114 research outputs found
Content name resolution service implementation for cache and forward network architecture
No full textCache aNd Forward (CNF) is a proposed architecture for content delivery services in the future Internet. The CNF architecture takes advantage of reductions in storage to design a network that directly addresses the mobile content delivery problem. The CNF architecture uses a content name resolution service protocol, along with a reliable hop-by-hop transport protocol, storage aware routing protocol in place of end-to-end TCP for reliable delivery of large files. This thesis presents the algorithms proposed for a distributed name resolution protocol and design and experimental evaluation of the protocol on ORBIT in context of a multi-hop wireless access network scenario. The protocol is designed using hashing technique such that when a host queries for a file, the name service will be triggered and will return the addresses of nodes that cache the file. Since our architecture is about caching and forwarding large content files, enabling hosts to retrieve files from the network and not necessarily from the origin server, we need to uniquely identify the files. To that effect, we propose to identify a file using a unique content identifier (CID) where CID is obtained by a one way hashing (SHA1) on the content itself. The aim here is to optimize selection of cache location and serve the host with the file from the nearest location. If the selected cache location is determined to be temporarily degraded, either due to poor channel conditions or mobility, the protocol uses multiple hash technique to provide alternate cache locations and the decision is based on the ETT metric provided by the routing protocol. The CNRS protocol over multi-hop 802.11 access networks with CNF routers has been implemented as a real-time proof-of-concept prototype on the ORBIT testbed. Baseline results for CNRS with hop-by-hop transport show that content based CNF network architecture performs better than TCP/IP stack. Using different content distributions, we have shown that multiple hashing, popularity based and location based caching provide significant gains over the baseline algorithm.M.S.Includes bibliographical referencesby Puneet Katari
Mutations in the cytoplasmic iron-sulfur assembly protein CIAO1 cause neuromuscular deficits
No full textDetermination of the octanol-water partition coefficient of indolicidin and indolicidin45 using micellar electrokinetic chromatography
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Giant axonal neuropathy–associated gigaxonin mutations impair intermediate filament protein degradation
No full textAuthor Posting. © American Society for Clinical Investigation, 2013. This article is posted here by permission of American Society for Clinical Investigation for personal use, not for redistribution. The definitive version was published in Journal of Clinical Investigation 123 (2013): 1964–1975, doi:10.1172/JCI66387.Giant axonal neuropathy (GAN) is an early-onset neurological disorder caused by mutations in the GAN gene (encoding for gigaxonin), which is predicted to be an E3 ligase adaptor. In GAN, aggregates of intermediate filaments (IFs) represent the main pathological feature detected in neurons and other cell types, including patients’ dermal fibroblasts. The molecular mechanism by which these mutations cause IFs to aggregate is unknown. Using fibroblasts from patients and normal individuals, as well as Gan–/– mice, we demonstrated that gigaxonin was responsible for the degradation of vimentin IFs. Gigaxonin was similarly involved in the degradation of peripherin and neurofilament IF proteins in neurons. Furthermore, proteasome inhibition by MG-132 reversed the clearance of IF proteins in cells overexpressing gigaxonin, demonstrating the involvement of the proteasomal degradation pathway. Together, these findings identify gigaxonin as a major factor in the degradation of cytoskeletal IFs and provide an explanation for IF aggregate accumulation, the subcellular hallmark of this devastating human disease.This work was
supported by NIH grants 1P01GM096971 (to R.D. Goldman) and
R01 NS062051 (to P. Opal) and a grant from Hannah’s Hope Fund
(to R.D. Goldman and P. Opal)
Genetic Instabilities and Hereditary Neurological Diseases R.D.WellsS.T.WarrenGenetic Instabilities and Hereditary Neurological Diseases1997Academic PressSan Diego829$159.95
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