Institution
University of Cologne
Education•Cologne, Germany•
About: University of Cologne is a education organization based out in Cologne, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 32050 authors who have published 66350 publications receiving 2210092 citations. The organization is also known as: Universität zu Köln & Universitatis Coloniensis.
Topics: Population, Gene, Transplantation, Medicine, Cancer
Papers published on a yearly basis
Papers
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Hebrew University of Jerusalem1, Case Western Reserve University2, Catholic University of Leuven3, Boston Children's Hospital4, Necker-Enfants Malades Hospital5, Queen's University Belfast6, University Medical Center Utrecht7, Paris Descartes University8, Vrije Universiteit Brussel9, Washington University in St. Louis10, Mount Sinai Hospital11, Northwestern University12, Sapienza University of Rome13, University of Cologne14, Johns Hopkins University15, University of Alabama at Birmingham16
TL;DR: Although ataluren did not improve lung function in the overall population of nonsense-mutation cystic fibrosis patients who received this treatment, it might be beneficial for patients not taking chronic inhaled tobramycin.
307 citations
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TL;DR: Unraveling the biology of gephyrin will further the understanding of glycinergic and GABAergic synapses in health and disease and highlight new research avenues based on a different structural model and a revised nomenclature for gephirin splice variants.
307 citations
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TL;DR: It is shown that POMC-specific disruption of Pten resulted in hyperphagia and sexually dimorphic diet-sensitive obesity, which indicates that PIP3-mediated signals are critical regulators of the melanocortin system via modulation of KATP channels.
Abstract: Leptin and insulin have been identified as fuel sensors acting in part through their hypothalamic receptors to inhibit food intake and stimulate energy expenditure. As their intracellular signaling converges at the PI3K pathway, we directly addressed the role of phosphatidylinositol3,4,5-trisphosphate-mediated (PIP3-mediated) signals in hypothalamic proopiomelanocortin (POMC) neurons by inactivating the gene for the PIP3 phosphatase Pten specifically in this cell type. Here we show that POMC-specific disruption of Pten resulted in hyperphagia and sexually dimorphic diet-sensitive obesity. Although leptin potently stimulated Stat3 phosphorylation in POMC neurons of POMC cell-restricted Pten knockout (PPKO) mice, it failed to significantly inhibit food intake in vivo. POMC neurons of PPKO mice showed a marked hyperpolarization and a reduction in basal firing rate due to increased ATP-sensitive potassium (KATP) channel activity. Leptin was not able to elicit electrical activity in PPKO POMC neurons, but application of the PI3K inhibitor LY294002 and the KATP blocker tolbutamide restored electrical activity and leptin-evoked firing of POMC neurons in these mice. Moreover, icv administration of tolbutamide abolished hyperphagia in PPKO mice. These data indicate that PIP3-mediated signals are critical regulators of the melanocortin system via modulation of KATP channels.
307 citations
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TL;DR: Crizotinib was highly active at treating lung cancer in patients with a ROS1 rearrangement, suggesting that patients with lung adenocarcinomas should be tested for ROS1.
Abstract: Approximately 1% of lung adenocarcinomas are driven by oncogenic ROS1 rearrangement. Crizotinib is a potent inhibitor of both ROS1 and ALK kinase domains. In the absence of a prospective clinical trial in Europe, we conducted a retrospective study in centers that tested for ROS1 rearrangement. Eligible patients had stage IV lung adenocarcinoma, had ROS1 rearrangement according to fluorescent in situ hybridization, and had received crizotinib therapy through an individual off-label use. Best response was assessed locally using RECIST (version 1.1). All other data were analyzed centrally. We identified 32 eligible patients. One patient was excluded because next-generation sequencing was negative for ROS1 fusion. Median age was 50.5 years, 64.5% of patients were women, and 67.7% were never-smokers. Thirty patients were evaluable for progression-free survival (PFS), and 29 patients were evaluable for best response. We observed four patients with disease progression, two patients with stable disease, and objective response in 24 patients, including five complete responses (overall response rate, 80%; disease control rate, 86.7%). Median PFS was 9.1 months, and the PFS rate at 12 months was 44%. No unexpected adverse effects were observed. Twenty-six patients received pemetrexed (either alone or in combination with platinum and either before or after crizotinib) and had a response rate of 57.7% and a median PFS of 7.2 months. Crizotinib was highly active at treating lung cancer in patients with a ROS1 rearrangement, suggesting that patients with lung adenocarcinomas should be tested for ROS1. Prospective clinical trials with crizotinib and other ROS1 inhibitors are ongoing or planned.
307 citations
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University of Bonn1, University of Göttingen2, Boston Children's Hospital3, University of Cambridge4, Harvard University5, Humboldt University of Berlin6, University of Cologne7, Leipzig University8, Otto-von-Guericke University Magdeburg9, University of Antwerp10, University of Iowa11, University of Pittsburgh12, Johns Hopkins University13, Johns Hopkins University School of Medicine14, University of Ferrara15, University of Dundee16
TL;DR: The first meta-analyses for nonsyndromic cleft lip with or without cleft palate (NSCL/P) using data from the two largest genome-wide association studies published to date identified the first specific genetic risk factor for NSCLP.
Abstract: We have conducted the first meta-analyses for nonsyndromic cleft lip with or without cleft palate (NSCL/P) using data from the two largest genome-wide association studies published to date. We confirmed associations with all previously identified loci and identified six additional susceptibility regions (1p36, 2p21, 3p11.1, 8q21.3, 13q31.1 and 15q22). Analysis of phenotypic variability identified the first specific genetic risk factor for NSCLP (nonsyndromic cleft lip plus palate) (rs8001641; PNSCLP = 6.51 × 10−11; homozygote relative risk = 2.41, 95% confidence interval (CI) 1.84–3.16).
307 citations
Authors
Showing all 32558 results
Name | H-index | Papers | Citations |
---|---|---|---|
Julie E. Buring | 186 | 950 | 132967 |
Stuart H. Orkin | 186 | 715 | 112182 |
Cornelia M. van Duijn | 183 | 1030 | 146009 |
Dorret I. Boomsma | 176 | 1507 | 136353 |
Frederick W. Alt | 171 | 577 | 95573 |
Donald E. Ingber | 164 | 610 | 100682 |
Klaus Müllen | 164 | 2125 | 140748 |
Klaus Rajewsky | 154 | 504 | 88793 |
Frederik Barkhof | 154 | 1449 | 104982 |
Stefanie Dimmeler | 147 | 574 | 81658 |
Detlef Weigel | 142 | 516 | 84670 |
Hidde L. Ploegh | 135 | 674 | 67437 |
Luca Valenziano | 130 | 437 | 94728 |
Peter Walter | 126 | 841 | 71580 |
Peter G. Martin | 125 | 553 | 97257 |