Detectors for the Gamma-Ray Resonant Absorption (GRA) Method of Explosives Detection in Cargo: A Comparative Study

Gamma-Ray Resonant Absorption (GRA) is an automatic-decision radiographic screening technique that combines high radiation penetration with very good sensitivity and specificity to nitrogenous explosives. The method is particularly well-suited to inspection of large, massive objects (since the incident gamma-ray probe is at 9.17 MeV) such as aviation and marine containers, heavy vehicles and railroad cars. Two kinds of gamma-ray detectors have been employed to date in GRA systems: 1) Resonant-response nitrogen-rich liquid scintillators and 2) BGO detectors. This paper analyses and compares the response of these detector-types to the resonant radiation, in terms of single-pixel figures of merit. The latter are sensitive not only to detector response, but also to accelerator-beam quality, via the properties of the nuclear reaction that produces the resonant gamma-rays. Generally, resonant detectors give rise to much higher nitrogen-contrast sensitivity in the radiographic image than their non-resonant detector counterparts and furthermore, do not require proton beams of high energy-resolution. By comparison, the non-resonant detectors have higher gamma-detection efficiency, but their contrast sensitivity is very sensitive to the quality of the accelerator beam. Implications of these detector/accelerator characteristics for eventual GRA field systems are discussed.Comment: 11 page

Different transcriptional response between susceptible and resistant common carp (Cyprinus carpio) fish hints on the mechanism of CyHV-3 disease resistance

Infectious disease outbreaks form major setbacks to aquaculture production and to further development of this important sector. Cyprinid herpes virus-3 (CyHV-3) is a dsDNA virus widely hampering production of common carp (Cyprinus carpio), one of the most farmed fish species worldwide. Genetically disease resistant strains are highly sought after as a sustainable solution to this problem. To study the genetic basis and cellular pathways underlying disease resistance, RNA-Seq was used to characterize transcriptional responses of susceptible and resistant fish at day 4 after CyHV-3 infection

Adoptive transfer of mRNA-Transfected T cells redirected against diabetogenic CD8 T cells can prevent diabetes

Chimeric major histocompatibility complex (MHC) molecules supplemented with T cell receptor (TCR) signaling motifs function as activation receptors and can redirect gene-modified T cells against pathogenic CD8 T cells. We have shown that β2 microglobulin (β2m) operates as a universal signaling component of MHC-I molecules when fused with the CD3-ζ chain. Linking the H-2Kd-binding insulin B chain peptide insulin B chain, amino acids 15–23 (InsB15–23) to the N terminus of β2m/CD3-ζ, redirected polyclonal CD8 T cells against pathogenic CD8 T cells in a peptide-specific manner in the non-obese diabetic (NOD) mouse. Here, we describe mRNA electroporation for delivering peptide/β2m/CD3-ζ genes to a reporter T cell line and purified primary mouse CD8 T cells. The peptide/β2m/CD3-ζ products paired with endogenous MHC-I chains and transmitted strong activation signals upon MHC-I cross-linking. The reporter T cell line transfected with InsB15–23/β2m/CD3-ζ mRNA was activated by an InsB15–23-H-2Kd-specific CD8 T cell hybrid only when the transfected T cells expressed H-2Kd. Primary NOD CD8 T cells expressing either InsB15–23/β2m/CD3-ζ or islet-specific glucose-6-phosphatase catalytic subunit-related protein, amino acids 206–214 (IGRP206–214)/β2m/CD3-ζ killed their respective autoreactive CD8 T cell targets in vitro. Furthermore, transfer of primary CD8 T cells transfected with InsB15–23/β2m/CD3-ζ mRNA significantly reduced insulitis and protected NOD mice from diabetes. Our results demonstrate that mRNA encoding chimeric MHC-I receptors can redirect effector CD8 against diabetogenic CD8 T cells, offering a new approach for the treatment of type 1 diabetes

The Costs of Sovereignty

Since the late 19th century, when the first Zionist settlers arrived in the area called Palestine, the relationship between the local Jews and the Arabs has been perceived as a zerosum game. A zero-sum game is one which generates solutions that favor one side or the other, but not both; the gain of one is the loss of the other. These games often produce equilibrium solutions, some of which are durable and stable. However, when they assume the form ascribed by Nash, or when the preferences of ..

Fine Tuning of a Type 1 Interferon Antagonist.

Type I interferons are multi-potent cytokines that serve as first line of defense against viruses and other pathogens, posses immunomudolatory functions and elicit a growth inhibitory response. In recent years it has been shown that interferons are also detrimental, for example in lupus, AIDS, tuberculosis and cognitive decline, highlighted the need to develop interferon antagonists. We have previously developed the antagonist IFN-1ant, with much reduced binding to the IFNAR1 receptor and enhanced binding to IFNAR2. Here, we further tune the IFN-1ant by producing three additional antagonists based on IFN-1ant but with altered activity profiles. We show that in all three cases the antiproliferative activity of interferons is blocked and the induction of gene transcription of immunomudolatory and antiproliferative associated genes are substantially decreased. Conversely, each of the new antagonists elicits a different degree of antiviral response, STAT phosphorylation and related gene induction. Two of the new antagonists promote decreased activity in relation to the original IFN-1ant, while one of them promotes increased activity. As we do not know the exact causes of the detrimental effects of IFNs, the four antagonists that were produced and analyzed provide the opportunity to investigate the extent of antagonistic and agonistic activity optimal for a given condition

Gene expression in response to antagonist treatment.

<p>Gene expression in OVCAR3, WISH and T47D cells in response to antagonists, YNS and IFNα2. (A) Cells were treated for 8 hours with 200 nM antagonists or 1nM YNS, and analyzed by qPCR. The data presented are the relative expression levels compared to those of untreated cells, normalized against HPRT1. (B) As described in (A), but cells were treated for 24 hours. (C) Cells were treated with a combination of 200 nM antagonist and 200 pM IFMα2. Gene induction was analyzed as described in (A). Error bars represent standard deviation of the data.</p