1,057 research outputs found

    A silver impregnation method for motor and sensory nerves and their endings in formalin-fixed mammalian muscles

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    A silver impregnation method is described which shows motor and sensory nerves and their endings in formalin-fixed mammalian muscles. The method works with the same reliability on flattened muscle pieces as well as on frozen sections. Large nerve bundles, myelinated and non-myelinated single axons, and terminals impregnated by this method stand out black against a light brown background

    Mechanism of the “dark” axonal degeneration in the central nervous system

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    Low-Complexity Blind Parameter Estimation in Wireless Systems with Noisy Sparse Signals

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    Baseband processing algorithms often require knowledge of the noise power, signal power, or signal-to-noise ratio (SNR). In practice, these parameters are typically unknown and must be estimated. Furthermore, the mean-square error (MSE) is a desirable metric to be minimized in a variety of estimation and signal recovery algorithms. However, the MSE cannot directly be used as it depends on the true signal that is generally unknown to the estimator. In this paper, we propose novel blind estimators for the average noise power, average receive signal power, SNR, and MSE. The proposed estimators can be computed at low complexity and solely rely on the large-dimensional and sparse nature of the processed data. Our estimators can be used (i) to quickly track some of the key system parameters while avoiding additional pilot overhead, (ii) to design low-complexity nonparametric algorithms that require such quantities, and (iii) to accelerate more sophisticated estimation or recovery algorithms. We conduct a theoretical analysis of the proposed estimators for a Bernoulli complex Gaussian (BCG) prior, and we demonstrate their efficacy via synthetic experiments. We also provide three application examples that deviate from the BCG prior in millimeter-wave multi-antenna and cell-free wireless systems for which we develop nonparametric denoising algorithms that improve channel-estimation accuracy with a performance comparable to denoisers that assume perfect knowledge of the system parameters

    NKT sejt szubpopulációk és aktiválódás sclerosis multiplexben = NKT cell subsets and activation in patients with multiple sclerosis

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    A vese- és agydaganatokban az NKT, valamint egy új, NKT sejtekhez hasonló T sejt, a MAIT sejtek invariáns receptora kimutatható, vagyis a sclerosis multiplex plakkokban észlelt NKT sejt deficiencia nem a központi idegrendszeri immunszabályozásssal függ össze, hanem a sclerosis multiplexre jellemző. A daganatokat infiltráló MAIT és NKT sejtek aktivált, döntően CD8+ sejtek, és CD56 molekulát nem expresszálnak, annak ellenére, hogy a perifériás vérben CD56+ csoportban is kimutathatók. A MAIT sejtek gyulladáskeltő citokin környezetben fordulnak elő a daganatokban, vagyis az NKT sejtekhez hasonlóan funkcionálisan heterogének. A MAIT és NKT sejteket tartalmazó CD56+ T sejtek sclerosis multiplex betegek vérében aktiváltak, és citotoxikus molekulákat expresszálnak. SSCP klonalitás módszerrel e sejtek klonális expanzióját mutattuk ki SM-ben. Jelen vannak e sejtek a liquorban is, és NK sejtekhez hasonlóan CD11c molekulát expresszálnak, mely a citokinválasszal összefügghet. Ugyanakkor e sejtek deficienciája mutatható ki órákon belül akut stroke-ban, a gyulladáskeltő citokinválasz és a citotoxicitás szuppressziójával. E korai, csak a gyulladáskeltő választ érintő deficiencia mellett a leukocyták aktivációja jellemzi az akut stroke-ot. A limfocita szuppresszió normalizálódásának elmaradása, illetve a korai leukocyta aktiváció deficitje a stroke-ot követő infekciókra hajlamosít, és a stroke kimenetelét szignifikánsan rontja. | The invariant T cell receptors of NKT cells and MAIT, a novel T cell subset with similar functions to NKT cell in mice, were shown in brain and kidney tumors. Thus, the previously observed deficiency of NKT cells in MS plaques is not related to the immunoregulation of the CNS, rather, it is connected to MS. The infiltrating T cells containing NKT and MAIT are activated, express CD8 but not CD56, although the MAIT TCR can be shown in the peripheral CD56+ T cell subset. The presence of pro-inflammatory cytokines in tumors, while anti-inflammatory cytokines are absent, indicates the functional heterogeneity of human MAIT similarly to NKT cells. We also showed that CD56+ T cells are activated and clonally expanded in the peripheral blood of MS, and express cytotoxic molecules. These cells are present in the CSF and express CD1c, which can be related to cytokine production. In contrast, the deficiency of these CD56+ T cells characterizes the acute phase of ischemic stroke: the pro-inflammatory cytokine production and cytotoxicity is suppressed within hours. Besides the early deficient lymphocyte responses, leukocytes are activated within hours in stroke. The delayed normalization of suppressed lymphocyte functions along with the deficiency of early leukocyte activation predispose to post-stroke infections and significantly worsen outcome
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