Groundstates for a local nonlinear perturbation of the Choquard equations with lower critical exponent

We prove the existence of ground state solutions by variational methods to the nonlinear Choquard equations with a nonlinear perturbation $$-{\Delta}u+ u=\big(I_\alpha*|u|^{\frac{\alpha}{N}+1}\big)|u|^{\frac{\alpha}{N}-1}u+f(x,u)\qquad \text{ in } \mathbb{R}^N$$ where $N\geq 1$, $I_\alpha$ is the Riesz potential of order $\alpha \in (0, N)$, the exponent $\frac{\alpha}{N}+1$ is critical with respect to the Hardy--Littlewood--Sobolev inequality and the nonlinear perturbation $f$ satisfies suitable growth and structural assumptions.Comment: 18 page

Standing waves with a critical frequency for nonlinear Choquard equations

In this paper, we study the nonlocal Choquard equation $$-\varepsilon^2 \Delta u_\varepsilon + V u_\varepsilon= (I_\alpha * |u_\varepsilon|^p)|u_\varepsilon|^{p-2}u_\varepsilon$$ where $N\geq 1$, $I_\alpha$ is the Riesz potential of order $\alpha \in (0, N)$ and $\varepsilon>0$ is a parameter. When the nonnegative potential $V\in C (\mathbb{R}^N)$ achieves $0$ with a homogeneous behaviour or on the closure of an open set but remains bounded away from $0$ at infinity, we show the existence of groundstate solutions for small $\varepsilon>0$ and exhibit the concentration behaviour as $\varepsilon\to 0$.Comment: 22 page

Adipocytes cause leukemia cell resistance to daunorubicin via oxidative stress response.

Adipocytes promote cancer progression and impair treatment, and have been shown to protect acute lymphoblastic leukemia (ALL) cells from chemotherapies. Here we investigate whether this protection is mediated by changes in oxidative stress. Co-culture experiments showed that adipocytes protect ALL cells from oxidative stress induced by drugs or irradiation. We demonstrated that ALL cells induce intracellular ROS and an oxidative stress response in adipocytes. This adipocyte oxidative stress response leads to the secretion of soluble factors which protect ALL cells from daunorubicin (DNR). Collectively, our investigation shows that ALL cells elicit an oxidative stress response in adipocytes, leading to adipocyte protection of ALL cells against DNR

Mini-NOVA: A Lightweight ARM-based Virtualization Microkernel Supporting Dynamic Partial Reconfiguration

International audienceToday, ARM is becoming the mainstream family of processors in the high-performance embedded systems domain. In this context, adding a run-time reconfigurable FPGA device to the ARM processor into a single chip makes it possible to combine high performance and flexibility. In this paper, we propose a low-complexity design of system virtualization running on the Zynq platform. Virtualization of software and hardware resources are managed by a custom microkernel. The dedicated features to efficiently manage the dynamic partial reconfiguration (DPR) technology are described in details. The performance of the DPR management is evaluated and presented at the end of this paper

Hydrogen Lyman-alpha and Lyman-beta radiances and profiles in polar coronal holes

The hydrogen Lyman-alpha plays a dominant role in the radiative energy transport in the lower transition region, and is important for the stud- ies of transition-region structure as well as solar wind origin. We investigate the Ly-alpha profiles obtained by SUMER in coronal holes and quiet Sun. In a subset of these observations, also the Hi Lyman-beta, Si iii, and O vi lines were (quasi-) simultaneously recorded. We find that the distances between the two peaks of Ly-alpha profiles are larger in coronal holes than in the quiet Sun, indicating a larger opacity in coronal holes. This difference might result from the different magnetic structures or the different radiation fields in the two regions. Most of the Ly-beta profiles in the coronal hole have a stronger blue peak, in contrast to those in quiet-Sun regions. Whilst in both regions the Ly-alpha profiles are stronger in the blue peak. Although the asymmetries are likely to be produced by differential flows in the solar atmosphere, their detailed formation processes are still unclear. The radiance ratio between Ly-alpha and Ly-beta decreases towards the limb in the coronal hole, which might be due to the different opacity of the two lines. We also find that the radiance distributions of the four lines are set by a combined effect of limb brightening and the different emission level between coronal holes and quiet Sun.Comment: 13 pages,4 figures, 1 talbe, accepted by Ap

The autophagic degradation of cytosolic pools of peroxisomal proteins by a new selective pathway.

Damaged or redundant peroxisomes and their luminal cargoes are removed by pexophagy, a selective autophagy pathway. In yeasts, pexophagy depends mostly on the pexophagy receptors, such as Atg30 for Pichia pastoris and Atg36 for Saccharomyces cerevisiae, the autophagy scaffold proteins, Atg11 and Atg17, and the core autophagy machinery. In P. pastoris, the receptors for peroxisomal matrix proteins containing peroxisomal targeting signals (PTSs) include the PTS1 receptor, Pex5, and the PTS2 receptor and co-receptor, Pex7 and Pex20, respectively. These shuttling receptors are predominantly cytosolic and only partially peroxisomal. It remains unresolved as to whether, when and how the cytosolic pools of peroxisomal receptors, as well as the peroxisomal matrix proteins, are degraded under pexophagy conditions. These cytosolic pools exist both in normal and mutant cells impaired in peroxisome biogenesis. We report here that Pex5 and Pex7, but not Pex20, are degraded by an Atg30-independent, selective autophagy pathway. To enter this selective autophagy pathway, Pex7 required its major PTS2 cargo, Pot1. Similarly, the degradation of Pex5 was inhibited in cells missing abundant PTS1 cargoes, such as alcohol oxidases and Fox2 (hydratase-dehydrogenase-epimerase). Furthermore, in cells deficient in PTS receptors, the cytosolic pools of peroxisomal matrix proteins, such as Pot1 and Fox2, were also removed by Atg30-independent, selective autophagy, under pexophagy conditions. In summary, the cytosolic pools of PTS receptors and their cargoes are degraded via a pexophagy-independent, selective autophagy pathway under pexophagy conditions. These autophagy pathways likely protect cells from futile enzymatic reactions that could potentially cause the accumulation of toxic cytosolic products.Abbreviations: ATG: autophagy related; Cvt: cytoplasm to vacuole targeting; Fox2: hydratase-dehydrogenase-epimerase; PAGE: polyacrylamide gel electrophoresis; Pot1: thiolase; PMP: peroxisomal membrane protein; Pgk1: 3-phosphoglycerate kinase; PTS: peroxisomal targeting signal; RADAR: receptor accumulation and degradation in the absence of recycling; RING: really interesting new gene; SDS: sodium dodecyl sulphate; TCA, trichloroacetic acid; Ub: ubiquitin; UPS: ubiquitin-proteasome system Vid: vacuole import and degradation

Generation of vortex lattices at the liquid-gas interface using rotating surface waves

In this paper, we demonstrate experimentally that by generating two orthogonal standing waves at the liquid surface, one can control the motion of floating microparticles. The mechanism of the vortex generation is somewhat similar to a classical Stokes drift in linear progression waves. By adjusting the relative phase between the waves, it is possible to generate a vortex lattice, seen as a stationary horizontal flow consisting of counter-rotating vortices. Two orthogonal waves which are phase-shifted by π/2 create locally rotating waves. Such waves induce nested circular drift orbits of the surface fluid particles. Such a configuration allows for the trapping of particles within a cell of the size about half the wavelength of the standing waves. By changing the relative phase, it is possible to either create or to destroy the vortex crystal. This method creates an opportunity to confine surface particles within cells, or to greatly increase mixing of the surface matter over the wave field surface.This work was supported by the Australian Research Council’s Discovery Projects funding scheme DP160100863 and Linkage Projects funding scheme LP160100477. H.X. acknowledges support from the Australian Research Council’s Future Fellowship (FT140100067). N.F. acknowledges support by the Australian Research Council’s DECRA award (DE160100742)