48 research outputs found
Effects of C, Cu and Be substitutions in superconducting MgB2
Density functional calculations are used to investigate the effects of
partial substitutional alloying of the B site in MgB2 with C and Be alone and
combined with alloying of the Mg site with Cu. The effect of such substitutions
on the electronic structure, electron phonon coupling and superconductivity are
discussed. We find that Be substitution for B is unfavorable for
superconductivity as it leads to a softer lattice and weaker electron-phonon
couplings. Replacement of Mg by Cu leads to an increase in the stiffness and
doping level at the same time, while the carrier concentration can be
controlled by partial replacement of B by C. We estimate that with full
replacement of Mg by Cu and fractional substitution of B by C, Tc values of 50K
may be attainable.Comment: 5 pages, 4 figure
Polarons with a twist
We consider a polaron model where molecular \emph{rotations} are important.
Here, the usual hopping between neighboring sites is affected directly by the
electron-phonon interaction via a {\em twist-dependent} hopping amplitude. This
model may be of relevance for electronic transport in complex molecules and
polymers with torsional degrees of freedom, such as DNA, as well as in
molecular electronics experiments where molecular twist motion is significant.
We use a tight-binding representation and find that very different polaronic
properties are already exhibited by a two-site model -- these are due to the
nonlinearity of the restoring force of the twist excitations, and of the
electron-phonon interaction in the model. In the adiabatic regime, where
electrons move in a {\em low}-frequency field of twisting-phonons, the
effective splitting of the energy levels increases with coupling strength. The
bandwidth in a long chain shows a power-law suppression with coupling, unlike
the typical exponential dependence due to linear phonons.Comment: revtex4 source and one eps figur
The Chiral Magnetic Effect and Axial Anomalies
We give an elementary derivation of the chiral magnetic effect based on a
strong magnetic field lowest-Landau-level projection in conjunction with the
well-known axial anomalies in two- and four-dimensional space-time. The
argument is general, based on a Schur decomposition of the Dirac operator. In
the dimensionally reduced theory, the chiral magnetic effect is directly
related to the relativistic form of the Peierls instability, leading to a
spiral form of the condensate, the chiral magnetic spiral. We then discuss the
competition between spin projection, due to a strong magnetic field, and
chirality projection, due to an instanton, for light fermions in QCD and QED.
The resulting asymmetric distortion of the zero modes and near-zero modes is
another aspect of the chiral magnetic effect.Comment: 33 pages, 5 figures, to appear in Lect. Notes Phys. "Strongly
interacting matter in magnetic fields" (Springer), edited by D. Kharzeev, K.
Landsteiner, A. Schmitt, H.-U. Ye
SYNTHESIZING POLITICS, RATIONALITY AND ADVOCACY: ENERGY POLICY ANALYSIS FOR MINORITY GROUPS
Altered TMPRSS2 usage by SARS-CoV-2 Omicron impacts infectivity and fusogenicity
The SARS-CoV-2 Omicron BA.1 variant emerged in 20211 and has multiple mutations in its spike protein2. Here we show that the spike protein of Omicron has a higher affinity for ACE2 compared with Delta, and a marked change in its antigenicity increases Omicron’s evasion of therapeutic monoclonal and vaccine-elicited polyclonal neutralizing antibodies after two doses. mRNA vaccination as a third vaccine dose rescues and broadens neutralization. Importantly, the antiviral drugs remdesivir and molnupiravir retain efficacy against Omicron BA.1. Replication was similar for Omicron and Delta virus isolates in human nasal epithelial cultures. However, in lung cells and gut cells, Omicron demonstrated lower replication. Omicron spike protein was less efficiently cleaved compared with Delta. The differences in replication were mapped to the entry efficiency of the virus on the basis of spike-pseudotyped virus assays. The defect in entry of Omicron pseudotyped virus to specific cell types effectively correlated with higher cellular RNA expression of TMPRSS2, and deletion of TMPRSS2 affected Delta entry to a greater extent than Omicron. Furthermore, drug inhibitors targeting specific entry pathways3 demonstrated that the Omicron spike inefficiently uses the cellular protease TMPRSS2, which promotes cell entry through plasma membrane fusion, with greater dependency on cell entry through the endocytic pathway. Consistent with suboptimal S1/S2 cleavage and inability to use TMPRSS2, syncytium formation by the Omicron spike was substantially impaired compared with the Delta spike. The less efficient spike cleavage of Omicron at S1/S2 is associated with a shift in cellular tropism away from TMPRSS2-expressing cells, with implications for altered pathogenesis
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