1,252 research outputs found

    Exclusive neuronal expression of SUCLA2 in the human brain

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    SUCLA2 encodes the ATP-forming subunit (A-SUCL-) of succinyl-CoA ligase, an enzyme of the citric acid cycle. Mutations in SUCLA2 lead to a mitochondrial disorder manifesting as encephalomyopathy with dystonia, deafness and lesions in the basal ganglia. Despite the distinct brain pathology associated with SUCLA2 mutations, the precise localization of SUCLA2 protein has never been investigated. Here we show that immunoreactivity of A-SUCL- in surgical human cortical tissue samples was present exclusively in neurons, identified by their morphology and visualized by double labeling with a fluorescent Nissl dye. A-SUCL- immunoreactivity co-localized >99% with that of the d subunit of the mitochondrial F0-F1 ATP synthase. Specificity of the anti-A-SUCL- antiserum was verified by the absence of labeling in fibroblasts from a patient with a complete deletion of SUCLA2. A-SUCL- immunoreactivity was absent in glial cells, identified by antibodies directed against the glial markers GFAP and S100. Furthermore, in situ hybridization histochemistry demonstrated that SUCLA2 mRNA was present in Nissl-labeled neurons but not glial cells labeled with S100. Immunoreactivity of the GTP-forming subunit (G-SUCL-) encoded by SUCLG2, or in situ hybridization histochemistry for SUCLG2 mRNA could not be demonstrated in either neurons or astrocytes. Western blotting of post mortem brain samples revealed minor G-SUCL- immunoreactivity that was however, not upregulated in samples obtained from diabetic versus non-diabetic patients, as has been described for murine brain. Our work establishes that SUCLA2 is expressed exclusively in neurons in the human cerebral cortex

    Non-Equilibrium Edge Channel Spectroscopy in the Integer Quantum Hall Regime

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    Heat transport has large potentialities to unveil new physics in mesoscopic systems. A striking illustration is the integer quantum Hall regime, where the robustness of Hall currents limits information accessible from charge transport. Consequently, the gapless edge excitations are incompletely understood. The effective edge states theory describes them as prototypal one-dimensional chiral fermions - a simple picture that explains a large body of observations and calls for quantum information experiments with quantum point contacts in the role of beam splitters. However, it is in ostensible disagreement with the prevailing theoretical framework that predicts, in most situations, additional gapless edge modes. Here, we present a setup which gives access to the energy distribution, and consequently to the energy current, in an edge channel brought out-of-equilibrium. This provides a stringent test of whether the additional states capture part of the injected energy. Our results show it is not the case and thereby demonstrate regarding energy transport, the quantum optics analogy of quantum point contacts and beam splitters. Beyond the quantum Hall regime, this novel spectroscopy technique opens a new window for heat transport and out-of-equilibrium experiments.Comment: 13 pages including supplementary information, Nature Physics in prin

    Subwavelength anti-diffracting beams propagating over more than 1,000 Rayleigh lengths

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    Propagating light beams with widths down to and below the optical wavelength require bulky large-aperture lenses and remain focused only for micrometric distances. Here, we report the observation of light beams that violate this localization/depth- of-focus law by shrinking as they propagate, allowing resolution to be maintained and increased over macroscopic propagation lengths. In nanodisordered ferroelectrics we observe a non-paraxial propagation of a sub-micrometre-sized beam for over 1,000 diffraction lengths, the narrowest visible beam reported to date. This unprecedented effect is caused by the nonlinear response of a dipolar glass, which transforms the leading opticalwave equation into a Klein-Gordon-type equation that describes a massive particle field. Our findings open the way to high-resolution optics over large depths of focus, and a route to merging bulk optics into nanodevices

    MAC Protocols for Wireless Mesh Networks with Multi-beam Antennas: A Survey

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    Multi-beam antenna technologies have provided lots of promising solutions to many current challenges faced in wireless mesh networks. The antenna can establish several beamformings simultaneously and initiate concurrent transmissions or receptions using multiple beams, thereby increasing the overall throughput of the network transmission. Multi-beam antenna has the ability to increase the spatial reuse, extend the transmission range, improve the transmission reliability, as well as save the power consumption. Traditional Medium Access Control (MAC) protocols for wireless network largely relied on the IEEE 802.11 Distributed Coordination Function(DCF) mechanism, however, IEEE 802.11 DCF cannot take the advantages of these unique capabilities provided by multi-beam antennas. This paper surveys the MAC protocols for wireless mesh networks with multi-beam antennas. The paper first discusses some basic information in designing multi-beam antenna system and MAC protocols, and then presents the main challenges for the MAC protocols in wireless mesh networks compared with the traditional MAC protocols. A qualitative comparison of the existing MAC protocols is provided to highlight their novel features, which provides a reference for designing the new MAC protocols. To provide some insights on future research, several open issues of MAC protocols are discussed for wireless mesh networks using multi-beam antennas.Comment: 22 pages, 6 figures, Future of Information and Communication Conference (FICC) 2019, https://doi.org/10.1007/978-3-030-12388-8_

    Determining the neurotransmitter concentration profile at active synapses

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    Establishing the temporal and concentration profiles of neurotransmitters during synaptic release is an essential step towards understanding the basic properties of inter-neuronal communication in the central nervous system. A variety of ingenious attempts has been made to gain insights into this process, but the general inaccessibility of central synapses, intrinsic limitations of the techniques used, and natural variety of different synaptic environments have hindered a comprehensive description of this fundamental phenomenon. Here, we describe a number of experimental and theoretical findings that has been instrumental for advancing our knowledge of various features of neurotransmitter release, as well as newly developed tools that could overcome some limits of traditional pharmacological approaches and bring new impetus to the description of the complex mechanisms of synaptic transmission

    Neuroinflammation, Mast Cells, and Glia: Dangerous Liaisons

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    The perspective of neuroinflammation as an epiphenomenon following neuron damage is being replaced by the awareness of glia and their importance in neural functions and disorders. Systemic inflammation generates signals that communicate with the brain and leads to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Identification of potential peripheral-to-central cellular links is thus a critical step in designing effective therapeutics. Mast cells may fulfill such a role. These resident immune cells are found close to and within peripheral nerves and in brain parenchyma/meninges, where they exercise a key role in orchestrating the inflammatory process from initiation through chronic activation. Mast cells and glia engage in crosstalk that contributes to accelerate disease progression; such interactions become exaggerated with aging and increased cell sensitivity to stress. Emerging evidence for oligodendrocytes, independent of myelin and support of axonal integrity, points to their having strong immune functions, innate immune receptor expression, and production/response to chemokines and cytokines that modulate immune responses in the central nervous system while engaging in crosstalk with microglia and astrocytes. In this review, we summarize the findings related to our understanding of the biology and cellular signaling mechanisms of neuroinflammation, with emphasis on mast cell-glia interactions
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