A blind decision feedback equalizer incorporating fixed lag smoothing

Copyright © 2000 IEEEA new type of blind decision feedback equalizer (DFE) incorporating fixed lag smoothing is developed in this paper. The structure is motivated by the fact that if we make full use of the dependence of the observed data on a given transmitted symbol, delayed decisions may produce better estimates of that symbol. To this end, we use a hidden Markov model (HMM) suboptimal formulation that offers a good tradeoff between computational complexity and bit error rate (BER) performance. The proposed equalizer also provides estimates of the channel coefficients and operates adaptively (so that it can adapt to a fading channel for instance) by means of an online version of the expectation-maximization (EM) algorithm. The resulting equalizer structure takes the form of a linear feedback system including a quantizer, and hence, it is easily implemented. In fact, because of its feedback structure, the proposed equalizer shows some similarities with the well-known DFE. A full theoretical analysis of the initial version of the algorithm is not available, but a characterization of a simplified version is provided. We demonstrate that compared to the zero-forcing DFE (ZF-DFE), the algorithm yields many improvements. A large range of simulations on finite impulse response (FIR) channels and on typical fading GSM channel models illustrate the potential of the proposed equalizer.Sylvie Perreau, Langford B. White and Pierre Duhame

Cancer and HIV-1 Infection: Patterns of Chronic Antigen Exposure.

The main role of the human immune system is to eliminate cells presenting foreign antigens and abnormal patterns, while maintaining self-tolerance. However, when facing highly variable pathogens or antigens very similar to self-antigens, this system can fail in completely eliminating the anomalies, leading to the establishment of chronic pathologies. Prototypical examples of immune system defeat are cancer and Human Immunodeficiency Virus-1 (HIV-1) infection. In both conditions, the immune system is persistently exposed to antigens leading to systemic inflammation, lack of generation of long-term memory and exhaustion of effector cells. This triggers a negative feedback loop where effector cells are unable to resolve the pathology and cannot be replaced due to the lack of a pool of undifferentiated, self-renewing memory T cells. In addition, in an attempt to reduce tissue damage due to chronic inflammation, antigen presenting cells and myeloid components of the immune system activate systemic regulatory and tolerogenic programs. Beside these homologies shared between cancer and HIV-1 infection, the immune system can be shaped differently depending on the type and distribution of the eliciting antigens with ultimate consequences at the phenotypic and functional level of immune exhaustion. T cell differentiation, functionality, cytotoxic potential and proliferation reserve, immune-cell polarization, upregulation of negative regulators (immune checkpoint molecules) are indeed directly linked to the quantitative and qualitative differences in priming and recalling conditions. Better understanding of distinct mechanisms and functional consequences underlying disease-specific immune cell dysfunction will contribute to further improve and personalize immunotherapy. In the present review, we describe relevant players of immune cell exhaustion in cancer and HIV-1 infection, and enumerate the best-defined hallmarks of T cell dysfunction. Moreover, we highlight shared and divergent aspects of T cell exhaustion and T cell activation to the best of current knowledge

Lattice Green functions and diffusion for modelling traffic routing in ad hoc networks

We describe basic properties of Markov chains on finite state spaces and their application to Green functions, partial differential equations, and their (approximate) solution using random walks on a graph. Attention is paid to the influence of boundary conditions (Dirichlet/von Neumann). We apply these ideas to the study of traffic propagation and distribution in ad hoc networks

Positive and Negative Regulation of Cellular Immune Responses in Physiologic Conditions and Diseases

The immune system has evolved to allow robust responses against pathogens while avoiding autoimmunity. This is notably enabled by stimulatory and inhibitory signals which contribute to the regulation of immune responses. In the presence of a pathogen, a specific and effective immune response must be induced and this leads to antigen-specific T-cell proliferation, cytokines production, and induction of T-cell differentiation toward an effector phenotype. After clearance or control of the pathogen, the effector immune response must be terminated in order to avoid tissue damage and chronic inflammation and this process involves coinhibitory molecules. When the immune system fails to eliminate or control the pathogen, continuous stimulation of T cells prevents the full contraction and leads to the functional exhaustion of effector T cells. Several evidences both in vitro and in vivo suggest that this anergic state can be reverted by blocking the interactions between coinhibitory molecules and their ligands. The potential to revert exhausted or inactivated T-cell responses following selective blocking of their function made these markers interesting targets for therapeutic interventions in patients with persistent viral infections or cancer

The Control Of Zealactone Biosynthesis And Exudation Is Involved In The Response To Nitrogen In Maize Root.

Nitrate acts as a signal in regulating plant development in response to environment. In particular nitric oxide (NO), auxin and strigolactones (SLs) were supposed to cooperate to regulate the maize root response to this anion. In this study, a combined approach based on LC-MS/MS and on physiological and molecular analyses was adopted to specify the involvement of SLs in the maize response to N. Our results showed that N deficiency strongly induces SL exudation, likely through stimulating their biosynthesis. Nitrate provision early counteracts and also ammonium lowers SL exudation, but less markedly. Exudates obtained from N-starved and ammonium-provided seedlings stimulated Phelipanche germination, whereas when seeds were treated with exudates harvested from nitrate-provided plants no germination was observed. Furthermore, our findings support the idea that the inhibition of SL production observed in response to nitrate and ammonium would contribute to the regulation of lateral root development. Moreover, the transcriptional regulation of a gene encoding a putative maize WBC transporter, in response to various nitrogen supplies, together with its mRNA tissue localization, supported its role in SL allocation. Our results highlight the dual role of SLs as molecules able to signal outwards a nutritional need and as endogenous regulators of root architecture adjustments to N, thus synchronizing plant growth with nitrogen acquisitio

Tree indexed Markov processes and long range dependency

Langford B. White and Sylvie L. Perrea

A Metal-Polymer Interface Study using Electropolymerized Acrylonitrile on Nickel Surfaces

Studies of the interface between mineral and organic materials have been realized for a couple formed between pure transition metal and a polar and polarizable molecule (acrylonitrile). The results presented show the effects of a local electric field on the activation processes associated with adsorption sites and the molecule, interaction mechanisms and the resulting types of chemical bond. The structural, electronic and chemical properties of a nickel-polyacrylonitrile interface are described. Molecular and energetic qualitative models for the interaction mechanisms are proposed

Joint Power Control and Spreading Gain Optimisation for Minimising the Energy Consumption in CDMA based Ad hoc Networks

This paper addresses the impact of the spreading gain on the efficiency of mobile Ad Hoc networks using Code Division Multiple Access (CDMA) as a mode of transmission. In particular, we concentrate on the trade off between the increase in transmission data rate, hence decrease of transmission time, and the necessary power needed to reach acceptable levels of interference in the system. We formulate this trade off as an optimisation problem with associated constraints, where the cost function is the overall energy consumed in the network and the constraints are the acceptable signal to interference ratio for each node. The solution to this optimisation problem provide optimal values for both the transmission spreading gains and powers that need to be allocated to each node in order to minimise the total energy consumption of the network

Personalized Cytokine-Directed Therapy With Tocilizumab for Refractory Immune Checkpoint Inhibitor-Related Cholangiohepatitis.

For patients with corticosteroid (CS)-refractory immune checkpoint inhibitor-related cholangiohepatitis (irCH), no consensus exists regarding treatment, and outcomes remain poor. We evaluated the possibility of personalized treatment according to the patient's cytokine profile and the immunohistopathologic assessment of the predominant immune infiltrate type of liver tissue. NSCLCs with CS-refractory irCH were analyzed by immunohistochemistry of liver biopsy specimen, serum cytokine panel, and assessment of peripheral blood mononuclear cell immune cell monitoring by mass cytometry. A total of three consecutive patients with irCH were identified. We found a predominant T-cell infiltrate and an interferon-gamma or T helper 1 proinflammatory cytokine profile. Here, we report for the first time that a T-cell-targeted therapy with the interleukin (IL)-6 receptor-neutralizing antibody tocilizumab, which inhibits signaling downstream of interferon-gamma and several other Janus kinase-dependent cytokines, is an effective single cytokine-directed therapy for CS-refractory irCH. Three patients with severe, CS-refractory irCH who were treated with tocilizumab were found to have persistent clinical and biological remission. Dysregulation of the IL-6/T-cell axis may contribute to the pathogenesis of CS-refractory irCH. Our observations suggest that IL-6 blockade seems to have promise in the treatment of CS-refractory irCH. The results from our three patients need to be confirmed in a larger patient population