Nitrogen atom detection in low-pressure flames by two-photon laser-excited fluorescence

Bittner J, Lawitzki A, Meier U, Kohse-Höinghaus K. Nitrogen atom detection in low-pressure flames by two-photon laser-excited fluorescence. Applied Physics, B. 1991;52(2):108-116.Nitrogen atoms have been detected in stoichiometric flat premixed H2/O2/N2 flames at 33 and 96 mbar doped with small amounts of NH3, HCN, and (CN)2 using two-photon laser excitation at 211 nm and fluorescence detection around 870 nm. The shape of the fluorescence intensity profiles versus height above the burner surface is markedly different for the different additives. Using measured quenching rate coefficients and calibrating with the aid of known N-atom concentrations in a discharge flow reactor, peak N-atom concentrations in these flames are estimated to be on the order of 10 12–5×10 13 cm –3; the detection limit is about 1×10 11 cm –3

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

Crystal structure of bis(benzamide-2-thiolato)(μ 2-bis(diphenylphosphino)-ethane)digold(I), C40H 36Au2N2O2P2S2

Zeitschrift fur Kristallographie - New Crystal Structures2173361-36

Crystal structure of benzamide-2-thiolato(tri-o-tolylphosphine)gold(I), C28H27AuNOPS

Zeitschrift fur Kristallographie - New Crystal Structures2173357-35

Crystal structure of bis(benzamide-2-thiolato)(μ 2-bis(diphenylphosphino)-propane)digold(I) dimethanol solvate, C 43H46Au2N2O4P 2S2

Zeitschrift fur Kristallographie - New Crystal Structures2173363-36