Low-energy electron-impact ionization of the helium atom using the multiconfiguration Hartree-Fock method

We have extended the multiconfiguration Hartree-Fock method for electron-impact ionization of atoms to investigate the effects of polarization and electron correlation of the target in the initial state. As a test case, the method is applied to calculate triple differential cross sections for electron-impact ionization of He atom at an excess energy of 2 eV for the coplanar theta(12) = pi geometry for equal and unequal energies of two final-state outgoing electrons. To determine the effects of electron correlation between the two outgoing electrons in the final state, the variationally determined screening potential approximation is used. It is found that target correlation in the initial state has smaller effect on the triple differential cross section but the polarization of the target by the incident electron has considerable effect on the triple differential cross section at low incident energy. The results are compared with absolute measurement and other available theoretical results

Extension of the multiconfiguration Hartree-Fock method to allow double photoionization of atoms

Very recently we were successful in extending the multiconfiguration Hartree-Fock (MCHF) method for electron-impact ionization of atoms to allow double photoionization of atoms. We report, as a test case, the results of our calculation of the triple differential cross section (TDCS) for double photoionization of helium. We have calculated the initial state in the Hartree-Fock and the MCHF approximations and the final state in the Coulomb approximation and the screening potential approximation in order to compare with previously published works. We compare the present results calculated at 30-eV excess photon energy shared equally by two final-state continuum electrons, with other similar theoretical calculations. Finally, we also calculate the TDCS at 20-eV excess photon energy to compare with experimental observation

Hartree-Fock studies of the triple differential cross section for electron-impact ionization of the hydrogen atom

We report absolute triple differential cross sections in coplanar theta(12)=pi geometry for the ionization of atomic hydrogen by electron impact at low energies. We used our recently extended multiconfiguration Hartree-Fock method successfully to calculate triple differential cross sections of H for incident energies E(0) of 14.6, 15.6, 17.6, 20, and 25 eV for equal energy sharing of excess energies by the two final state continuum electrons. It has been shown that there is very little difference between the results obtained in the Hartree-Fock and the screening potential approximations implying that in the case of H and theta(12)=pi configuration distortion effects between the two outgoing electrons are small even at low energies. Our results are compared with available absolute and relative experimental data and other existing theoretical calculations and are found to be in very good agreement

Large electron correlation effects in the nondipole asymmetry parameters near photoionization thresholds

The nondipole corrections to the dipole approximation for the angular distribution of photoelectrons are calculated for Ar 3s subshell in the Hartree-Fock (HF) approximation for photoelectron energies ranging from threshold to 2 keV. The effects of electron correlation which are very important have been taken into account using the multiconfiguration HF approximation. It is found that near the threshold from 0 to 50 eV photoelectron energy, the nondipole parameters show oscillatory structure due to large electron correlation effects. The results are compared with existing theoretical and experimental data

K-Shell Photoionization of Beryllium

The numerical multiconfiguration Hartree-Fock method is used to study in detail the photoionization of atomic beryllium near the 1s threshold. Electron correlation effects, which are found to be very important in the K-shell partial photoionization cross section, have been taken into account very accurately through the configuration-interaction procedure. The present results are compared with experimental measurements of the relative contributions of the three major ionization channels and are found to be in excellent agreement. The existence of the principal resonances reported by the experiment has been confirmed and assignments made to these contributions based on accurate energ

HIV-1 gp120 Induces Expression of IL-6 through a Nuclear Factor-Kappa B-Dependent Mechanism: Suppression by gp120 Specific Small Interfering RNA

In addition to its role in virus entry, HIV-1 gp120 has also been implicated in HIV-associated neurocognitive disorders. However, the mechanism(s) responsible for gp120-mediated neuroinflammation remain undefined. In view of increased levels of IL-6 in HIV-positive individuals with neurological manifestations, we sought to address whether gp120 is involved in IL-6 over-expression in astrocytes. Transfection of a human astrocyte cell line with a plasmid encoding gp120 resulted in increased expression of IL-6 at the levels of mRNA and protein by 51.3±2.1 and 11.6±2.2 fold respectively; this effect of gp120 on IL-6 expression was also demonstrated using primary human fetal astrocytes. A similar effect on IL-6 expression was observed when primary astrocytes were treated with gp120 protein derived from different strains of X4 and R5 tropic HIV-1. The induction of IL-6 could be abrogated by use of gp120-specific siRNA. Furthermore, this study showed that the NF-κB pathway is involved in gp120-mediated IL-6 over-expression, as IKK-2 and IKKβ inhibitors inhibited IL-6 expression by 56.5% and 60.8%, respectively. These results were also confirmed through the use of NF-κB specific siRNA. We also showed that gp120 could increase the phosphorylation of IκBα. Furthermore, gp120 transfection in the SVGA cells increased translocation of NF-κB from cytoplasm to nucleus. These results demonstrate that HIV-1 gp120-mediated over-expression of IL-6 in astrocytes is one mechanism responsible for neuroinflammation in HIV-infected individuals and this is mediated by the NF-κB pathway

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 hospitalization2–4 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