Institution
Technion – Israel Institute of Technology
Education•Haifa, Israel•
About: Technion – Israel Institute of Technology is a education organization based out in Haifa, Israel. It is known for research contribution in the topics: Population & Nonlinear system. The organization has 31714 authors who have published 79377 publications receiving 2603976 citations. The organization is also known as: Technion Israel Institute of Technology & Ṭekhniyon, Makhon ṭekhnologi le-Yiśraʼel.
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Papers
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25 Feb 2010TL;DR: The role of this recent model in image processing, its rationale, and models related to it are reviewed; ways to employ these tools for various image-processing tasks are discussed and several applications in which state-of-the-art results are obtained.
Abstract: Much of the progress made in image processing in the past decades can be attributed to better modeling of image content and a wise deployment of these models in relevant applications. This path of models spans from the simple l2-norm smoothness through robust, thus edge preserving, measures of smoothness (e.g. total variation), and until the very recent models that employ sparse and redundant representations. In this paper, we review the role of this recent model in image processing, its rationale, and models related to it. As it turns out, the field of image processing is one of the main beneficiaries from the recent progress made in the theory and practice of sparse and redundant representations. We discuss ways to employ these tools for various image-processing tasks and present several applications in which state-of-the-art results are obtained.
710 citations
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University College London1, University of Oxford2, Case Western Reserve University3, Mayo Clinic4, University of Pennsylvania5, University Hospitals Bristol NHS Foundation Trust6, Scottish National Blood Transfusion Service7, Nottingham University Hospitals NHS Trust8, Northwestern University9, Technion – Israel Institute of Technology10
TL;DR: It is concluded from a large, unselected series with mature follow-up that most adults with recurring ALL cannot be rescued using currently available therapies and prevention of recurrence is the best strategy for long-term survival in this disease.
710 citations
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TL;DR: The FOG questionnaire that was constructed is highly reliable in assessing freezing of gait, unrelated to falls, in patients with PD.
704 citations
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TL;DR: It is shown that ENaC is a short‐lived protein that is ubiquitinated in vivo on the α and γ (but not β) subunits, and a paradigm for ubiquitination‐mediated regulation of ion channels is proposed.
Abstract: The epithelial Na+ channel (ENaC), composed of three subunits (alpha beta gamma), plays a critical role in salt and fluid homeostasis. Abnormalities in channel opening and numbers have been linked to several genetic disorders, including cystic fibrosis, pseudohypoaldosteronism type I and Liddle syndrome. We have recently identified the ubiquitin-protein ligase Nedd4 as an interacting protein of ENaC. Here we show that ENaC is a short-lived protein (t1/2 approximately 1 h) that is ubiquitinated in vivo on the alpha and gamma (but not beta) subunits. Mutation of a cluster of Lys residues (to Arg) at the N-terminus of gamma ENaC leads to both inhibition of ubiquitination and increased channel activity, an effect augmented by N-terminal Lys to Arg mutations in alpha ENaC, but not in beta ENaC. This elevated channel activity is caused by an increase in the number of channels present at the plasma membrane; it represents increases in both cell-surface retention or recycling of ENaC and incorporation of new channels at the plasma membrane, as determined by Brefeldin A treatment. In addition, we find that the rapid turnover of the total pool of cellular ENaC is attenuated by inhibitors of both the proteasome and the lysosomal/endosomal degradation systems, and propose that whereas the unassembled subunits are degraded by the proteasome, the assembled alpha beta gamma ENaC complex is targeted for lysosomal degradation. Our results suggest that ENaC function is regulated by ubiquitination, and propose a paradigm for ubiquitination-mediated regulation of ion channels.
702 citations
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TL;DR: The natural phenotypic variability in a large population of motile epithelial keratocytes from fish to reveal mechanisms of shape determination is harnessed and it is found that the cells inhabit a low-dimensional, highly correlated spectrum of possible functional states.
Abstract: The shape of motile cells is determined by many dynamic processes spanning several orders of magnitude in space and time, from local polymerization of actin monomers at subsecond timescales to global, cell-scale geometry that may persist for hours. Understanding the mechanism of shape determination in cells has proved to be extremely challenging due to the numerous components involved and the complexity of their interactions. Here we harness the natural phenotypic variability in a large population of motile epithelial keratocytes from fish (Hypsophrys nicaraguensis) to reveal mechanisms of shape determination. We find that the cells inhabit a low-dimensional, highly correlated spectrum of possible functional states. We further show that a model of actin network treadmilling in an inextensible membrane bag can quantitatively recapitulate this spectrum and predict both cell shape and speed. Our model provides a simple biochemical and biophysical basis for the observed morphology and behaviour of motile cells.
701 citations
Authors
Showing all 31937 results
Name | H-index | Papers | Citations |
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Robert Langer | 281 | 2324 | 326306 |
Nicholas G. Martin | 192 | 1770 | 161952 |
Tobin J. Marks | 159 | 1621 | 111604 |
Grant W. Montgomery | 157 | 926 | 108118 |
David Eisenberg | 156 | 697 | 112460 |
David J. Mooney | 156 | 695 | 94172 |
Dirk Inzé | 149 | 647 | 74468 |
Jerrold M. Olefsky | 143 | 595 | 77356 |
Joseph J.Y. Sung | 142 | 1240 | 92035 |
Deborah Estrin | 135 | 562 | 106177 |
Bruce Yabsley | 133 | 1191 | 84889 |
Jerry W. Shay | 133 | 639 | 74774 |
Richard N. Bergman | 130 | 477 | 91718 |
Shlomit Tarem | 129 | 1306 | 86919 |
Allen Mincer | 129 | 1040 | 80059 |