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Institution

University of Marburg

EducationMarburg, Germany
About: University of Marburg is a education organization based out in Marburg, Germany. It is known for research contribution in the topics: Population & Virus. The organization has 23195 authors who have published 42907 publications receiving 1506069 citations. The organization is also known as: Philipps University of Marburg & Philipps-Universität.
Topics: Population, Virus, Gene, Exciton, Photoluminescence


Papers
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Journal ArticleDOI
TL;DR: These findings, together with the zebrafish model of human nephrotic syndrome generated by plce1 knockdown, open new inroads into pathophysiology and treatment mechanisms of nephrotsic syndrome.
Abstract: Nephrotic syndrome, a malfunction of the kidney glomerular filter, leads to proteinuria, edema and, in steroid-resistant nephrotic syndrome, end-stage kidney disease. Using positional cloning, we identified mutations in the phospholipase C epsilon gene (PLCE1) as causing early-onset nephrotic syndrome with end-stage kidney disease. Kidney histology of affected individuals showed diffuse mesangial sclerosis (DMS). Using immunofluorescence, we found PLCepsilon1 expression in developing and mature glomerular podocytes and showed that DMS represents an arrest of normal glomerular development. We identified IQ motif-containing GTPase-activating protein 1 as a new interaction partner of PLCepsilon1. Two siblings with a missense mutation in an exon encoding the PLCepsilon1 catalytic domain showed histology characteristic of focal segmental glomerulosclerosis. Notably, two other affected individuals responded to therapy, making this the first report of a molecular cause of nephrotic syndrome that may resolve after therapy. These findings, together with the zebrafish model of human nephrotic syndrome generated by plce1 knockdown, open new inroads into pathophysiology and treatment mechanisms of nephrotic syndrome.

505 citations

Journal ArticleDOI
TL;DR: PCs are complex tumors which require a multidisciplinary approach and long-term follow-up, and may be considered as first-line systemic antiproliferative treatment in unresectable PCs, particularly of low-grade TC and AC.

505 citations

Journal ArticleDOI
Günter U. Höglinger1, Nadine M. Melhem2, Dennis W. Dickson3, Patrick M. A. Sleiman4, Li-San Wang4, Lambertus Klei2, Rosa Rademakers3, Rohan de Silva5, Irene Litvan6, David E. Riley7, John C. van Swieten8, Peter Heutink9, Zbigniew K. Wszolek3, Ryan J. Uitti3, Jana Vandrovcova5, Howard I. Hurtig4, Rachel G. Gross4, Walter Maetzler10, Stefano Goldwurm, Eduardo Tolosa11, Barbara Borroni12, Pau Pastor13, Laura B. Cantwell4, Mi Ryung Han4, Allissa Dillman14, Marcel P. van der Brug15, J. Raphael Gibbs14, J. Raphael Gibbs5, Mark R. Cookson14, Dena G. Hernandez14, Dena G. Hernandez5, Andrew B. Singleton14, Matthew J. Farrer16, Chang En Yu17, Lawrence I. Golbe18, Tamas Revesz5, John Hardy5, Andrew J. Lees5, Bernie Devlin2, Hakon Hakonarson4, Ulrich Müller19, Gerard D. Schellenberg4, Roger L. Albin20, Elena Alonso13, Angelo Antonini, Manuela Apfelbacher21, Steven E. Arnold4, Jesús Avila22, Thomas G. Beach, Sherry Beecher4, Daniela Berg23, Thomas D. Bird, Nenad Bogdanovic24, Agnita J.W. Boon8, Yvette Bordelon25, Alexis Brice26, Alexis Brice27, Herbert Budka28, Margherita Canesi, Wang Zheng Chiu8, Roberto Cilia, Carlo Colosimo29, Peter Paul De Deyn30, Justo Garcãa De Yebenes, Laura Donker Kaat8, Ranjan Duara31, Alexandra Durr27, Alexandra Durr26, Sebastiaan Engelborghs30, Giovanni Fabbrini29, Nicole A. Finch3, Robyn Flook32, Matthew P. Frosch33, Carles Gaig11, Douglas Galasko34, Thomas Gasser23, Marla Gearing35, Evan T. Geller4, Bernardino Ghetti36, Neill R. Graff-Radford3, Murray Grossman4, Deborah A. Hall37, Lili-Naz Hazrati38, Matthias Höllerhage1, Joseph Jankovic39, Jorge L. Juncos35, Anna Karydas40, Hans A. Kretzschmar41, Isabelle Leber26, Isabelle Leber27, Virginia M.-Y. Lee4, Andrew P. Lieberman20, Kelly E. Lyons42, Claudio Mariani, Eliezer Masliah34, Luke A. Massey5, Catriona McLean43, Nicoletta Meucci, Bruce L. Miller40, Brit Mollenhauer44, Jens Carsten Möller1, Huw R. Morris45, Christopher Morris46, Sean S. O'Sullivan5, Wolfgang H. Oertel1, Donatella Ottaviani29, Alessandro Padovani12, Rajesh Pahwa42, Gianni Pezzoli, Stuart Pickering-Brown47, Werner Poewe48, Alberto Rábano49, Alex Rajput50, Stephen G. Reich51, Gesine Respondek1, Sigrun Roeber41, Jonathan D. Rohrer5, Owen A. Ross3, Martin N. Rossor5, Giorgio Sacilotto, William W. Seeley40, Klaus Seppi48, Laura Silveira-Moriyama5, Salvatore Spina36, Karin Srulijes23, Peter St George-Hyslop52, Maria Stamelou1, David G. Standaert53, Silvana Tesei, Wallace W. Tourtellotte54, Claudia Trenkwalder44, Claire Troakes55, John Q. Trojanowski4, Juan C. Troncoso56, Vivianna M. Van Deerlin4, Jean Paul G. Vonsattel57, Gregor K. Wenning48, Charles L. White58, Pia Winter19, Chris Zarow59, Anna Zecchinelli 
University of Marburg1, University of Pittsburgh2, Mayo Clinic3, University of Pennsylvania4, University College London5, University of Louisville6, Case Western Reserve University7, Erasmus University Rotterdam8, VU University Amsterdam9, University of Tübingen10, University of Barcelona11, University of Brescia12, University of Navarra13, National Institutes of Health14, Scripps Research Institute15, University of British Columbia16, University of Washington17, Rutgers University18, University of Giessen19, University of Michigan20, University of Würzburg21, Autonomous University of Madrid22, German Center for Neurodegenerative Diseases23, Karolinska Institutet24, University of California, Los Angeles25, French Institute of Health and Medical Research26, Centre national de la recherche scientifique27, Medical University of Vienna28, Sapienza University of Rome29, University of Antwerp30, Mount Sinai Hospital31, Flinders University32, Harvard University33, University of California, San Diego34, Emory University35, Indiana University36, Rush University Medical Center37, University of Toronto38, Baylor College of Medicine39, University of California, San Francisco40, Ludwig Maximilian University of Munich41, University of Kansas42, Mental Health Research Institute43, University of Göttingen44, Cardiff University45, Newcastle University46, University of Manchester47, Innsbruck Medical University48, Carlos III Health Institute49, University of Saskatchewan50, University of Maryland, Baltimore51, University of Cambridge52, University of Alabama at Birmingham53, Veterans Health Administration54, King's College London55, Johns Hopkins University56, Columbia University57, University of Texas Southwestern Medical Center58, University of Southern California59
TL;DR: Two independent variants in MAPT affecting risk for PSP are confirmed, one of which influences MAPT brain expression and the genes implicated encode proteins for vesicle-membrane fusion at the Golgi-endosomal interface and for a myelin structural component.
Abstract: Progressive supranuclear palsy (PSP) is a movement disorder with prominent tau neuropathology. Brain diseases with abnormal tau deposits are called tauopathies, the most common of which is Alzheimer's disease. Environmental causes of tauopathies include repetitive head trauma associated with some sports. To identify common genetic variation contributing to risk for tauopathies, we carried out a genome-wide association study of 1,114 individuals with PSP (cases) and 3,247 controls (stage 1) followed by a second stage in which we genotyped 1,051 cases and 3,560 controls for the stage 1 SNPs that yielded P ≤ 10−3. We found significant previously unidentified signals (P < 5 × 10−8) associated with PSP risk at STX6, EIF2AK3 and MOBP. We confirmed two independent variants in MAPT affecting risk for PSP, one of which influences MAPT brain expression. The genes implicated encode proteins for vesicle-membrane fusion at the Golgi-endosomal interface, for the endoplasmic reticulum unfolded protein response and for a myelin structural component.

504 citations

Journal ArticleDOI
TL;DR: In this article, the authors propose that the relationship between identification and turnover will be mediated by job satisfaction as the more specific evaluation of ones task and working conditions, which in turn predicts turnover intentions.
Abstract: The social identity approach is a powerful theoretical framework for the understanding of individuals behaviour The main argument is that individuals think and act on behalf of the group they belong to because this group membership adds to their social identity, which partly determines ones self-esteem In the organizational world, social identity and self-categorization theories state that a strong organizational identification is associated with low turnover intentions Because identification is the more general perception of shared fate between employee and organization, we propose that the relationship between identification and turnover will be mediated by job satisfaction as the more specific evaluation of ones task and working conditions In four samples we found organizational identification feeding into job satisfaction, which in turn predicts turnover intentions

501 citations

Journal ArticleDOI
TL;DR: The tissue origins of cfDNA and thus the rate of death of specific cell types can be determined in humans, offering a minimally invasive window for diagnosing and monitoring a broad spectrum of human pathologies as well as providing a better understanding of normal tissue dynamics.
Abstract: Minimally invasive detection of cell death could prove an invaluable resource in many physiologic and pathologic situations. Cell-free circulating DNA (cfDNA) released from dying cells is emerging as a diagnostic tool for monitoring cancer dynamics and graft failure. However, existing methods rely on differences in DNA sequences in source tissues, so that cell death cannot be identified in tissues with a normal genome. We developed a method of detecting tissue-specific cell death in humans based on tissue-specific methylation patterns in cfDNA. We interrogated tissue-specific methylome databases to identify cell type-specific DNA methylation signatures and developed a method to detect these signatures in mixed DNA samples. We isolated cfDNA from plasma or serum of donors, treated the cfDNA with bisulfite, PCR-amplified the cfDNA, and sequenced it to quantify cfDNA carrying the methylation markers of the cell type of interest. Pancreatic β-cell DNA was identified in the circulation of patients with recently diagnosed type-1 diabetes and islet-graft recipients; oligodendrocyte DNA was identified in patients with relapsing multiple sclerosis; neuronal/glial DNA was identified in patients after traumatic brain injury or cardiac arrest; and exocrine pancreas DNA was identified in patients with pancreatic cancer or pancreatitis. This proof-of-concept study demonstrates that the tissue origins of cfDNA and thus the rate of death of specific cell types can be determined in humans. The approach can be adapted to identify cfDNA derived from any cell type in the body, offering a minimally invasive window for diagnosing and monitoring a broad spectrum of human pathologies as well as providing a better understanding of normal tissue dynamics.

500 citations


Authors

Showing all 23488 results

NameH-indexPapersCitations
John C. Morris1831441168413
Russel J. Reiter1691646121010
Martin J. Blaser147820104104
Christopher T. Walsh13981974314
Markus Cristinziani131114084538
James C. Paulson12644352152
Markus F. Neurath12493462376
Nicholas W. Wood12361466270
Florian Lang116142166496
Howard I. Maibach116182160765
Thomas G. Ksiazek11339846108
Frank Glorius11366349305
Eberhard Ritz111110961530
Manfred T. Reetz11095942941
Wolfgang H. Oertel11065351147
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023142
2022412
20212,103
20201,918
20191,749
20181,592