USER'S GUIDE - GENERAL WEED MANAGEMENT MODEL VERSION 1.0 - DECEMBER 1994

Crop Production/Industries,

Superconductivity and single crystal growth of Ni0:05TaS2

Superconductivity was discovered in a Ni0:05TaS2 single crystal. A Ni0:05TaS2 single crystal was successfully grown via the NaCl/KCl flux method. The obtained lattice constant c of Ni0:05TaS2 is 1.1999 nm, which is significantly smaller than that of 2H-TaS2 (1.208 nm). Electrical resistivity and magnetization measurements reveal that the superconductivity transition temperature of Ni0:05TaS2 is enhanced from 0.8 K (2H-TaS2) to 3.9 K. The charge-density-wave transition of the matrix compound 2H-TaS2 is suppressed in Ni0:05TaS2. The success of Ni0:05TaS2 single crystal growth via a NaCl/KCl flux demonstrates that NaCl/KCl flux method will be a feasible method for single crystal growth of the layered transition metal dichalcogenides.Comment: 13pages, 6 figures, Published in SS

Elliptic curves of large rank and small conductor

For r=6,7,...,11 we find an elliptic curve E/Q of rank at least r and the smallest conductor known, improving on the previous records by factors ranging from 1.0136 (for r=6) to over 100 (for r=10 and r=11). We describe our search methods, and tabulate, for each r=5,6,...,11, the five curves of lowest conductor, and (except for r=11) also the five of lowest absolute discriminant, that we found.Comment: 16 pages, including tables and one .eps figure; to appear in the Proceedings of ANTS-6 (June 2004, Burlington, VT). Revised somewhat after comments by J.Silverman on the previous draft, and again to get the correct page break

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