Search for merger ejecta emission from late time radio observations of short GRBs using GMRT

Short gamma-ray bursts (GRBs) are the aftermath of compact binary mergers involving neutron stars. If the merger remnant is a millisecond magnetar instead of a black hole, a significant proportion of the rotational energy deposited to the emerging ejecta can produce a late-time radio brightening from its interaction with the ambient medium. Detection of this late-time radio emission from short GRBs can have profound implications for understanding the physics of the progenitor. We report the radio observations of five short GRBs - 050709, 061210, 100625A, 140903A, and 160821B using the Giant Metrewave Radio Telescope (GMRT) at 1250, 610, and 325 MHz frequencies after $\sim$ $2 - 11$ years from the time of the burst. The GMRT observations at low frequencies are particularly important to detect the signature of merger ejecta emission at the peak. These observations are the most delayed searches associated with some of these GRBs for any late-time low-frequency emission. We find no evidence for such an emission. We find that none of these GRBs are consistent with maximally rotating magnetar with a rotational energy of $\sim 10^{53}\, {\rm ergs}$. However, magnetars with lower rotational energies cannot be completely ruled out. Despite the non detection, our study underscores the power of radio observations in the search for magnetar signatures associated with short GRBs. However, only future radio observatories may have the capabilities to either detect these signatures or put more stringent constraints on the model.Comment: 10 pages, 4 figures, Published in MNRA

Determination of Magnetic Exchange Stiffness and Surface Anisotropy Constants in Epitaxial Ni_ {1-x} Co_ {x}(001) Films

Magnetic characteristics of epitaxial Ni1-xCox(001) (x=0, 0.16, and 0.50) films with nominal 200 nm thickness on Cu(001)/Si(100) substrates have been investigated by magnetization and ferromagnetic resonance measurements in order to better clarify the rationale for the large variation in the magnetic exchange stiffness constant A, previously determined from different measurements. The exchange constant as well as the saturation magnetization, effective demagnetizing field, fourth-order magnetocrystalline, and second-order perpendicular uniaxial magnetic anisotropy fields has been determined. The analyses of low-temperature saturation magnetization data on these films yield A values that increase from 0.82×10-6erg/cm for a pure Ni film to 2.27×10-6erg/cm for the Ni0.50Co0.50 film. Furthermore, spin-wave resonance volume modes observed in x=0 and 0.16 films indicate that the surface plays a role in the exchange stiffness constant determination as the surface anisotropy constants are found to be approximately 1 and 4 erg/cm2, respectively. The latter value is substantially larger than that for any other system reported so far

The Role of the Mucus Barrier in Digestion

Mucus forms a protective layer across a variety of epithelial surfaces. In the gastrointestinal (GI) tract, the barrier has to permit the uptake of nutrients, while excluding potential hazards, such as pathogenic bacteria. In this short review article, we look at recent literature on the structure, location, and properties of the mammalian intestinal secreted mucins and the mucus layer they form over a wide range of length scales. In particular, we look at the structure of the gel-forming glycoprotein MUC2, the primary intestinal secreted mucin, and the influence this has on the properties of the mucus layer. We show that, even at the level of the protein backbone, MUC2 is highly heterogeneous and that this is reflected in the networks it forms. It is evident that a combination of charge and pore size determines what can diffuse through the layer to the underlying gut epithelium. This information is important for the targeted delivery of bioactive molecules, including nutrients and pharmaceuticals, and for understanding how GI health is maintained

Hard X-Ray Polarization Catalog for a Five-year Sample of Gamma-Ray Bursts Using AstroSat CZT Imager

The Cadmium Zinc Telluride Imager (CZTI) on board AstroSat has been regularly detecting gamma-ray bursts (GRBs) since its launch in 2015. Its sensitivity to polarization measurements at energies above 100 keV allows CZTI to attempt spectropolarimetric studies of GRBs. Here, we present the first catalog of GRB polarization measurements made by CZTI during its first five years of operation. This includes the time-integrated polarization measurements of the prompt emission of 20 GRBs in the energy range 100-600 keV. The sample includes the bright GRBs that were detected within an angle range of 0 degrees-60 degrees and 120 degrees-180 degrees where the instrument has useful polarization sensitivity and is less prone to systematics. We implement a few new modifications in the analysis to enhance the polarimetric sensitivity of the instrument. The majority of the GRBs in the sample are found to possess less/null polarization across the total bursts' duration in contrast to a small fraction of five GRBs that exhibit high polarization. The low polarization across the bursts might be due either to the burst being intrinsically weakly polarized or to a varying polarization angle within the burst even when it is highly polarized. In comparison to POLAR measurements, CZTI has detected a larger number of cases with high polarization. This may be a consequence of the higher energy window of CZTI observations, which results in the sampling of a shorter duration of burst emissions than POLAR, thereby probing emissions with less temporal variation in polarization properties

Clinical pharmacology of exogenously administered alkaline phosphatase

Purpose: To evaluate the clinical pharmacology of exogenous alkaline phosphatase (AP). Methods: Randomized, double-blind, placebo-controlled sequential protocols of (1) ascending doses and infusion duration (volunteers) and (2) fixed dose and duration (patients) were conducted at clinical pharmacology and intensive care units. A total of 103 subjects (67 male volunteers and 36 patients with severe sepsis) were administered exogenous, 10-min IV infusions (three ascending doses) or 24-72 h continuous (132.5-200 U kg-124 h-1) IV infusion with/without preceding loading dose and experimental endotoxemia for evaluations of pharmacokinetics, pharmacodynamics, safety parameters, antigenicity, inflammatory markers, and outcomes. Results: Linearity and dose-proportionality were shown during 10-min infusions. The relatively short elimination half-life necessitated a loading dose to achieve stable enzyme levels. Pharmacokinetic parameters in volunteers and patients were similar. Innate immunity response was not significantly influenced by AP, while renal function significantly improved in sepsis patients. Conclusions: The pharmacokinetics of exogenous AP is linear, dose-proportional, exhibit a short half-life, and are not influenced by renal impairment or dialysis

Loss of Adenomatous polyposis coli function renders intestinal epithelial cells resistant to the cytokine IL-22

Interleukin-22 (IL-22) is a critical immune defence cytokine that maintains intestinal homeostasis and promotes wound healing and tissue regeneration, which can support the growth of colorectal tumours. Mutations in the adenomatous polyposis coli gene (Apc) are a major driver of familial colorectal cancers (CRCs). How IL-22 contributes to APC-mediated tumorigenesis is poorly understood. To investigate IL-22 signalling in wild-type (WT) and APC-mutant cells, we performed RNA sequencing (RNAseq) of IL-22-treated murine small intestinal epithelial organoids. In WT epithelia, antimicrobial defence and cellular stress response pathways were most strongly induced by IL-22. Surprisingly, although IL-22 activates signal transducer and activator of transcription 3 (STAT3) in APC-mutant cells, STAT3 target genes were not induced. Our analyses revealed that ApcMin/Min cells are resistant to IL-22 due to reduced expression of the IL-22 receptor, and increased expression of inhibitors of STAT3, particularly histone deacetylases (HDACs). We further show that IL-22 increases DNA damage and genomic instability, which can accelerate cellular transition from heterozygosity (ApcMin/+) to homozygosity (ApcMin/Min) to drive tumour formation. Our data reveal an unexpected role for IL-22 in promoting early tumorigenesis while excluding a function for IL-22 in transformed epithelial cells

Paneth cells as a site of origin for intestinal inflammation.

The recognition of autophagy related 16-like 1 (ATG16L1) as a genetic risk factor has exposed the critical role of autophagy in Crohn's disease. Homozygosity for the highly prevalent ATG16L1 risk allele, or murine hypomorphic (HM) activity, causes Paneth cell dysfunction. As Atg16l1(HM) mice do not develop spontaneous intestinal inflammation, the mechanism(s) by which ATG16L1 contributes to disease remains obscure. Deletion of the unfolded protein response (UPR) transcription factor X-box binding protein-1 (Xbp1) in intestinal epithelial cells, the human orthologue of which harbours rare inflammatory bowel disease risk variants, results in endoplasmic reticulum (ER) stress, Paneth cell impairment and spontaneous enteritis. Unresolved ER stress is a common feature of inflammatory bowel disease epithelium, and several genetic risk factors of Crohn's disease affect Paneth cells. Here we show that impairment in either UPR (Xbp1(ΔIEC)) or autophagy function (Atg16l1(ΔIEC) or Atg7(ΔIEC)) in intestinal epithelial cells results in each other's compensatory engagement, and severe spontaneous Crohn's-disease-like transmural ileitis if both mechanisms are compromised. Xbp1(ΔIEC) mice show autophagosome formation in hypomorphic Paneth cells, which is linked to ER stress via protein kinase RNA-like endoplasmic reticulum kinase (PERK), elongation initiation factor 2α (eIF2α) and activating transcription factor 4 (ATF4). Ileitis is dependent on commensal microbiota and derives from increased intestinal epithelial cell death, inositol requiring enzyme 1α (IRE1α)-regulated NF-κB activation and tumour-necrosis factor signalling, which are synergistically increased when autophagy is deficient. ATG16L1 restrains IRE1α activity, and augmentation of autophagy in intestinal epithelial cells ameliorates ER stress-induced intestinal inflammation and eases NF-κB overactivation and intestinal epithelial cell death. ER stress, autophagy induction and spontaneous ileitis emerge from Paneth-cell-specific deletion of Xbp1. Genetically and environmentally controlled UPR function within Paneth cells may therefore set the threshold for the development of intestinal inflammation upon hypomorphic ATG16L1 function and implicate ileal Crohn's disease as a specific disorder of Paneth cells

Daksha: On Alert for High Energy Transients

We present Daksha, a proposed high energy transients mission for the study of electromagnetic counterparts of gravitational wave sources, and gamma ray bursts. Daksha will comprise of two satellites in low earth equatorial orbits, on opposite sides of earth. Each satellite will carry three types of detectors to cover the entire sky in an energy range from 1 keV to >1 MeV. Any transients detected on-board will be announced publicly within minutes of discovery. All photon data will be downloaded in ground station passes to obtain source positions, spectra, and light curves. In addition, Daksha will address a wide range of science cases including monitoring X-ray pulsars, studies of magnetars, solar flares, searches for fast radio burst counterparts, routine monitoring of bright persistent high energy sources, terrestrial gamma-ray flashes, and probing primordial black hole abundances through lensing. In this paper, we discuss the technical capabilities of Daksha, while the detailed science case is discussed in a separate paper.Comment: 9 pages, 3 figures, 1 table. Additional information about the mission is available at https://www.dakshasat.in