Does Solar Physics Provide Constraints to Weakly Interacting Massive Particles?

We investigate whether present data on helioseismology and solar neutrino fluxes may constrain WIMP--matter interactions in the range of WIMP parameters under current exploration in WIMP searches. We find that, for a WIMP mass of 30 GeV, once the effect of the presence of WIMPs in the Sun's interior is maximized, the squared isothermal sound speed is modified, with respect to the standard solar model, by at most 0.4% at the Sun's center. The maximal effect on the Boron-8 solar neutrino flux is a reduction of 4.5%. Larger masses lead to smaller effects. These results imply that present sensitivities in the measurements of solar properties, though greatly improved in recent years, do not provide information or constraints on WIMP properties of relevance for dark matter. Furthermore, we show that, when current bounds from direct WIMP searches are taken into account, the effect induced by WIMPs with dominant coherent interactions are drastically reduced as compared to the values quoted above. The case of neutralinos in the minimal supersymmetric standard model is also discussed.Comment: 31 pages, 2 tables and 9 figures, typeset with ReVTeX4. The paper may also be found at http://www.to.infn.it/~fornengo/papers/helio.ps.gz or through http://www.to.infn.it/astropart/index.htm

Changes in the ceIl membrane of Lactobacillus bulgaricus during storage following freeze-drying

The mechanism of inactivation of freeze-dried Lactobacillus bulgaricus during storage in maltodextrin under controlled humidity was investigated. Evidence is presented supporting the hypothesis that membrane damage occurs during storage. A study on the lipid composition of the cells by gas chromatography showed a decrease in the unsaturated and saturated fatty acid content of the cell. Further evidence indicating membrane damage includes a decrease in membrane bound proton-translocating ATPase activity

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