Radon Mitigation Applications at the Laboratorio Subterraneo de Canfranc (LSC)

The Laboratorio Subterraneo de Canfranc (LSC) is the Spanish national hub for low radioactivity techniques and the associated scientific and technological applications. The concentration of the airborne radon is a major component of the radioactive budget in the neighborhood of the detectors. The LSC hosts a Radon Abatement System, which delivers a radon suppressed air with 1.1 & PLUSMN;0.2 mBq/m(3) of Rn-222. The radon content in the air is continuously monitored with an Electrostatic Radon Monitor. Measurements with the double beta decay demonstrators NEXT-NEW and CROSS and the gamma HPGe detectors show the important reduction of the radioactive background due to the purified air in the vicinity of the detectors. We also discuss the use of this facility in the LSC current program which includes NEXT-100, low background biology experiments and radiopure copper electroformation equipment placed in the radon-free clean room

miR-146a is a pivotal regulator of neutrophil extracellular trap formation promoting thrombosis.

Neutrophil extracellular traps (NETs) induce a procoagulant response linking inflammation and thrombosis. Low levels of miR-146a, a brake of inflammatory response, are involved in higher risk for cardiovascular events, but the mechanisms explaining how miR-146a exerts its function remain largely undefined. The aim of this study was to explore the impact of miR-146a deficiency in NETosis both, in sterile and non-sterile models in vivo, and to inquire into the underlying mechanism. Two models of inflammation were performed: 1) Ldlr-/- mice transplanted with bone marrow from miR-146a-/- or wild type (WT) were fed high-fat diet, generating an atherosclerosis model; and 2) an acute inflammation model was generated by injecting lipopolysaccharide (LPS) (1 mg/Kg) into miR-146a-/- and WT mice. miR-146a deficiency increased NETosis in both models. Accordingly, miR-146a-/- mice showed significant reduced carotid occlusion time and elevated levels of NETs in thrombi following FeCl3-induced thrombosis. Infusion of DNAse I abolished arterial thrombosis in WT and miR-146a-/- mice. Interestingly, miR-146a deficient mice have aged, hyperreactive and pro-inflammatory neutrophils in circulation that are more prone to form NETs independently of the stimulus. Furthermore, we demonstrated that community acquired pneumonia (CAP) patients with reduced miR-146a levels associated with the T variant of the functional rs2431697, presented an increased risk for cardiovascular events due in part to an increased generation of NETs.This work was supported by research grants from Instituto de Salud Carlos III (ISCIII), Fondo Europeo de Desarrollo Regional “Investing in your future” (PI17/00051 y PI17/01421) (PFIS18/0045: A.M. de los Reyes-García) (CD18/00044: S. Águila), and Fundación Séneca (19873/GERM/15). The CNIC is supported by the ISCIII, the Ministerio de Ciencia, Innovación y Universidades (MCIU), and the Fundación Pro CNIC, and is a Severo Ochoa Center of Excellence (SEV-2015-0505). A.B. Arroyo has a research fellowship from Sociedad Española de Trombosis y Hemostasia (SETH). The MCIU supported A.dM. (predoctoral contract BES-2014-067791).S