On the Potential of Generic Modeling for VANET Data Aggregation Protocols

In-network data aggregation is a promising communication mechanism to reduce bandwidth requirements of applications in vehicular ad-hoc networks (VANETs). Many aggregation schemes have been proposed, often with varying features. Most aggregation schemes are tailored to specific application scenarios and for specific aggregation operations. Comparative evaluation of different aggregation schemes is therefore difficult. An application centric view of aggregation does also not tap into the potential of cross application aggregation. Generic modeling may help to unlock this potential. We outline a generic modeling approach to enable improved comparability of aggregation schemes and facilitate joint optimization for different applications of aggregation schemes for VANETs. This work outlines the requirements and general concept of a generic modeling approach and identifies open challenges

Uncovering the Mechanism of Aggregation of Human Transthyretin.

The tetrameric thyroxine transport protein transthyretin (TTR) forms amyloid fibrils upon dissociation and monomer unfolding. The aggregation of transthyretin has been reported as the cause of the life-threatening transthyretin amyloidosis. The standard treatment of familial cases of TTR amyloidosis has been liver transplantation. Although aggregation-preventing strategies involving ligands are known, understanding the mechanism of TTR aggregation can lead to additional inhibition approaches. Several models of TTR amyloid fibrils have been proposed, but the segments that drive aggregation of the protein have remained unknown. Here we identify β-strands F and H as necessary for TTR aggregation. Based on the crystal structures of these segments, we designed two non-natural peptide inhibitors that block aggregation. This work provides the first characterization of peptide inhibitors for TTR aggregation, establishing a novel therapeutic strategy

Diamond Aggregation

Internal diffusion-limited aggregation is a growth model based on random walk in Z^d. We study how the shape of the aggregate depends on the law of the underlying walk, focusing on a family of walks in Z^2 for which the limiting shape is a diamond. Certain of these walks -- those with a directional bias toward the origin -- have at most logarithmic fluctuations around the limiting shape. This contrasts with the simple random walk, where the limiting shape is a disk and the best known bound on the fluctuations, due to Lawler, is a power law. Our walks enjoy a uniform layering property which simplifies many of the proofs.Comment: v2 addresses referee comments, new section on the abelian propert

Unexpected cell type-dependent effects of autophagy on polyglutamine aggregation revealed by natural genetic variation in C. elegans.

BACKGROUND: Monogenic protein aggregation diseases, in addition to cell selectivity, exhibit clinical variation in the age of onset and progression, driven in part by inter-individual genetic variation. While natural genetic variants may pinpoint plastic networks amenable to intervention, the mechanisms by which they impact individual susceptibility to proteotoxicity are still largely unknown. RESULTS: We have previously shown that natural variation modifies polyglutamine (polyQ) aggregation phenotypes in C. elegans muscle cells. Here, we find that a genomic locus from C. elegans wild isolate DR1350 causes two genetically separable aggregation phenotypes, without changing the basal activity of muscle proteostasis pathways known to affect polyQ aggregation. We find that the increased aggregation phenotype was due to regulatory variants in the gene encoding a conserved autophagy protein ATG-5. The atg-5 gene itself conferred dosage-dependent enhancement of aggregation, with the DR1350-derived allele behaving as hypermorph. Surprisingly, increased aggregation in animals carrying the modifier locus was accompanied by enhanced autophagy activation in response to activating treatment. Because autophagy is expected to clear, not increase, protein aggregates, we activated autophagy in three different polyQ models and found a striking tissue-dependent effect: activation of autophagy decreased polyQ aggregation in neurons and intestine, but increased it in the muscle cells. CONCLUSIONS: Our data show that cryptic natural variants in genes encoding proteostasis components, although not causing detectable phenotypes in wild-type individuals, can have profound effects on aggregation-prone proteins. Clinical applications of autophagy activators for aggregation diseases may need to consider the unexpected divergent effects of autophagy in different cell types

Cross-Scale Cost Aggregation for Stereo Matching

Human beings process stereoscopic correspondence across multiple scales. However, this bio-inspiration is ignored by state-of-the-art cost aggregation methods for dense stereo correspondence. In this paper, a generic cross-scale cost aggregation framework is proposed to allow multi-scale interaction in cost aggregation. We firstly reformulate cost aggregation from a unified optimization perspective and show that different cost aggregation methods essentially differ in the choices of similarity kernels. Then, an inter-scale regularizer is introduced into optimization and solving this new optimization problem leads to the proposed framework. Since the regularization term is independent of the similarity kernel, various cost aggregation methods can be integrated into the proposed general framework. We show that the cross-scale framework is important as it effectively and efficiently expands state-of-the-art cost aggregation methods and leads to significant improvements, when evaluated on Middlebury, KITTI and New Tsukuba datasets.Comment: To Appear in 2013 IEEE Conference on Computer Vision and Pattern Recognition (CVPR). 2014 (poster, 29.88%