Compressibility Effect on the Rayleigh–Taylor Instability with Sheared Magnetic Fields

We study the effect of plasma compressibility on the Rayleigh–Taylor instability of a magnetic interface with a sheared magnetic field. We assume that the plasma is ideal and the equilibrium quantities are constant above and below the interface. We derive the dispersion equation. Written in dimensionless variables, it contains seven dimensionless parameters: the ratio of plasma densities above and below the interface ζζ, the ratio of magnetic field magnitude squared χχ, the shear angle αα, the plasma beta above and below the interface, β2β2 and β1β1, the angle between the perturbation wave number and the magnetic field direction above the interface ϕϕ, and the dimensionless wave number κκ. Only six of these parameters are independent because χχ, β1β1, and β2β2 are related by the condition of total pressure continuity at the interface. Only perturbations with the wave number smaller than the critical wave number are unstable. The critical wave number depends on ϕϕ, but it is independent of β1β1 and β2β2, and is the same as that in the incompressible plasma approximation. The dispersion equation is solved numerically with ζ=100ζ=100, χ=1χ=1, and β1=β2=ββ1=β2=β. We obtain the following results. When ββ decreases, so does the maximum instability increment. However, the effect is very moderate. It is more pronounced for high values of αα. We also calculate the dependence on ϕϕ of the maximum instability increment with respect to κκ. The instability increment takes its maximum at ϕ=ϕmϕ=ϕm. Again, the decrease of ββ results in the reduction of the instability increment. This reduction is more pronounced for high values of |ϕ−ϕm||ϕ−ϕm|. When both αα and |ϕ−ϕm||ϕ−ϕm| are small, the reduction effect is practically negligible. The theoretical results are applied to the magnetic Rayleigh–Taylor instability of prominence threads in the solar atmosphere

Identification of independent association signals and putative functional variants for breast cancer risk through fine-scale mapping of the 12p11 locus.

BACKGROUND: Multiple recent genome-wide association studies (GWAS) have identified a single nucleotide polymorphism (SNP), rs10771399, at 12p11 that is associated with breast cancer risk. METHOD: We performed a fine-scale mapping study of a 700 kb region including 441 genotyped and more than 1300 imputed genetic variants in 48,155 cases and 43,612 controls of European descent, 6269 cases and 6624 controls of East Asian descent and 1116 cases and 932 controls of African descent in the Breast Cancer Association Consortium (BCAC; http://bcac.ccge.medschl.cam.ac.uk/ ), and in 15,252 BRCA1 mutation carriers in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). Stepwise regression analyses were performed to identify independent association signals. Data from the Encyclopedia of DNA Elements project (ENCODE) and the Cancer Genome Atlas (TCGA) were used for functional annotation. RESULTS: Analysis of data from European descendants found evidence for four independent association signals at 12p11, represented by rs7297051 (odds ratio (OR) = 1.09, 95 % confidence interval (CI) = 1.06-1.12; P = 3 × 10(-9)), rs805510 (OR = 1.08, 95 % CI = 1.04-1.12, P = 2 × 10(-5)), and rs1871152 (OR = 1.04, 95 % CI = 1.02-1.06; P = 2 × 10(-4)) identified in the general populations, and rs113824616 (P = 7 × 10(-5)) identified in the meta-analysis of BCAC ER-negative cases and BRCA1 mutation carriers. SNPs rs7297051, rs805510 and rs113824616 were also associated with breast cancer risk at P < 0.05 in East Asians, but none of the associations were statistically significant in African descendants. Multiple candidate functional variants are located in putative enhancer sequences. Chromatin interaction data suggested that PTHLH was the likely target gene of these enhancers. Of the six variants with the strongest evidence of potential functionality, rs11049453 was statistically significantly associated with the expression of PTHLH and its nearby gene CCDC91 at P < 0.05. CONCLUSION: This study identified four independent association signals at 12p11 and revealed potentially functional variants, providing additional insights into the underlying biological mechanism(s) for the association observed between variants at 12p11 and breast cancer risk.UK funding includes Cancer Research UK and NIH.This is the final version of the article. It first appeared from BioMed Central via http://dx.doi.org/10.1186/s13058-016-0718-

The Cytoplasmic Tail of Invariant Chain Regulates Endosome Fusion and Morphology

The major histocompatibility complex class II associated invariant chain (Ii) has been shown to inhibit endocytic transport and to increase the size of endosomes. We have recently found that this property has a significant impact on antigen processing and presentation. Here, we show in a cell-free endosome fusion assay that expression of Ii can increase fusion after phosphatidylinositol 3-kinase activity is blocked by wortmannin. In live cells wortmannin was also not able to block formation of the Ii-induced enlarged endosomes. The effects of Ii on endosomal transport and morphology depend on elements within the cytoplasmic tail. Data from mutagenesis analysis and nuclear magnetic resonance-based structure calculations of the Ii cytoplasmic tail demonstrate that free negative charges that are not involved in internal salt bridges are essential for both interactions between the tails and for the formation of enlarged endosomes. This correlation indicates that it is interactions between the Ii cytoplasmic tails that are involved in endosome fusion. The combined data from live cells, cell-free assays, and molecular dynamic simulations suggest that Ii molecules on different vesicles can promote endosome docking and fusion and thereby control endosomal traffic of membrane proteins and endosomal content