Precision Requirements for Space-based XCO2 Data

Precision requirements have been determined for the column-averaged CO2 dry air mole fraction (X(sub CO2)) data products to be delivered by the Orbiting Carbon Observatory (OCO). These requirements result from an assessment of the amplitude and spatial gradients in X(sub CO2), the relationship between X(sub CO2) precision and surface CO2 flux uncertainties calculated from inversions of the X(sub CO2) data, and the effects of X,,Z biases on CO2 flux inversions. Observing system simulation experiments and synthesis inversion modeling demonstrate that the OCO mission design and sampling strategy provide the means to achieve the X(sub CO2) precision requirements. The impact of X(sub CO2) biases on CO2 flux uncertainties depend on their spatial and temporal extent since CO2 sources and sinks are inferred from regional-scale X(sub CO2) gradients. Simulated OCO sampling of the TRACE-P CO2 fields shows the ability of X(sub CO2) data to constrain CO2 flux inversions over Asia and distinguish regional fluxes from India and China

Existence of superposition solutions for pulse propagation in nonlinear resonant media

Existence of self-similar, superposed pulse-train solutions of the nonlinear, coupled Maxwell-Schr\"odinger equations, with the frequencies controlled by the oscillator strengths of the transitions, is established. Some of these excitations are specific to the resonant media, with energy levels in the configurations of $\Lambda$ and $N$ and arise because of the interference effects of cnoidal waves, as evidenced from some recently discovered identities involving the Jacobian elliptic functions. Interestingly, these excitations also admit a dual interpretation as single pulse-trains, with widely different amplitudes, which can lead to substantially different field intensities and population densities in different atomic levels.Comment: 11 Pages, 6 Figures, presentation changed and 3 figures adde

Resonant nonstationary amplification of polychromatic laser pulses and conical emission in an optically dense ensemble of neon metastable atoms

Experimental and numerical investigation of single-beam and pump-probe interaction with a resonantly absorbing dense extended medium under strong and weak field-matter coupling is presented. Significant probe beam amplification and conical emission were observed. Under relatively weak pumping and high medium density, when the condition of strong coupling between field and resonant matter is fulfilled, the probe amplification spectrum has a form of spectral doublet. Stronger pumping leads to the appearance of a single peak of the probe beam amplification at the transition frequency. The greater probe intensity results in an asymmetrical transmission spectrum with amplification at the blue wing of the absorption line and attenuation at the red one. Under high medium density, a broad band of amplification appears. Theoretical model is based on the solution of the Maxwell-Bloch equations for a two-level system. Different types of probe transmission spectra obtained are attributed to complex dynamics of a coherent medium response to broadband polychromatic radiation of a multimode dye laser.Comment: 9 pages, 13 figures, corrected, Fig.8 was changed, to be published in Phys. Rev.

A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk

Combined analyses of gene networks and DNA sequence variation can provide new insights into the aetiology of common diseases that may not be apparent from genome-wide association studies alone. Recent advances in rat genomics are facilitating systems-genetics approaches. Here we report the use of integrated genome-wide approaches across seven rat tissues to identify gene networks and the loci underlying their regulation. We defined an interferon regulatory factor 7 (IRF7)-driven inflammatory network (IDIN) enriched for viral response genes, which represents a molecular biomarker for macrophages and which was regulated in multiple tissues by a locus on rat chromosome 15q25. We show that Epstein-Barr virus induced gene 2 (Ebi2, also known as Gpr183), which lies at this locus and controls B lymphocyte migration, is expressed in macrophages and regulates the IDIN. The human orthologous locus on chromosome 13q32 controlled the human equivalent of the IDIN, which was conserved in monocytes. IDIN genes were more likely to associate with susceptibility to type 1 diabetes (T1D)-a macrophage-associated autoimmune disease-than randomly selected immune response genes (P = 8.85 x 10(-6)). The human locus controlling the IDIN was associated with the risk of T1D at single nucleotide polymorphism rs9585056 (P = 7.0 x 10(-10); odds ratio, 1.15), which was one of five single nucleotide polymorphisms in this region associated with EBI2 (GPR183) expression. These data implicate IRF7 network genes and their regulatory locus in the pathogenesis of T1D

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease