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 & Gene. 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, Gene, Immune system, Receptor, CAS Registry Number
Papers published on a yearly basis
Papers
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TL;DR: The development of ambient stable organic n-channel semiconductor molecules for thin-film transistors has experienced a tremendous impetus in the last decade to close the gap in performance in comparison to that of their p-channel counterparts.
479 citations
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University of Pennsylvania1, Autonomous University of Barcelona2, Mayo Clinic3, University of Manchester4, Erasmus University Rotterdam5, VU University Amsterdam6, Indiana University – Purdue University Indianapolis7, University of Siena8, National Institutes of Health9, Neuroscience Research Australia10, University of Cambridge11, University of Michigan12, Oregon Health & Science University13, Northwestern University14, King's College London15, University of Texas at Dallas16, University of Texas Southwestern Medical Center17, University of Barcelona18, University of Zurich19, Ludwig Maximilian University of Munich20, Duke University21, University of California, San Francisco22, Boston University23, Veterans Health Administration24, Emory University25, University College London26, University of British Columbia27, University of Pittsburgh28, University of Virginia29, Flanders Institute for Biotechnology30, University of Antwerp31, Columbia University32, Johns Hopkins University33, University of Sydney34, University of New South Wales35, University of Washington36, University of Sheffield37, Washington University in St. Louis38, Alfred Hospital39, University of California, Davis40, Harvard University41, Icahn School of Medicine at Mount Sinai42, Rush University Medical Center43, University of Arizona44, University of California, Los Angeles45, University of Southern California46, Uppsala University47, University of Eastern Finland48, Pierre-and-Marie-Curie University49, University of California, San Diego50, University of California, Irvine51, University of Toronto52, University of Alabama at Birmingham53, University of Würzburg54, Karolinska Institutet55
TL;DR: It is found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM 106B, which implicate variants in TMEM106B as a strong risk factor for FTLD, suggesting an underlying pathogenic mechanism.
Abstract: Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. The predominant neuropathology is FTLD with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). FTLD-TDP is frequently familial, resulting from mutations in GRN (which encodes progranulin). We assembled an international collaboration to identify susceptibility loci for FTLD-TDP through a genome-wide association study of 515 individuals with FTLD-TDP. We found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM106B. Three SNPs retained genome-wide significance following Bonferroni correction (top SNP rs1990622, P = 1.08 x 10(-11); odds ratio, minor allele (C) 0.61, 95% CI 0.53-0.71). The association replicated in 89 FTLD-TDP cases (rs1990622; P = 2 x 10(-4)). TMEM106B variants may confer risk of FTLD-TDP by increasing TMEM106B expression. TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism.
479 citations
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Brigham and Women's Hospital1, Memorial Hermann Texas Medical Center2, University of Cologne3, University of Chicago4, Duke University5, University of California, Davis6, Henry Ford Hospital7, Stanford University8, Fred Hutchinson Cancer Research Center9, University of Würzburg10, University of Strasbourg11, Katholieke Universiteit Leuven12, Rambam Health Care Campus13, University of Alabama at Birmingham14, Masaryk University15, Sheba Medical Center16, Universidade Federal de Minas Gerais17, Charité18, University of Minnesota19, Khon Kaen University20, Prince of Songkla University21, American University of Beirut22, Center for Global Development23
TL;DR: Isavuconazole showed activity against mucormycosis with efficacy similar to amphotericin B, and can be used for treatment of mucormYcosis and is well tolerated.
Abstract: Summary Background Mucormycosis is an uncommon invasive fungal disease with high mortality and few treatment options. Isavuconazole is a triazole active in vitro and in animal models against moulds of the order Mucorales. We assessed the efficacy and safety of isavuconazole for treatment of mucormycosis and compared its efficacy with amphotericin B in a matched case-control analysis. Methods In a single-arm open-label trial (VITAL study), adult patients (≥18 years) with invasive fungal disease caused by rare fungi, including mucormycosis, were recruited from 34 centres worldwide. Patients were given isavuconazole 200 mg (as its intravenous or oral water-soluble prodrug, isavuconazonium sulfate) three times daily for six doses, followed by 200 mg/day until invasive fungal disease resolution, failure, or for 180 days or more. The primary endpoint was independent data review committee-determined overall response—ie, complete or partial response (treatment success) or stable or progressive disease (treatment failure)—according to prespecified criteria. Mucormycosis cases treated with isavuconazole as primary treatment were matched with controls from the FungiScope Registry, recruited from 17 centres worldwide, who received primary amphotericin B-based treatment, and were analysed for day-42 all-cause mortality. VITAL is registered with ClinicalTrials.gov, number NCT00634049. FungiScope is registered with ClinicalTrials.gov, number NCT01731353. Findings Within the VITAL study, from April 22, 2008, to June 21, 2013, 37 patients with mucormycosis received isavuconazole for a median of 84 days (IQR 19–179, range 2–882). By day 42, four patients (11%) had a partial response, 16 (43%) had stable invasive fungal disease, one (3%) had invasive fungal disease progression, three (8%) had missing assessments, and 13 (35%) had died. 35 patients (95%) had adverse events (28 [76%] serious). Day-42 crude all-cause mortality in seven (33%) of 21 primary-treatment isavuconazole cases was similar to 13 (39%) of 33 amphotericin B-treated matched controls (weighted all-cause mortality: 33% vs 41%; p=0·595). Interpretation Isavuconazole showed activity against mucormycosis with efficacy similar to amphotericin B. Isavuconazole can be used for treatment of mucormycosis and is well tolerated. Funding Astellas Pharma Global Development, Basilea Pharmaceutica International.
478 citations
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TL;DR: The previous EFNS guidelines on neuropathic pain assessment aimed to provide recommendations for the diagnostic process, screening tools and questionnaires, quantitative sensory testing (QST), microneurography, pain‐related reflexes and evoked potentials, functional neuroimaging and skin biopsy.
Abstract: Background and purpose: We have revised the previous EFNS guidelines on neuropathic pain (NP) assessment, which aimed to provide recommendations for the diagnostic process, screening tools and questionnaires, quantitative sensory testing (QST), microneurography, pain-related reflexes and evoked potentials, functional neuroimaging and skin biopsy.
Methods: We have checked and rated the literature published in the period 2004–2009, according to the EFNS method of classification for diagnostic procedures.
Results: Most of the previous recommendations were reinforced by the new studies. The main revisions relate to: (i) the new definition of NP and a diagnostic grading system; (ii) several new validated clinical screening tools that identify NP components, and questionnaires which assess the different types of NP; (iii) recent high-quality studies on laser-evoked potentials (LEPs) and skin biopsy.
Conclusions: History and bedside examination are still fundamental to a correct diagnosis, whilst screening tools and questionnaires are useful in indicating probable NP; QST is also useful for indicating the latter, and to assess provoked pains and treatment response. Amongst laboratory tests, LEPs are the best tool for assessing Aδ pathway dysfunction, and skin biopsy for assessing neuropathies with distal loss of unmyelinated nerve fibres.
478 citations
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TL;DR: The oxidative stress theory of neurodegeneration, on excitotoxin-induced cell damage and on impairment of mitochondrial function are focused on as three major noxae being the most likely causes of cell death either independently or in connection with each other.
477 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 |