Neutrino imaging of the Galactic Centre and Millisecond Pulsar Population

Despite the potentially large population of millisecond pulsars in the Galactic Centre, direct detection of them is almost impossible using the current radio telescopes, due to severe pulse broadening caused by radiation scattering. We propose that imaging the Galactic Centre using neutrinos provides us a way to constrain the millisecond pulsar population. Millisecond pulsars are proposed cosmic-ray accelerators. The high-energy protons they produce will collide with the baryonic matter in the central molecular zone, which creates charged and neutral pions that decay into neutrinos and γ rays, respectively. The specific fluxes of neutrino and γ -ray emission for the case with CS emission as the baryon tracer in the Central Molecular Zone that we computed, subjected to γ -ray observation by H.E.S.S., set a conservative upper limit of NMSP<10,000 for the Galactic Centre millisecond pulsar population, with an injecting proton energy spectral index Γ=−1 and an efficiency of fp=1% converting the pulsar's rotational power to cosmic-ray power. This population of millisecond pulsars could explain the GeV γ -ray excess in the Galactic Centre

Electrical stimulation modulates Wnt signaling and regulates genes for the motor endplate and calcium binding in muscle of rats with spinal cord transection

Background Spinal cord injury (SCI) results in muscle atrophy and a shift of slow oxidative to fast glycolytic fibers. Electrical stimulation (ES) at least partially restores muscle mass and fiber type distribution. The objective of this study was to was to characterize the early molecular adaptations that occur in rat soleus muscle after initiating isometric resistance exercise by ES for one hour per day for 1, 3 or 7 days when ES was begun 16 weeks after SCI. Additionally, changes in mRNA levels after ES were compared with those induced in soleus at the same time points after gastrocnemius tenotomy (GA). Results ES increased expression of Hey1 and Pitx2 suggesting increased Notch and Wnt signaling, respectively, but did not normalize RCAN1.4, a measure of calcineurin/NFAT signaling, or PGC-1ß mRNA levels. ES increased PGC-1α expression but not that of slow myofibrillar genes. Microarray analysis showed that after ES, genes coding for calcium binding proteins and nicotinic acetylcholine receptors were increased, and the expression of genes involved in blood vessel formation and morphogenesis was altered. Of the 165 genes altered by ES only 16 were also differentially expressed after GA, of which 12 were altered in the same direction by ES and GA. In contrast to ES, GA induced expression of genes related to oxidative phosphorylation. Conclusions Notch and Wnt signaling may be involved in ES-induced increases in the mass of paralyzed muscle. Molecular adaptations of paralyzed soleus to resistance exercise are delayed or defective compared to normally innervated muscle

Two-channel anomalous Hall effect in SrRuO3

The Hall effect in SrRuO$_3$ thin-films near the thickness limit for ferromagnetism shows an extra peak in addition to the ordinary and anomalous Hall effects. This extra peak has been attributed to a topological Hall effect due to two-dimensional skyrmions in the film around the coercive field; however, the sign of the anomalous Hall effect in SrRuO$_3$ can change as a function of saturation magnetization. Here we report Hall peaks in SrRuO$_3$ in which volumetric magnetometry measurements and magnetic force microscopy indicate that the peaks result from the superposition of two anomalous Hall channels with opposite sign. These channels likely form due to thickness variations in SrRuO$_3$, creating two spatially separated magnetic regions with different saturation magnetizations and coercive fields. The results are central to the development of strongly correlated materials for spintronics.This work is supported by the EPSRC through the Core-to-Core International Network “Oxide Superspin” (EP/P026311/1) and the Doctoral Training Partnership Grant (EP/N509620/1). Additional support from the Office of Basic Energy Sciences Division of Materials Sciences and Engineering, US Department of Energy under Award numbers de-sc0018153, and the Research Center Program of IBS (Institute for Basic Science) in Korea (IBS-R009-D1)

Measuring the signal-to-noise ratio of a neuron

The signal-to-noise ratio (SNR), a commonly used measure of fidelity in physical systems, is defined as the ratio of the squared amplitude or variance of a signal relative to the variance of the noise. This definition is not appropriate for neural systems in which spiking activity is more accurately represented as point processes. We show that the SNR estimates a ratio of expected prediction errors and extend the standard definition to one appropriate for single neurons by representing neural spiking activity using point process generalized linear models (PP-GLM). We estimate the prediction errors using the residual deviances from the PP-GLM fits. Because the deviance is an approximate χ2 random variable, we compute a bias-corrected SNR estimate appropriate for single-neuron analysis and use the bootstrap to assess its uncertainty. In the analyses of four systems neuroscience experiments, we show that the SNRs are -10 dB to -3 dB for guinea pig auditory cortex neurons, -18 dB to -7 dB for rat thalamic neurons, -28 dB to -14 dB for monkey hippocampal neurons, and -29 dB to -20 dB for human subthalamic neurons. The new SNR definition makes explicit in the measure commonly used for physical systems the often-quoted observation that single neurons have low SNRs. The neuron's spiking history is frequently a more informative covariate for predicting spiking propensity than the applied stimulus. Our new SNR definition extends to any GLM system in which the factors modulating the response can be expressed as separate components of a likelihood function

Deactivation of carbon electrode for elimination of carbon dioxide evolution from rechargeable lithium-oxygen cells

Carbon has unfaired advantages in material properties to be used as electrodes. It offers a low cost, light weight cathode that minimizes the loss in specific energy of lithium-oxygen batteries as well. To date, however, carbon dioxide evolution has been an unavoidable event during the operation of non-aqueous lithium-oxygen batteries with carbon electrodes, due to the reactivity of carbon against self-decomposition and catalytic decomposition of electrolyte. Here we report a simple but potent approach to eliminate carbon dioxide evolution by using an ionic solvate of dimethoxyethane and lithium nitrate. We show that the solvate leads to deactivation of the carbon against parasitic reactions by electrochemical doping of nitrogen into carbon. This work demonstrates that one could take full advantage of carbon by mitigating the undesired activity. &copy; 2014 Macmillan Publishers Limited. All rights reserved.open8

RUNDC3A regulates SNAP25-mediated chemotherapy resistance by binding AKT in gastric neuroendocrine carcinoma (GNEC)

Gastric neuroendocrine carcinoma (GNEC) is a common type of neuroendocrine carcinoma (NEC) with a poor prognosis and limited therapeutic options. The underlying mechanisms of chemoresistance in patients with GNEC and those with NEC are largely unknown, and thus, reliable biomarkers and therapeutic targets that could improve treatment outcomes in patients with NECs are lacking. The aim of this study was to identify specific targets and investigate their roles in GNEC progression and treatment resistance. Differentially expressed genes (DEGs) were identified in GNEC specimens and were further analysed by focusing on their roles in chemoresistance. Gene Ontology (GO) and pathway enrichment analyses of GNEC DEGs revealed that synapse-related function was the most prominent cellular function perturbed in GNEC. SNAP25 was identified as the target gene involved in most of the enriched pathways. In vitro and in vivo experiments showed that SNAP25 plays a role in proliferation and chemoresistance in GNEC cell lines. AKT has been identified as a downstream target, and SNAP25 binds to AKT protein and promotes AKT protein half-life. Further analysis of other types of NEC as well as small cell lung cancer, which resembles NEC on a molecular level, has identified RUNDC3A as an upstream molecule that regulates SNAP25 expression and the associated phenotypes that could enhance chemoresistance in NECs. Our results show that SNAP25 expression in GNEC is mediated by RUNDC3A and promotes GNEC progression and chemoresistance via posttranslational modification of AKT. Thus, our results suggest that the RUNDC3A/SNAP25/Akt axis could be a potential therapeutic target in GNEC

Directed self-organization of graphene nanoribbons on SiC

Realization of post-CMOS graphene electronics requires production of semiconducting graphene, which has been a labor-intensive process. We present tailoring of silicon carbide crystals via conventional photolithography and microelectronics processing to enable templated graphene growth on 4H-SiC{1-10n} (n = 8) crystal facets rather than the customary {0001} planes. This allows self-organized growth of graphene nanoribbons with dimensions defined by those of the facet. Preferential growth is confirmed by Raman spectroscopy and high-resolution transmission electron microscopy (HRTEM) measurements, and electrical characterization of prototypic graphene devices is presented. Fabrication of > 10,000 top-gated graphene transistors on a 0.24 cm2 SiC chip demonstrates scalability of this process and represents the highest density of graphene devices reported to date.Comment: 13 pages, 5 figure