Finite size effects and error-free communication in Gaussian channels

The efficacy of a specially constructed Gallager-type error-correcting code to communication in a Gaussian channel is being examined. The construction is based on the introduction of complex matrices, used in both encoding and decoding, which comprise sub-matrices of cascading connection values. The finite size effects are estimated for comparing the results to the bounds set by Shannon. The critical noise level achieved for certain code-rates and infinitely large systems nearly saturates the bounds set by Shannon even when the connectivity used is low

Statistical mechanics of error exponents for error-correcting codes

Error exponents characterize the exponential decay, when increasing message length, of the probability of error of many error-correcting codes. To tackle the long standing problem of computing them exactly, we introduce a general, thermodynamic, formalism that we illustrate with maximum-likelihood decoding of low-density parity-check (LDPC) codes on the binary erasure channel (BEC) and the binary symmetric channel (BSC). In this formalism, we apply the cavity method for large deviations to derive expressions for both the average and typical error exponents, which differ by the procedure used to select the codes from specified ensembles. When decreasing the noise intensity, we find that two phase transitions take place, at two different levels: a glass to ferromagnetic transition in the space of codewords, and a paramagnetic to glass transition in the space of codes.Comment: 32 pages, 13 figure

Gain-of-Function Mutation in Filamin A Potentiates Platelet Integrin αβ Activation

OBJECTIVE: Dominant mutations of the X-linked filamin A () gene are responsible for filaminopathies A, which are rare disorders including brain periventricular nodular heterotopia, congenital intestinal pseudo-obstruction, cardiac valves or skeleton malformations, and often macrothrombocytopenia. APPROACH AND RESULTS: We studied a male patient with periventricular nodular heterotopia and congenital intestinal pseudo-obstruction, his unique X-linked allele carrying a stop codon mutation resulting in a 100-amino acid-long FLNa C-terminal extension (NP_001447.2: ). Platelet counts were normal, with few enlarged platelets. FLNa was detectable in all platelets but at 30% of control levels. Surprisingly, all platelet functions were significantly upregulated, including platelet aggregation and secretion, as induced by ADP, collagen, or von Willebrand factor in the presence of ristocetin, as well as thrombus formation in blood flow on a collagen or on a von Willebrand factor matrix. Most importantly, patient platelets stimulated with ADP exhibited a marked increase in αβ integrin activation and a parallel increase in talin recruitment to β, contrasting with normal Rap1 activation. These results are consistent with the mutant FLNa affecting the last step of αβ activation. Overexpression of mutant FLNa in the HEL megakaryocytic cell line correlated with an increase (compared with wild-type FLNa) in PMA-induced fibrinogen binding to and in talin and kindlin-3 recruitment by αβ. CONCLUSIONS: Altogether, our results are consistent with a less binding of mutant FLNa to β and the facilitated recruitment of talin by β on platelet stimulation, explaining the increased αβ activation and the ensuing gain-of-platelet functions

Error-correcting codes that nearly saturate Shannon's bound

Gallager-type error-correcting codes that nearly saturate Shannon's bound are constructed using insight gained from mapping the problem onto that of an Ising spin system. The performance of the suggested codes is evaluated for different code rates in both finite and infinite message length

On encoding symbol degrees of array BP-XOR codes

Low density parity check (LDPC) codes, LT codes and digital fountain techniques have received significant attention from both academics and industry in the past few years. By employing the underlying ideas of efficient Belief Propagation (BP) decoding process (also called iterative message passing decoding process) on binary erasure channels (BEC) in LDPC codes, Wang has recently introduced the concept of array BP-XOR codes and showed the necessary and sufficient conditions for MDS [k + 2,k] and [n,2] array BP-XOR codes. In this paper, we analyze the encoding symbol degree requirements for array BP-XOR codes and present new necessary conditions for array BP-XOR codes. These new necessary conditions are used as a guideline for constructing several array BP-XOR codes and for presenting a complete characterization (necessary and sufficient conditions) of degree two array BP-XOR codes and for designing new edge-colored graphs. Meanwhile, these new necessary conditions are used to show that the codes by Feng, Deng, Bao, and Shen in IEEE Transactions on Computers are incorrect

A survey of three-dimensional turbo codes and recent performance enhancements

This paper presents a survey of two techniques intended for improving the performance of conventional turbo codes (TCs). The first part of this work is dedicated to explore a hybrid concatenation structure combining both parallel and serial concatenation based on a three-dimensional (3D) code. The 3D structure, recently introduced by Berrou et al., is able to ensure large asymptotic gains at very low error rates at the expense of an increase in complexity and a loss in the convergence threshold. In order to reduce the loss in the convergence threshold, the authors consider first a time-varying construction of the post-encoded parity. Then, they investigate the association of the 3D TC with high-order modulations according to the bit-interleaved coded modulation approach. The second part of this study deals with irregular TCs. In contrast to 3D TCs, although irregular TCs can achieve performance closer to capacity, their asymptotic performance is very poor. Therefore, the authors propose irregular turbo coding schemes with suitable interleavers in order to improve their distance properties. Finally, a modified encoding procedure, inspired from the 3D TC, makes it possible to obtain irregular TCs which perform better than the corresponding regular codes in both the waterfall and the error floor regions

Survival in dialysis patients is not different between patients with diabetes as primary renal disease and patients with diabetes as a co-morbid condition

On dialysis, survival among patients with diabetes mellitus is inferior to survival of non-diabetic patients. We hypothesized that patients with diabetes as primary renal disease have worse survival compared to patients with diabetes as a co-morbid condition and aimed to compare all-cause mortality between these patient groups. Data were collected from the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD), a multicenter, prospective cohort study in which new patients with end stage renal disease (ESRD) were monitored until transplantation or death. Patients with diabetes as primary cause of ESRD were compared with patients with diabetes as co-morbid condition and both of these patient groups were compared to patients without diabetes. Analysis was performed using Kaplan-Meier and Cox regression. Fifteen % of the patients had diabetic nephropathy as primary renal disease (N = 281); 6% had diabetes as co-morbid condition (N = 107) and 79% had no diabetes (N = 1465). During follow-up 42% of patients (N = 787) died. Compared to non-diabetic patients, mortality risk was increased for both patients with diabetes as primary renal disease HR: 1.9 (95% CI 1.6, 2.3) and for patients with diabetes as co-morbid condition HR: 1.7 (95% CI 1.3, 2.2). Mortality was not significantly higher in patients with diabetes as primary renal disease compared to patients with diabetes as co-morbid condition (HR 1.06; 95% CI 0.79, 1.43). This study in patients with ESRD showed no survival difference between patients with diabetes as primary renal disease and patients with diabetes as a co-morbid condition. Both conditions were associated with increased mortality risk compared to non-diabetic patient

Small molecule sensitization to TRAIL is mediated via nuclear localization, phosphorylation and inhibition of chaperone activity of Hsp27

10.1038/cddis.2013.413Cell Death and Disease410

Systems biology of platelet-vessel wall interactions

Platelets are small, anucleated cells that participate in primary hemostasis by forming a hemostatic plug at the site of a blood vessel's breach, preventing blood loss. However, hemostatic events can lead to excessive thrombosis, resulting in life-threatening strokes, emboli, or infarction. Development of multi-scale models coupling processes at several scales and running predictive model simulations on powerful computer clusters can help interdisciplinary groups of researchers to suggest and test new patient-specific treatment strategies

Differential regulation of cell death pathways by the microenvironment correlates with chemoresistance and survival in leukaemia

Glucocorticoids (GCs) and topoisomerase II inhibitors are used to treat acute lymphoblastic leukaemia (ALL) as they induce death in lymphoid cells through the glucocorticoid receptor (GR) and p53 respectively. Mechanisms underlying ALL cell death and the contribution of the bone marrow microenvironment to drug response/resistance remain unclear. The role of the microenvironment and the identification of chemoresistance determinants were studied by transcriptomic analysis in ALL cells treated with Dexamethasone (Dex), and Etoposide (Etop) grown in the presence or absence of bone marrow conditioned media (CM). The necroptotic (RIPK1) and the apoptotic (caspase-8/3) markers were downregulated by CM, whereas the inhibitory effects of chemotherapy on the autophagy marker Beclin-1 (BECN1) were reduced suggesting CM exerts cytoprotective effects. GCs upregulated the RIPK1 ubiquitinating factor BIRC3 (cIAP2), in GC-sensitive (CEM-C7-14) but not in resistant (CEM-C1-15) cells. In addition, CM selectively affected GR phosphorylation in a site and cell-specific manner. GR is recruited to RIPK1, BECN1 and BIRC3 promoters in the sensitive but not in the resistant cells with phosphorylated GR forms being generally less recruited in the presence of hormone. FACS analysis and caspase-8 assays demonstrated that CM promoted a pro-survival trend. High molecular weight proteins reacting with the RIPK1 antibody were modified upon incubation with the BIRC3 inhibitor AT406 in CEM-C7-14 cells suggesting that they represent ubiquitinated forms of RIPK1. Our data suggest that there is a correlation between microenvironment-induced ALL proliferation and altered response to chemotherapy