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Institution

University of Texas at Dallas

EducationRichardson, Texas, United States
About: University of Texas at Dallas is a education organization based out in Richardson, Texas, United States. It is known for research contribution in the topics: Population & Computer science. The organization has 14986 authors who have published 35589 publications receiving 1293714 citations. The organization is also known as: UT-Dallas & UT Dallas.


Papers
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Journal ArticleDOI
TL;DR: Using solution spinning, which involves an intermediate gel-state, they obtained exceptionally strong carbon nanotube fibers that are tougher than either spider silk or any fiber used for mechanical reinforcement as discussed by the authors.
Abstract: Using solution spinning, which involves an intermediate gel-state, we obtained exceptionally strong carbon nanotube fibers that are tougher than either spider silk or any fiber used for mechanical reinforcement. We use these fibers to make 100 micron diameter supercapacitors and electronic textiles. Per weight, the energy needed to break these fibers is about 4× higher than spider dragline silk and 20× higher than steel wire. This article describes this advance, comparisons with the prior art, potential applications, and present barriers for large volume applications.

250 citations

Journal ArticleDOI
TL;DR: It is found that NAc MSNs have more stubby spine structures with smaller postsynaptic densities and an increase in the frequency of mEPSCs after social defeat, and activation of IKK signaling pathways during social defeat is both necessary and sufficient to induce synaptic alterations and behavioral effects of the stress.
Abstract: The neurobiological underpinnings of mood and anxiety disorders have been linked to the nucleus accumbens (NAc), a region important in processing the rewarding and emotional salience of stimuli. Using chronic social defeat stress, an animal model of mood and anxiety disorders, we investigated whether alterations in synaptic plasticity are responsible for the long-lasting behavioral symptoms induced by this form of stress. We hypothesized that chronic social defeat stress alters synaptic strength or connectivity of medium spiny neurons (MSNs) in the NAc to induce social avoidance. To test this, we analyzed the synaptic profile of MSNs via confocal imaging of Lucifer-yellow-filled cells, ultrastructural analysis of the postsynaptic density, and electrophysiological recordings of miniature EPSCs (mEPSCs) in mice after social defeat. We found that NAc MSNs have more stubby spine structures with smaller postsynaptic densities and an increase in the frequency of mEPSCs after social defeat. In parallel to these structural changes, we observed significant increases in IκB kinase (IKK) in the NAc after social defeat, a molecular pathway that has been shown to regulate neuronal morphology. Indeed, we find using viral-mediated gene transfer of dominant-negative and constitutively active IKK mutants that activation of IKK signaling pathways during social defeat is both necessary and sufficient to induce synaptic alterations and behavioral effects of the stress. These studies establish a causal role for IKK in regulating stress-induced adaptive plasticity and may present a novel target for drug development in the treatment of mood and anxiety disorders in humans.

250 citations

Journal Article
TL;DR: The expression of alpha-SM actin was directly correlated to corneal wound contraction, appearing at the initiation of and disappearing at the completion of the contraction process, suggesting that local environmental factors unique to the wound may play an important role in myofibroblast transformation.
Abstract: Purpose The purpose of this study was to correlate the temporal expression of alpha-smooth muscle specific actin (alpha-SM actin), a molecular marker for myofibroblast transformation, with corneal wound contraction. Methods After full-thickness, central corneal injury in rabbit eyes, the anterior width of the wound (wound gape) was measured in the same animals using in vivo confocal microscopy. In addition, animals were sacrificed at various times after injury for the determination of alpha-SM actin expression by immunofluorescent microscopy using a mouse monoclonal antibody specific for human alpha-actin. Antibody specificity was confirmed by Western blot analysis of normal and wound fibroblasts. Expression of alpha-SM actin also was related spatially to f-actin and the wound margin by co-localization with phalloidin and DTAF (5([4,6-dichlorotriazin-2yl]amino)fluorescein), a fluorescent marker bound to the wound margin. Results Wound contraction was most evident from days 7 to 42, when wound gape progressively decreased from 574 +/- 120 microns to 250 +/- 61 microns. Thereafter, the wound remained stable to day 84 (304 +/- 58 microns). Expression of alpha-SM actin directly correlated with wound contraction--appearing across the wound at day 7, the full thickness of the wound at day 14, and the posterior wound at day 28. alpha-SM actin was localized exclusively to phalloidin-stained, f-actin microfilament bundles or stress fibers within wound healing fibroblasts, and the disappearance of alpha-SM actin correlated with the concomitant disappearance of stress fibers at days 28 to 42. Staining of the wound margin with DTAF confirmed that the expression of alpha-SM actin was limited to fibroblasts within the wound. Conclusions The expression of alpha-SM actin was directly correlated to corneal wound contraction, appearing at the initiation of and disappearing at the completion of the contraction process. Furthermore, the exclusive expression of alpha-SM actin by fibroblasts present only within the wound suggests that local environmental factors unique to the wound may play an important role in myofibroblast transformation.

250 citations

Journal ArticleDOI
Georges Aad1, Brad Abbott2, J. Abdallah, A. A. Abdelalim3  +3034 moreInstitutions (195)
TL;DR: In this paper, the production cross sections of the inclusive Drell-Yan processes W-+/- -> l nu and Z/gamma* -> ll (l = e, mu) are measured in proton-proton collisions at root s = 7 TeV with the ATLAS detector.
Abstract: The production cross sections of the inclusive Drell-Yan processes W-+/- -> l nu and Z/gamma* -> ll (l = e, mu) are measured in proton-proton collisions at root s = 7 TeV with the ATLAS detector. The cross sections are reported integrated over a fiducial kinematic range, extrapolated to the full range, and also evaluated differentially as a function of the W decay lepton pseudorapidity and the Z boson rapidity, respectively. Based on an integrated luminosity of about 35 pb(-1) collected in 2010, the precision of these measurements reaches a few percent. The integrated and the differential W-+/- and Z/gamma* cross sections in the e and mu channels are combined, and compared with perturbative QCD calculations, based on a number of different parton distribution sets available at next-to-next-to-leading order.

250 citations

Journal ArticleDOI
TL;DR: A role for LRP is proposed in the clearance of plasminogen activator-inhibitor complexes that is analogous to its function in the endocytosis of alpha 2-macroglobulin-protease complexes.
Abstract: Tissue-type plasminogen activator and urokinase are serine proteases secreted by many cell types that participate in biological processes, such as tissue restructuring, cell migration, and tumor metastasis. Clinically, these proteases are used to dissolve coronary fibrin clots that are the proximal causes of acute myocardial infarction. In vivo, the activity of these enzymes is controlled by plasminogen-activator inhibitors, members of the serpin family of protease inhibitors. This study shows that tissue-type plasminogen activator-inhibitor complexes bind in solution to low density lipoprotein receptor-related protein (LRP), a large heterodimeric ubiquitous membrane receptor. In cultured cells, endocytosis and degradation of these complexes is reduced by polyclonal antibodies directed against LRP and inhibited by a M(r) 39,000 protein that binds to LRP and inhibits its interaction with previously known ligands, including apolipoprotein E and alpha 2-macroglobulin. We propose a role for LRP in the clearance of plasminogen activator-inhibitor complexes that is analogous to its function in the endocytosis of alpha 2-macroglobulin-protease complexes.

249 citations


Authors

Showing all 15148 results

NameH-indexPapersCitations
Eugene Braunwald2301711264576
Younan Xia216943175757
Eric N. Olson206814144586
Thomas C. Südhof191653118007
Scott M. Grundy187841231821
Jing Wang1844046202769
Eric Boerwinkle1831321170971
Eric J. Nestler178748116947
John D. Minna169951106363
Elliott M. Antman161716179462
Adi F. Gazdar157776104116
Bruce D. Walker15577986020
R. Kowalewski1431815135517
Joseph Izen137143398900
James A. Richardson13636375778
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20241
202371
2022217
20212,152
20202,227
20192,192