A Randomized Greedy Algorithm for Near-Optimal Sensor Scheduling in Large-Scale Sensor Networks

We study the problem of scheduling sensors in a resource-constrained linear dynamical system, where the objective is to select a small subset of sensors from a large network to perform the state estimation task. We formulate this problem as the maximization of a monotone set function under a matroid constraint. We propose a randomized greedy algorithm that is significantly faster than state-of-the-art methods. By introducing the notion of curvature which quantifies how close a function is to being submodular, we analyze the performance of the proposed algorithm and find a bound on the expected mean square error (MSE) of the estimator that uses the selected sensors in terms of the optimal MSE. Moreover, we derive a probabilistic bound on the curvature for the scenario where{\color{black}{ the measurements are i.i.d. random vectors with bounded $\ell_2$ norm.}} Simulation results demonstrate efficacy of the randomized greedy algorithm in a comparison with greedy and semidefinite programming relaxation methods

MRI data part 1

Contains Bruker scan data (including localizer scans) as 2dseq files and can be easily read with Bruker ParaVision software. On request, data can be converted to Nifti/Dicom

MRI data part 2

Contains Bruker scan data (including localizer scans) as 2dseq files and can be easily read with Bruker ParaVision software. On request, data can be converted to Nifti/Dicom

Data from: Influence of full-length dystrophin on brain volumes in mouse models of Duchenne muscular dystrophy

Duchenne muscular dystrophy (DMD) affects besides muscle also the brain, resulting in memory and behavioral problems. The consequences of dystrophinopathy on gross macroscopic alterations are unclear. To elucidate the effect of dystrophin expression on brain morphology, we used high-resolution post-mortem MRI in mouse models that either express 0% (mdx), 100% (BL10) or a low amount of full-length dystrophin (mdx-Xist∆hs). While absence or low amounts of dystrophin did not result in significantly different whole brain volume and skull morphology, we found differences in volume of individual brain structures. The found results are in line with observations in humans, where whole brain volume was found to be reduced only in patients lacking both full-length dystrophin and the shorter isoform Dp140

Template and brain volumes

This zip file contains the following information: mouse brain template, brain ROIs, registration settings and the processed data. Each mouse brain was registered to a template mouse brain and volumes (whole brain + 22 structures) were extracted using the ROIs. Volumes are stored [per structure per mouse] and volumes are stored [per structure per strain]

Prednisolone Treatment Does Not Interfere with 2′- O

In Duchenne muscular dystrophy (DMD), dystrophin deficiency leading to progressive muscular degeneration is caused by frame-shifting mutations in the DMD gene. Antisense oligonucleotides (AONs) aim to restore the reading frame by skipping of a specific exon(s), thereby allowing the production of a shorter, but semifunctional protein, as is found in the mostly more mildly affected patients with Becker muscular dystrophy. AONs are currently being investigated in phase 3 placebo-controlled clinical trials. Most of the participating patients are treated symptomatically with corticosteroids (mainly predniso[lo]ne) to stabilize the muscle fibers, which might affect the uptake and/or efficiency of AONs. Therefore the effect of prednisolone on 2'-O-methyl phosphorothioate AON efficacy in patient-derived cultured muscle cells and the mdx mouse model (after local and systemic AON treatment) was assessed in this study. Both in vitro and in vivo skip efficiency and biomarker expression were comparable between saline- and prednisolone-cotreated cells and mice. After systemic exon 23-specific AON (23AON) treatment for 8 weeks, dystrophin was detectable in all treated mice. Western blot analyses indicated slightly higher dystrophin levels in prednisolone-treated mice, which might be explained by better muscle condition and consequently more target dystrophin pre-mRNA. In addition, fibrotic and regeneration biomarkers were normalized to some extent in prednisolone- and/or 23AON-treated mice. Overall these results show that the use of prednisone forms no barrier to participation in clinical trials with AONs

Data from: Influence of full-length dystrophin on brain volumes in mouse models of Duchenne muscular dystrophy

Duchenne muscular dystrophy (DMD) affects besides muscle also the brain, resulting in memory and behavioral problems. The consequences of dystrophinopathy on gross macroscopic alterations are unclear. To elucidate the effect of dystrophin expression on brain morphology, we used high-resolution post-mortem MRI in mouse models that either express 0% (mdx), 100% (BL10) or a low amount of full-length dystrophin (mdx-Xist∆hs). While absence or low amounts of dystrophin did not result in significantly different whole brain volume and skull morphology, we found differences in volume of individual brain structures. The found results are in line with observations in humans, where whole brain volume was found to be reduced only in patients lacking both full-length dystrophin and the shorter isoform Dp140

A modified diet does not ameliorate muscle pathology in a mouse model for Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is caused by a lack of dystrophin protein. Next to direct effects on the muscles, this has also metabolic consequences. The influence of nutrition on disease progression becomes more and more recognized. Protein intake by DMD patients may be insufficient to meet the increased demand of the constantly regenerating muscle fibers. This led to the hypothesis that improving protein uptake by the muscles could have therapeutic effects. The present study examined the effects of a modified diet, which composition might stimulate muscle growth, on disease pathology in the D2-mdx mouse model. D2-mdx males were fed with either a control diet or modified diet, containing high amounts of branched-chain amino acids, vitamin D3 and ursolic acid, for six weeks. Our study indicates that the modified diet could not ameliorate the muscle pathology. No effects on bodyweight or weight of individual muscles were observed. Neither did the diet affect severity of fibrosis or calcification of the muscles