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 Physics of Irregular Low-Density Parity-Check Codes

Low-density parity-check codes with irregular constructions have been recently shown to outperform the most advanced error-correcting codes to date. In this paper we apply methods of statistical physics to study the typical properties of simple irregular codes. We use the replica method to find a phase transition which coincides with Shannon's coding bound when appropriate parameters are chosen. The decoding by belief propagation is also studied using statistical physics arguments; the theoretical solutions obtained are in good agreement with simulations. We compare the performance of irregular with that of regular codes and discuss the factors that contribute to the improvement in performance.Comment: 20 pages, 9 figures, revised version submitted to JP

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

Statistical physics of low density parity check error correcting codes

We study the performance of Low Density Parity Check (LDPC) error-correcting codes using the methods of statistical physics. LDPC codes are based on the generation of codewords using Boolean sums of the original message bits by employing two randomly-constructed sparse matrices. These codes can be mapped onto Ising spin models and studied using common methods of statistical physics. We examine various regular constructions and obtain insight into their theoretical and practical limitations. We also briefly report on results obtained for irregular code constructions, for codes with non-binary alphabet, and on how a finite system size effects the error probability

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

463 Understanding the role of nurses in deprescribing medicines for older people: A systematic review

Introduction:It is predicted that by 2035, two-thirds of people aged over 65 in the UK will be living with multiple health conditions requiring a life-long intake of multiple medicines (1). Recent reports suggest that over 8.4 million people take 5+ medicines, and 3.8 million take 8+ medicines (2). Polypharmacy, the concurrent intake of multiple medicines (5+) by one person is not problematic if the multiple medicines are prescribed appropriately to achieve clear therapeutic objectives and minimise harm. However, problematic polypharmacy arises if the risks of medicines exceed their benefits due to drug interactions and adverse drug reactions. Deprescribing is a personalised medicine optimisation intervention to ensure the safe and effective withdrawal of medicines that are no longer appropriate, beneficial or wanted. Several studies explored the role of pharmacists and doctors in deprescribing medicines for older people, and the benefits to patients and the health care system. However, literature on the nurses’ role in this process remains scarce, despite their frequent contact with older people.Aim:To review the relevant studies to identify the role nurses play in deprescribing for older people.Methods:This is a systematic review of qualitative and quantitative studies, published in Embase, CINHAL, Google Scholar, British Nursing Database and PubMed, between 2012 and 2022. A manual search of reference lists of included studies was also conducted. We used key words such as nurse, nurse prescriber, deprescribing and medication optimisation to search for studies reporting on the role of nurses in deprescribing medicines for older people >65 years of age, in all healthcare settings. The quality of studies was appraised using the Critical Appraisal Skills Programme (CASP) tool. Thematic analysis was used to identify recurrent themes or concepts from the included studies, and these were then synthesised to answer the research question.Results:Twelve studies met the inclusion criteria, 11 of which were of qualitative design. All of the included studies were of moderate to high quality. Five critical roles of nurses in deprescribing were identified including: (i) Assessors; (ii) Co-ordinators; (iii) Facilitators, (iv) Communicators; and (v) Educators. Deprescribing requires multidisciplinary collaboration with clear communication between healthcare providers, and nurses are key players through their management of patients and physically effecting prescribing and deprescribing. They also have a role in assessing patients for deprescribing opportunity, coordinating multidisciplinary healthcare professional support, communicating with patients, relatives and other healthcare professionals, and educating nurses and other healthcare professionals on the importance of deprescribing as a discipline. Despite this, deprescribing is not yet integrated into nurse medication administration, prescribing, and initial or continued professional development.Conclusion:Evidence on the role of nurses in deprescribing for the older people is limited. However, the studies included in this systematic review highlight the crucial role nurses play in all stages of the process. Further exploration is required to understand the role of the nurse in deprescribing and how their initial and continued professional development can be optimised to support it

Improving the distance properties of turbo codes using a third component code: 3D turbo codes

International audienc

Identification of metabolic biomarkers to follow wound evolution

International audienc

Adding a rate-1 third dimension to turbo codes

International audienceThanks to the message passing principle, turbo decoding is able to provide strong error correction near the theoretical (Shannon) limit. However, the minimum Hamming distance (MHD) of a turbo code may not be sufficient to prevent a detrimental change in the error rate vs. signal to noise ratio curve, the so-called flattening. Increasing the MHD of a turbo code may involve using component encoders with a large number of states, devising more sophisticated internal permutations, or increasing the dimension of the turbo code, i.e. the number of component encoders. This paper addresses the latter option and proposes a modified turbo code, in which some of the parity bits stemming from the classical component encoders are encoded by a rate-1, third encoder. The result is a significantly increased MHD, which improves turbo decoder performance at low error rates, at the expense of a very small increase in complexity. In this paper, we compare the performance of the proposed turbo code with that of the DVB-RCS turbo code and the DVB-S2 LDPC code. Comparisons with more complex 16-state TCs are also reported