Critical weak-LpL^{p} differentiability of singular integrals

We establish that for every function $u \in L^1_\mathrm{loc}(\Omega)$ whose distributional Laplacian $\Delta u$ is a signed Borel measure in an open set $\Omega$ in $\mathbb{R}^{N}$, the distributional gradient $\nabla u$ is differentiable almost everywhere in $\Omega$ with respect to the weak-$L^{\frac{N}{N-1}}$ Marcinkiewicz norm. We show in addition that the absolutely continuous part of $\Delta u$ with respect to the Lebesgue measure equals zero almost everywhere on the level sets $\{u = \alpha\}$ and $\{\nabla u = e\}$, for every $\alpha \in \mathbb{R}$ and $e \in \mathbb{R}^N$. Our proofs rely on an adaptation of Calder\'on and Zygmund's singular-integral estimates inspired by subsequent work by Hajlasz.Comment: Accepted for publication in Revista Matem\'atica Iberoamerican

Push or Pull? An Empirical Analysis of the Demand for Individual Project Grants from the Swiss National Science Foundation

This study empirically analyses on the basis of a panel of grant requests to the Swiss National Science Foundation (SNSF. From the results it can be concluded, that the different scientific disciplines react in very different ways to the institutional and financial framework conditions set by the funding agency. Regarding the expansion of the tertiary educational system it can concluded that it has an impact on research funding in the form of two contrary influences. These two effects offset each other to the extent that they do not suffice to explain the rising trend in terms of the number of requests observable as from the year 2000.research funding, universities, panel estimations

Chronologie de l'activité volcanique historique de l'arc insulaire des Nouvelles-Hébrides de 1595 à 1991 = Chronology of the historic volcanic activity of the New Hebrides island arc from 1595 to 1991

Etude chronologique, volcan par volcan, de l'activité historique ou récente des volcans de l'arc insulaire des Nouvelles-Hébride

Rho-ROCK and Rac-PAK signaling pathways have opposing effects on the cell-to-cell spread of Marek's Disease Virus.

Marek's Disease Virus (MDV) is an avian alpha-herpesvirus that only spreads from cell-to-cell in cell culture. While its cell-to-cell spread has been shown to be dependent on actin filament dynamics, the mechanisms regulating this spread remain largely unknown. Using a recombinant BAC20 virus expressing an EGFPVP22 tegument protein, we found that the actin cytoskeleton arrangements and cell-cell contacts differ in the center and periphery of MDV infection plaques, with cells in the latter areas showing stress fibers and rare cellular projections. Using specific inhibitors and activators, we determined that Rho-ROCK pathway, known to regulate stress fiber formation, and Rac-PAK, known to promote lamellipodia formation and destabilize stress fibers, had strong contrasting effects on MDV cell-to-cell spread in primary chicken embryo skin cells (CESCs). Inhibition of Rho and its ROCKs effectors led to reduced plaque sizes whereas inhibition of Rac or its group I-PAKs effectors had the adverse effect. Importantly, we observed that the shape of MDV plaques is related to the semi-ordered arrangement of the elongated cells, at the monolayer level in the vicinity of the plaques. Inhibition of Rho-ROCK signaling also resulted in a perturbation of the cell arrangement and a rounding of plaques. These opposing effects of Rho and Rac pathways in MDV cell-to-cell spread were validated for two parental MDV recombinant viruses with different ex vivo spread efficiencies. Finally, we demonstrated that Rho/Rac pathways have opposing effects on the accumulation of N-cadherin at cell-cell contact regions between CESCs, and defined these contacts as adherens junctions. Considering the importance of adherens junctions in HSV-1 cell-to-cell spread in some cell types, this result makes of adherens junctions maintenance one potential and attractive hypothesis to explain the Rho/Rac effects on MDV cell-to-cell spread. Our study provides the first evidence that MDV cell-to-cell spread is regulated by Rho/Rac signaling