Two-loop cusp anomaly in ABJM at strong coupling

We compute the null cusp anomalous dimension of ABJM theory at strong coupling up to two-loop order. This is done by evaluating corrections to the corresponding superstring partition function, weighted by the AdS 4 × ℂℙ3 action in AdS light-cone gauge. We compare our result, where we use an anomalous shift in the AdS 4 radius, with the cusp anomaly of N = 4 SYM, and extract the two-loop contribution to the non-trivial integrable coupling h(λ) of ABJM theory. It coincides with the strong coupling expansion of the exact expression for h(λ) recently conjectured by Gromov and Sizov. Our work provides thus a non-trivial perturbative check for the latter, as well as evidence for two-loop UV-finiteness and quantum integrability of the Type IIA AdS 4 × ℂℙ3 superstring in this gauge

Ex Vivo Thrombus Magnetic Resonance Imaging Features and Patient Clinical Data Enable Prediction of Acute Ischemic Stroke Cause

The cause of ischemic stroke often remains elusive even after full stroke workup is completed. Cardioembolic mechanisms in particular are frequently presumed but challenging to definitively diagnose. Quantitative thrombus texture analysis is emerging as a powerful tool for stroke characterization, having shown the ability to predict response to stroke treatment,1 but its ability to predict stroke cause and complement machine learning models built from standard clinical features has not been studied.2, 3 The purpose of this study is to evaluate the ability of radiomics features extracted from quantitative magnetic resonance images of retrieved ischemic stroke thrombi (R2*(=1/T2*), quantitative susceptibility mapping, and fat fraction) to improve the accuracy of machine learning models built from clinical data for the prediction of cardioembolic stroke

The NIKA2 instrument, a dual-band kilopixel KID array for millimetric astronomy

NIKA2 (New IRAM KID Array 2) is a camera dedicated to millimeter wave astronomy based upon kilopixel arrays of Kinetic Inductance Detectors (KID). The pathfinder instrument, NIKA, has already shown state-of-the-art detector performance. NIKA2 builds upon this experience but goes one step further, increasing the total pixel count by a factor $\sim$10 while maintaining the same per pixel performance. For the next decade, this camera will be the resident photometric instrument of the Institut de Radio Astronomie Millimetrique (IRAM) 30m telescope in Sierra Nevada (Spain). In this paper we give an overview of the main components of NIKA2, and describe the achieved detector performance. The camera has been permanently installed at the IRAM 30m telescope in October 2015. It will be made accessible to the scientific community at the end of 2016, after a one-year commissioning period. When this happens, NIKA2 will become a fundamental tool for astronomers worldwide.Comment: Proceedings of the 16th Low Temperature Detectors workshop. To be published in the Journal of Low Temperature Physics. 8 pages, 4 figures, 1 tabl

Muon-induced background in the EDELWEISS dark matter search

A dedicated analysis of the muon-induced background in the EDELWEISS dark matter search has been performed on a data set acquired in 2009 and 2010. The total muon flux underground in the Laboratoire Souterrain de Modane (LSM) was measured to be $\Phi_{\mu}=(5.4\pm 0.2 ^{+0.5}_{-0.9})$\,muons/m$^2$/d. The modular design of the muon-veto system allows the reconstruction of the muon trajectory and hence the determination of the angular dependent muon flux in LSM. The results are in good agreement with both MC simulations and earlier measurements. Synchronization of the muon-veto system with the phonon and ionization signals of the Ge detector array allowed identification of muon-induced events. Rates for all muon-induced events $\Gamma^{\mu}=(0.172 \pm 0.012)\, \rm{evts}/(\rm{kg \cdot d})$ and of WIMP-like events $\Gamma^{\mu-n} = 0.008^{+0.005}_{-0.004}\, \rm{evts}/(\rm{kg \cdot d})$ were extracted. After vetoing, the remaining rate of accepted muon-induced neutrons in the EDELWEISS-II dark matter search was determined to be $\Gamma^{\mu-n}_{\rm irred} < 6\cdot 10^{-4} \, \rm{evts}/(\rm{kg \cdot d})$ at 90%\,C.L. Based on these results, the muon-induced background expectation for an anticipated exposure of 3000\,\kgd\ for EDELWEISS-3 is $N^{\mu-n}_{3000 kg\cdot d} < 0.6$ events.Comment: 21 pages, 16 figures, Accepted for publication in Astropart. Phy

Expression of the Serpin Serine Protease Inhibitor 6 Protects Dendritic Cells from Cytotoxic T Lymphocyte–Induced Apoptosis: Differential Modulation by T Helper Type 1 and Type 2 Cells

Dendritic cells (DCs) play a central role in the immune system as they drive activation of T lymphocytes by cognate interactions. However, as DCs express high levels of major histocompatibility complex class I, this intimate contact may also result in elimination of DCs by activated cytotoxic T lymphocytes (CTLs) and thereby limit induction of immunity. We show here that immature DCs are indeed susceptible to CTL-induced killing, but become resistant upon maturation with anti-CD40 or lipopolysaccharide. Protection is achieved by expression of serine protease inhibitor (SPI)-6, a member of the serpin family that specifically inactivates granzyme B and thereby blocks CTL-induced apoptosis. Anti-CD40 and LPS-induced SPI-6 expression is sustained for long periods of time, suggesting a role for SPI-6 in the longevity of DCs. Importantly, T helper 1 cells, which mature DCs and boost CTL immunity, induce SPI-6 expression and subsequent DC resistance. In contrast, T helper 2 cells neither induce SPI-6 nor convey protection, despite the fact that they trigger DC maturation with comparable efficiency. Our data identify SPI-6 as a novel marker for DC function, which protects DCs against CTL-induced apoptosis

A siRNA-Based Screen for Genes Involved in Chromosome End Protection

Telomeres are nucleoprotein complexes which protect the ends of linear chromosomes from detection as DNA damage and provide a sequence buffer against replication-associated shortening. In mammals, telomeres consist of repetitive DNA sequence (TTAGGG) and associated proteins. The telomeric core complex is called shelterin and is comprised of the proteins TRF1, TRF2, POT1, TIN2, TPP1 and RAP1. Excessive telomere shortening or de-protection of telomeres through the loss of shelterin subunits allows the detection of telomeres as DNA damage, which can be visualized as DNA damage protein foci at chromosome ends called TIF (Telomere Dysfunction-Induced Foci). We sought to exploit the TIF phenotype as marker for telomere dysfunction to identify novel genes involved in telomere protection by siRNA-mediated knock-down of a set of 386 candidates. Here we report the establishment, specificity and feasibility of such a screen and the results of the genes tested. Only one of the candidate genes showed a unique TIF phenotype comparable to the suppression of the main shelterin components TRF2 or TRF1 and that gene was identified as a TRF1-like pseudogene. We also identified a weak TIF phenotype for SKIIP (SNW1), a splicing factor and transcriptional co-activator. However, the knock-down of SKIIP also induced a general, not telomere-specific DNA damage response, which complicates conclusions about a telomeric role. In summary, this report is a technical demonstration of the feasibility of a cell-based screen for telomere deprotection with the potential of scaling it to a high-throughput approach