16 research outputs found
Prospects for photon blockade in four level systems in the N configuration with more than one atom
We show that for appropriate choices of parameters it is possible to achieve
photon blockade in idealised one, two and three atom systems. We also include
realistic parameter ranges for rubidium as the atomic species. Our results
circumvent the doubts cast by recent discussion in the literature (Grangier et
al Phys. Rev Lett. 81, 2833 (1998), Imamoglu et al Phys. Rev. Lett. 81, 2836
(1998)) on the possibility of photon blockade in multi-atom systems.Comment: 8 page, revtex, 7 figures, gif. Submitted to Journal of Optics B:
Quantum and Semiclassical Optic
Resistance related metabolic pathways for drug target identification in Mycobacterium tuberculosis
Genetic mechanisms of critical illness in COVID-19.
Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 × 10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice