The Fallout of Catastrophic Technogenic Emissions of Toxic Gases Can Negatively Affect Covid-19 Clinical Course

The coronavirus D-19 (Covid-19) pandemic has shaken almost every country in the world: as we stand, 6,3 million deaths from the infection have already been recorded, 167,000 and 380,000 of which are in Italy and the Russian Federation, respectively. In the first wave of the pandemic, Italy suffered an abnormally high death toll. A detailed analysis of available epidemiological data suggests that that rate was shockingly high in the Northern regions and in Lombardy, in particular, whilst in the southern region the situation was less dire. This inexplicably high mortality rate in conditions of a very well-developed health care system such as the one in Lombardy recognized as one of the best in Italy certainly cries for a convincing explanation. In 1976, the small city of Seveso, Lombardy, experienced a release of dioxin into the atmosphere after a massive technogenic accident. The immediate effects of the industrial disaster did not become apparent until a surge in the number of tumors in the affected population in the subsequent years. In this paper, we endeavor to prove our hypothesis that the release of dioxin was a negative cofactor that contributed to a worsening of the clinical course of COVID-19 in Lombardy

Scintillation proportional Xe counter with WLS fiber readout for low-energy X-rays

A gas Xe based scintillation proportional counter with cylindrical geometry and wavelength shifting (WLS) fiber readout for X-rays of energy 0.5 - 100 keV is proposed. With such a design large sizes and sensitive area of the counter with a fairly well uniformity is possible. The counter could be used for "dark matter" search and neutrino magnetic moment measurement and for detection of small amounts or traces of radioactive elements in substances or environment.Comment: LaTeX 4 pages, 3 figures in eps, Submitted to NI

Steps toward translocation-independent RNA polymerase inactivation by terminator ATPase ρ

Factor-dependent transcription termination mechanisms are poorly understood. We determined a series of cryo–electron microscopy structures portraying the hexameric adenosine triphosphatase (ATPase) ρ on a pathway to terminating NusA/NusG-modified elongation complexes. An open ρ ring contacts NusA, NusG, and multiple regions of RNA polymerase, trapping and locally unwinding proximal upstream DNA. NusA wedges into the ρ ring, initially sequestering RNA. Upon deflection of distal upstream DNA over the RNA polymerase zinc-binding domain, NusA rotates underneath one capping ρ subunit, which subsequently captures RNA. After detachment of NusG and clamp opening, RNA polymerase loses its grip on the RNA:DNA hybrid and is inactivated. Our structural and functional analyses suggest that ρ, and other termination factors across life, may use analogous strategies to allosterically trap transcription complexes in a moribund state

Detector array for the 7^7H nucleus multi-neutron decay study

Setup fitting the requirements for the detailed study of the five-body decay of the 7H nucleus obtained as a result of the proton transfer from the 8He projectiles to the deuterium target nuclei is being built at the radioactive beam line of ACCULINNA-2 separator in the G.N. Flerov Laboratory of Nuclear Reactions. Described here is the assembly of 100 BC-404 plastic scintillators, intended for neutron detection, the annular Si detector telescope for the 3He recoils, and the detector array providing the $\Delta E$-$E$-TOF registration of 3H nuclei emitted at the 7H decay. Results obtained by the Monte Carlo simulations made for the energy values and flight passes of all these particles are given together with the luminosity expected for the discussed experiments

Lineage-specific variations in the trigger loop modulate RNA proofreading by bacterial RNA polymerases

RNA cleavage by bacterial RNA polymerase (RNAP) has been implicated in transcriptional proofreading and reactivation of arrested transcription elongation complexes but its molecular mechanism is less understood than the mechanism of nucleotide addition, despite both reactions taking place in the same active site. RNAP from the radioresistant bacterium Deinococcus radiodurans is characterized by highly efficient intrinsic RNA cleavage in comparison with Escherichia coli RNAP. We find that the enhanced RNA cleavage activity largely derives from amino acid substitutions in the trigger loop (TL), a mobile element of the active site involved in various RNAP activities. The differences in RNA cleavage between these RNAPs disappear when the TL is deleted, or in the presence of GreA cleavage factors, which replace the TL in the active site. We propose that the TL substitutions modulate the RNA cleavage activity by altering the TL folding and its contacts with substrate RNA and that the resulting differences in transcriptional proofreading may play a role in bacterial stress adaptation.</p

Flux Modulations seen by the Muon Veto of the GERDA Experiment

The GERDA experiment at LNGS of INFN is equipped with an active muon veto. The main part of the system is a water Cherenkov veto with 66~PMTs in the water tank surrounding the GERDA cryostat. The muon flux recorded by this veto shows a seasonal modulation. Two effects have been identified which are caused by secondary muons from the CNGS neutrino beam (2.2 %) and a temperature modulation of the atmosphere (1.4 %). A mean cosmic muon rate of $I^0_{\mu} = (3.477 \pm 0.002_{\textrm{stat}} \pm 0.067_{\textrm{sys}}) \times 10^{-4}$/(s$\cdot$m$^2$) was found in good agreement with other experiments at LNGS at a depth of 3500~meter water equivalent.Comment: 7 pages, 6 figure

Diagnostics of autoimmune neurodegeneration using fluorescent probing

© 2018, The Author(s). The discovery of antibody-mediated catalysis was a breakthrough that showed antibody function is not limited to specific binding interactions, and that immunoglobulins (Igs) may also chemically transform their target antigens. Recently, so-called “natural catalytic antibodies” have been intimately linked with several pathologies, where they either protect the organism or contribute to the development of autoimmune abnormalities. Previously, we showed that myelin-reactive autoantibodies from patients with multiple sclerosis (MS) and mice with experimental autoimmune encephalomyelitis (EAE) exhibit the ability to recognize and hydrolyse distinct epitopes within myelin basic protein (MBP). Further, the antibody-mediated cleavage of encephalitogenic MBP peptide 81–103, flanked by two fluorescent proteins, can serve as a novel biomarker for MS. Here, we report the next generation of this biomarker, based on the antibody-mediated degradation of a novel chemically synthesized FRET substrate, comprising the fluorophore Cy5 and the quencher QXL680, interconnected by the MBP peptide 81–99: Cy5-MBP81–99-QXL680. This substrate is degraded upon incubation with either purified antibodies from MS patients but not healthy donors or purified antibodies and splenocytes from EAE but not from non-immunized mice. Data presented herein suggest the elaboration of potential specific, rapid, and sensitive diagnostic criteria of active progressive MS

Characterization of 30 76^{76}Ge enriched Broad Energy Ge detectors for GERDA Phase II

The GERmanium Detector Array (GERDA) is a low background experiment located at the Laboratori Nazionali del Gran Sasso in Italy, which searches for neutrinoless double beta decay of $^{76}$Ge into $^{76}$Se+2e$^-$. GERDA has been conceived in two phases. Phase II, which started in December 2015, features several novelties including 30 new Ge detectors. These were manufactured according to the Broad Energy Germanium (BEGe) detector design that has a better background discrimination capability and energy resolution compared to formerly widely-used types. Prior to their installation, the new BEGe detectors were mounted in vacuum cryostats and characterized in detail in the HADES underground laboratory in Belgium. This paper describes the properties and the overall performance of these detectors during operation in vacuum. The characterization campaign provided not only direct input for GERDA Phase II data collection and analyses, but also allowed to study detector phenomena, detector correlations as well as to test the strength of pulse shape simulation codes.Comment: 29 pages, 18 figure

Exposure to the Epstein-Barr viral antigen latent membrane protein 1 induces myelin-reactive antibodies in vivo

© 2017 Lomakin, Arapidi, Chernov, Ziganshin, Tcyganov, Lyadova, Butenko, Osetrova, Ponomarenko, Telegin, Govorun, Gabibov and Belogurov. Multiple sclerosis (MS) is an autoimmune chronic inflammatory disease of the central nervous system (CNS). Cross-reactivity of neuronal proteins with exogenous antigens is considered one of the possible mechanisms of MS triggering. Previously, we showed that monoclonal myelin basic protein (MBP)-specific antibodies from MS patients cross-react with Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1). In this study, we report that exposure of mice to LMP1 results in induction of myelin-reactive autoantibodies in vivo. We posit that chronic exposure or multiple acute exposures to viral antigen may redirect B cells from production of antiviral antibodies to antibodies, specific to myelin antigen. However, even in inbred animals, which are almost identical in terms of their genomes, such an effect is only observed in 20-50% of animals, indicating that this change occurs by chance, rather than systematically. Cross-immunoprecipitation analysis showed that only part of anti-MBP antibodies from LMP1-immunized mice might simultaneously bind LMP1. In contrast, the majority of anti-LMP1 antibodies from MBP-immunized mice bind MBP. De novo sequencing of anti-LMP1 and anti-MBP antibodies by mass spectrometry demonstrated enhanced clonal diversity in LMP1-immunized mice in comparison with MBP-immunized mice. We suggest that induction of MBP-reactive antibodies in LMP1-immunized mice may be caused by either Follicular dendritic cells (FDCs) or by T cells that are primed by myelin antigens directly in CNS. Our findings help to elucidate the still enigmatic link between EBV infection and MS development, suggesting that myelin-reactive antibodies raised as a response toward EBV protein LMP1 are not truly cross-reactive but are primarily caused by epitope spreading