Institution
University of Würzburg
Education•Wurzburg, Bayern, Germany•
About: University of Würzburg is a education organization based out in Wurzburg, Bayern, Germany. It is known for research contribution in the topics: Population & CAS Registry Number. The organization has 31437 authors who have published 62203 publications receiving 2337033 citations. The organization is also known as: Julius-Maximilians-Universität Würzburg & Würzburg University.
Topics: Population, CAS Registry Number, Immune system, Gene, T cell
Papers published on a yearly basis
Papers
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TL;DR: In this paper, a search for new phenomena in final states with an energetic jet and large missing transverse momentum is reported, and the results are translated into exclusion limits in models with pair-produced weakly interacting dark-matter candidates, large extra spatial dimensions, and supersymmetric particles in several compressed scenarios.
Abstract: Results of a search for new phenomena in final states with an energetic jet and large missing transverse momentum are reported. The search uses proton-proton collision data corresponding to an integrated luminosity of 36.1 fb−1 at a centre-of-mass energy of 13 TeV collected in 2015 and 2016 with the ATLAS detector at the Large Hadron Collider. Events are required to have at least one jet with a transverse momentum above 250 GeV and no leptons (e or μ). Several signal regions are considered with increasing requirements on the missing transverse momentum above 250 GeV. Good agreement is observed between the number of events in data and Standard Model predictions. The results are translated into exclusion limits in models with pair-produced weakly interacting dark-matter candidates, large extra spatial dimensions, and supersymmetric particles in several compressed scenarios.
358 citations
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358 citations
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TL;DR: In this paper, the authors provided direct evidence that an autoimmune attack directed against the cardiac beta(1)-adrenergic receptor may play a causal role in dilated cardiomyopathy.
Abstract: Today, dilated cardiomyopathy (DCM) represents the main cause of severe heart failure and disability in younger adults and thus is a challenge for public health. About 30% of DCM cases are genetic in origin; however, the large majority of cases are sporadic, and a viral or immune pathogenesis is suspected. Following the established postulates for pathogenesis of autoimmune diseases, here we provide direct evidence that an autoimmune attack directed against the cardiac beta(1)-adrenergic receptor may play a causal role in DCM. First, we immunized inbred rats against the second extracellular beta(1)-receptor loop (beta(1)-EC(II); 100% sequence identity between human and rat) every month. All these rats developed first, receptor-stimulating anti-beta(1)-EC(II) Ab's and then, after 9 months, progressive severe left ventricular dilatation and dysfunction. Second, we transferred sera from anti-beta(1)-EC(II)-positive and Ab-negative animals every month to healthy rats of the same strain. Strikingly, all anti-beta(1)-EC(II)-transferred rats also developed a similar cardiomyopathic phenotype within a similar time frame, underlining the pathogenic potential of these receptor Ab's. As a consequence, beta(1)-adrenergic receptor-targeted autoimmune DCM should now be categorized with other known receptor Ab-mediated autoimmune diseases, such as Graves disease or myasthenia gravis. Although carried out in an experimental animal model, our findings should further encourage the development of therapeutic strategies that combat harmful anti-beta(1)-EC(II) in receptor Ab-positive DCM patients.
357 citations
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University of Mississippi Medical Center1, Veterans Health Administration2, University of Louisville3, University at Buffalo4, The Heart Research Institute5, Albert Einstein College of Medicine6, University of Würzburg7, Virginia Tech8, University of Virginia9, Huntington Medical Research Institutes10, University of Southern California11, Louisiana State University12, Harvard University13, National Institutes of Health14, University of California, Los Angeles15, Wayne State University16, Sant'Anna School of Advanced Studies17, Temple University18, University of California, Davis19, Cedars-Sinai Medical Center20, University of Duisburg-Essen21
TL;DR: The goal of this review is to provide best practice information regarding myocardial ischemia-reperfusion and infarction models and to provide increasing awareness of the need for rigor and reproducibility in designing and performing scientific research to ensure validation of results.
Abstract: Myocardial infarction is a prevalent major cardiovascular event that arises from myocardial ischemia with or without reperfusion, and basic and translational research is needed to better understand...
357 citations
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TL;DR: This summary of the pathophysiology of heart failure tries to give a compact overview of basic mechanisms and of the novel unfolding, progressive theory ofHeart failure to contribute to a more comprehensive knowledge of the disease.
Abstract: Heart failure is considered an epidemic disease in the modern world affecting approximately 1% to 2% of adult population. It presents a multifactorial, systemic disease, in which--after cardiac injury--structural, neurohumoral, cellular, and molecular mechanisms are activated and act as a network to maintain physiological functioning. These coordinated, complex processes lead to excessive volume overload, increased sympathetic activity, circulation redistribution, and result in different, parallel developing clinical signs and symptoms. These signs and symptoms sum up to an unspecific clinical picture; thus invasive and noninvasive diagnostic tools are used to get an accurate diagnosis and to specify the underlying cause. The most important, outcome determining factor in heart failure is its constant progression. Constant optimizing of pharmatherapeutical regimes, novel targets, and fine regulation of these processes try to keep these compensatory mechanisms in a physiological range. Beside pharmacological therapy, interventional and surgical therapy options give new chances in the management of heart failure. For the optimization and establishment of these and novel therapeutical approaches, complete and comprehensive understanding of the underlying mechanisms is essentially needed. Besides diagnosis and treatment, efforts should be made for better prevention in heart failure by treatment of risk factors, or identifying and following risk groups. This summary of the pathophysiology of heart failure tries to give a compact overview of basic mechanisms and of the novel unfolding, progressive theory of heart failure to contribute to a more comprehensive knowledge of the disease.
357 citations
Authors
Showing all 31653 results
Name | H-index | Papers | Citations |
---|---|---|---|
Peer Bork | 206 | 697 | 245427 |
Cyrus Cooper | 204 | 1869 | 206782 |
D. M. Strom | 176 | 3167 | 194314 |
George P. Chrousos | 169 | 1612 | 120752 |
David A. Bennett | 167 | 1142 | 109844 |
Marc W. Kirschner | 162 | 457 | 102145 |
Josef M. Penninger | 154 | 700 | 107295 |
William A. Catterall | 154 | 536 | 83561 |
Rui Zhang | 151 | 2625 | 107917 |
Niels Birbaumer | 142 | 835 | 77853 |
Kim Nasmyth | 142 | 294 | 59231 |
James J. Gross | 139 | 529 | 100206 |
Michael Schmitt | 134 | 2007 | 114667 |
Jean-Luc Brédas | 134 | 1026 | 85803 |
Alexander Schmidt | 134 | 1185 | 83879 |