Considering the power exponent of the degree distribution, \gamma, as a control parameter, we show that random networks exhibit transitions between three regimes. In each regime the subgraph number of appearances follows a different scaling law, \mean{G} ~ N^{\alpha}, where \alpha=n-g+s-1 for \gamma<2, \alpha=n-g+s+1-\gamma for 2<\gamma<\gamma_c, and \alpha=n-g for \gamma>\gamma_c, s is the maximal outdegree in the subgraph, and \gamma_c=s+1. We find that certain subgraphs appear much more frequently than in Erdos networks. These results are in very good agreement with numerical simulations. This has implications for detecting network motifs, subgraphs that occur in natural networks significantly more than in their randomized counterparts.Comment: 8 pages, 5 figure

Mixing Bandt-Pompe and Lempel-Ziv approaches: another way to analyze the complexity of continuous-states sequences

In this paper, we propose to mix the approach underlying Bandt-Pompe permutation entropy with Lempel-Ziv complexity, to design what we call Lempel-Ziv permutation complexity. The principle consists of two steps: (i) transformation of a continuous-state series that is intrinsically multivariate or arises from embedding into a sequence of permutation vectors, where the components are the positions of the components of the initial vector when re-arranged; (ii) performing the Lempel-Ziv complexity for this series of `symbols', as part of a discrete finite-size alphabet. On the one hand, the permutation entropy of Bandt-Pompe aims at the study of the entropy of such a sequence; i.e., the entropy of patterns in a sequence (e.g., local increases or decreases). On the other hand, the Lempel-Ziv complexity of a discrete-state sequence aims at the study of the temporal organization of the symbols (i.e., the rate of compressibility of the sequence). Thus, the Lempel-Ziv permutation complexity aims to take advantage of both of these methods. The potential from such a combined approach - of a permutation procedure and a complexity analysis - is evaluated through the illustration of some simulated data and some real data. In both cases, we compare the individual approaches and the combined approach.Comment: 30 pages, 4 figure

Ataxia-telangiectasia: Linkage analysis in highly inbred Arab and Druze families and differentiation from an ataxia-microcephaly-cataract syndrome

Ataxia-telangiectasia (A-T) is a progressive autosomal recessive disease featuring neurodegeneration, immunodeficiency, chromosomal instability, radiation sensitivity and a highly increased proneness to cancer. A-T is ethnically widespread and genetically heterogeneous, as indicated by the existence of four complementation groups in this disease. Several "A-T-like" genetic diseases share various clinical and cellular characteristics with A-T. By using linkage analysis to study North American and Turkish A-O families, the ATA (A-T, complementation group A) gene has been mapped to chromosome 11q23. A number of Israeli Arab A-T patients coming from large, highly inbred families were assigned to group A In one of these families, an additional autosomal recessive disease was identified, characterized by ataxia, hypotonia, microcephaly and bilateral congenital cataracts. In two patients with this syndrome, normal levels of serum immunoglobulins and alpha-fetoprotein, chromosomal stability in peripheral blood lymphocytes and skin fibroblasts, and normal cellular response to treatments with X-rays and the radiomimetic drug neocarzinostatin indicated that this disease does not share, with A-T, any additional features other than ataxia. These tests also showed that another patient in this family, who is also mentally retarded, is affected with both disorders. This conclusion was further supported by linkage analysis with 11q23 markers. Lod scores between A-O and these markers, cumulated over three large Arab families, were significant and confirmed the localization of the ATA gene to aq23. However, another Druze family unassigned to a specific complementation group, showed several recombinants between A-T and the same markers, leaving the localization of the A-T gene in this family open