Noisy random resistor networks: renormalized field theory for the multifractal moments of the current distribution

We study the multifractal moments of the current distribution in randomly diluted resistor networks near the percolation treshold. When an external current is applied between to terminals $x$ and $x^\prime$ of the network, the $l$th multifractal moment scales as $M_I^{(l)} (x, x^\prime) \sim | x - x^\prime |^{\psi_l /\nu}$, where $\nu$ is the correlation length exponent of the isotropic percolation universality class. By applying our concept of master operators [Europhys. Lett. {\bf 51}, 539 (2000)] we calculate the family of multifractal exponents $\{\psi_l \}$ for $l \geq 0$ to two-loop order. We find that our result is in good agreement with numerical data for three dimensions.Comment: 30 pages, 6 figure

Modeling of ACTN4-based podocytopathy using Drosophila nephrocytes

INTRODUCTION: Genetic disorders are among the most prevalent causes leading to progressive glomerular disease and, ultimately, end-stage renal disease in children and adolescents. Identification of underlying genetic causes is indispensable for targeted treatment strategies and counseling of affected patients and their families. METHODS: Here, we report a boy who presented at four years of age with proteinuria and biopsy-proven focal segmental glomerulosclerosis that was temporarily responsive to treatment with Ciclosporin A. Molecular genetic testing identified a novel mutation in alpha-actinin-4 (p.M240T). We describe a feasible and efficient experimental approach to test its pathogenicity by combining in silico, in vitro, and in vivo analyses. RESULTS: The de novo p.M240T mutation led to decreased alpha-Actinin-4 stability as well as protein mislocalization and actin cytoskeleton rearrangements. Transgenic expression of wild-type human alpha-Actinin-4 in Drosophila melanogaster nephrocytes was able to ameliorate phenotypes associated with the knockdown of endogenous Actinin. In contrast, p.M240T, as well as other established disease variants p.W59R and p.K255E, failed to rescue these phenotypes, underlining the pathogenicity of the novel alpha-Actinin-4 variant. CONCLUSION: Our data highligh that the newly identified alpha-actinin-4 mutation indeed encodes for a disease-causing variant of the protein and promote the Drosophila model as a simple and convenient tool to study monogenic kidney disease in vivo