Calculation of electronic properties of amorphous alloys

We describe the application of the locally-self-consistent-multiple-scattering (LSMS)[1] method to amorphous alloys. The LSMS algorithm is optimized for the Intel XP/S-150, a multiple-instruction-multiple-data parallel computer with 1024 nodes and 2 compute processors per node. The electron density at each site is determined by solving the multiple scattering equation for atoms within a specified distance of the atom under consideration. Because this method is carried out in real space it is ideal for treating amorphous alloys. We have adapted the code to the calculation of the electronic properties of amorphous alloys. In these calculations we determine the potentials in the atomic sphere approximation self consistently at each site, unlike previous calculations[2] where we determined the potentials self consistently at an average site. With these self-consistent potentials, we then calculate electronic properties of various amorphous alloy systems. We present calculated total electronic densities of states for amorphous Ni$_{80}$P$_{20}$ and Ni$_{40}$Pd$_{40}$P$_{20}$ with 300 atoms in a supercell.Comment: 10 pages, plain tex, 2 figures. Paper accepted for publication in Proceedings of LAM-9 and Journal of non-Crystalline Solids. Please request preprints from J.C. Swihart ([email protected]

Effects of copper sulfate and zinc oxide on weanling pig growth and plasma mineral levels

A total of 216 weanling pigs (PIC TR4 × 1050, initially 13.6 lb and 21 d of age) were used in a 42-d growth trial to compare the effects of supplemental zinc and copper and changing mineral regimens on growth performance and plasma mineral levels. The 6 dietary treatments included a 2 × 2 factorial arrangement with main effects of added copper from copper sulfate (0 or 125 ppm) and added zinc from zinc oxide (0 or 3,000 ppm from d 0 to 14 and 0 or 2,000 ppm from d 14 to 42). For the final 2 treatments, either zinc oxide alone or the combinations of zinc and copper were fed from d 0 to 14, with copper sulfate fed from d 14 to 42. There were 6 pens per treatment with 6 pigs per pen. All diets were supplemented with an additional 165 ppm zinc and 16.5 ppm copper from the trace mineral premix. Plasma was collected from 2 pigs per pen on d 14 and 42. From d 0 to 14, ADG, ADFI, and F/G were improved (P < 0.04) with the addition of dietary zinc. Copper supplementation also tended to increase (P < 0.07) ADFI from d 0 to 14. From d 14 to 42, added copper increased (P < 0.003) ADG and ADFI. Over the entire trial, continuous supplemental zinc increased (P < 0.03) ADG and tended to increase (P < 0.09) ADFI. Dietary copper also increased (P < 0.004) ADG and ADFI when fed from d 0 to 42. The most advantageous values for ADG and ADFI were seen in the treatment containing high levels of zinc from d 0 to 14 and high copper levels from d 14 to 42. The addition of either zinc or copper increased (P < 0.02) feed cost per pound of gain. However, income over feed cost was improved (P < 0.006) with the addition of copper, with the greatest value obtained when high zinc was fed from d 0 to 14 and high copper was fed from d 14 to 42. Plasma zinc levels were increased (P < 0.001) with zinc supplementation on d 14. These results indicate the optimal mineral regimen was supplementing zinc oxide from d 0 to 14 and copper sulfate from d 14 to 42

Insights into malaria susceptibility using genome-wide data on 17,000 individuals from Africa, Asia and Oceania

The human genetic factors that affect resistance to infectious disease are poorly understood. Here we report a genome-wide association study in 17,000 severe malaria cases and population controls from 11 countries, informed by sequencing of family trios and by direct typing of candidate loci in an additional 15,000 samples. We identify five replicable associations with genome-wide levels of evidence including a newly implicated variant on chromosome 6. Jointly, these variants account for around one-tenth of the heritability of severe malaria, which we estimate as -23% using genome-wide genotypes. We interrogate available functional data and discover an erythroid-specific transcription start site underlying the known association in ATP2B4, but are unable to identify a likely causal mechanism at the chromosome 6 locus. Previously reported HLA associations do not replicate in these samples. This large dataset will provide a foundation for further research on thegenetic determinants of malaria resistance in diverse populations.Peer reviewe

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

Effects of copper sulfate, tri-basic copper chloride, and zinc oxide on weanling pig growth and plasma mineral concentrations

Two 28-d experiments were conducted to determine the effects of increasing dietary zinc and copper levels on weanling pig performance. In each experiment, 180 weanling pigs (PIC, 21 d of age, 12.5 lb in Exp. 1 and 13.2 lb in Exp. 2) were allotted to 1 of 6 treatments with 5 and 6 replications in Exp. 1 and 2, respectively. Diets were fed in 2 phases (d 0 to 14 and 14 to 28), and the trace mineral premix provided 165 ppm zinc and 16.5 ppm copper to all diets. In Exp. 1, treatments were arranged as a 2 × 3 factorial with 2 levels of added copper from tri-basic copper chloride (TBCC; 0 or 150 ppm) and 3 levels of added zinc from zinc oxide (0, 1,500, or 3,000 ppm from d 0 to 14 and 0, 1,000, or 2,000 ppm from d 14 to 28). In addition, blood collected on d 14 was analyzed for plasma zinc, copper, and phosphorus concentrations. No copper × zinc interactions were observed (P > 0.25) for any of the growth data. Addition of TBCC in-creased (P 0.10) were observed for any performance data. Adding zinc oxide to the diet improved (P < 0.03) ADG, ADFI, and F/G from d 0 to 14 and ADG and ADFI from d 0 to 28. Adding copper to the diet increased (P < 0.05) ADG, ADFI, and F/G from d 0 to 14 and 0 to 28 with pigs fed copper sulfate having greater (P < 0.02) ADG and ADFI from d 0 to 14 than pigs fed TBCC. Similar to Exp. 1, plasma zinc was increased (P < 0.001) in pigs fed high levels of dietary zinc at d 14. Unlike many previous research trials, these two trials found additive effects to feeding high levels of dietary copper and zinc in diets for nursery pigs

Multi-teraflops spin dynamics studies of the magnetic structure of FeMn/Co interfaces

The authors have used the power of massively parallel computers to perform first principles spin dynamics (SD) simulations of the magnetic structure of Iron-Manganese/Cobalt (FeMn/Co) interfaces. These large scale quantum mechanical simulations, involving 2016-atom super-cell models, reveal details of the orientational configuration of the magnetic moments at the interface that are unobtainable by any other means. Exchange bias, which involves the use of an antiferromagnetic (AFM) layer such as FeMn to pin the orientation of the magnetic moment of a proximate ferromagnetic (FM) layer such as Co, is of fundamental importance in magnetic multilayer storage and read head devices. Here the equation of motion of first principles SD is used to perform relaxations of model magnetic structures to the true ground (equilibrium) state. Our code is intrinsically parallel and has achieved a maximum execution rate of 2.46 Teraflops on the IBM SP at the National Energy Research Scientific Computing Center (NERSC)