Institution
University of Hamburg
Education•Hamburg, Germany•
About: University of Hamburg is a education organization based out in Hamburg, Germany. It is known for research contribution in the topics: Population & Laser. The organization has 45564 authors who have published 89286 publications receiving 2850161 citations. The organization is also known as: Hamburg University.
Topics: Population, Laser, Transplantation, Large Hadron Collider, Higgs boson
Papers published on a yearly basis
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University of Pennsylvania1, Pierre-and-Marie-Curie University2, University of Cambridge3, Leiden University Medical Center4, Wellcome Trust Sanger Institute5, British Heart Foundation6, University of Glasgow7, Glasgow Clinical Research Facility8, International Centre for Diarrhoeal Disease Research, Bangladesh9, University of Michigan10, University of Lübeck11, Copenhagen University Hospital12, University of Copenhagen13, National Institutes of Health14, Pennsylvania State University15, University of Hamburg16, Pasteur Institute17, University of Strasbourg18, University of Toulouse19, Ludwig Maximilian University of Munich20, University of Insubria21, Queen's University Belfast22, National Institute for Health Research23, Technische Universität München24, Harvard University25, Washington University in St. Louis26
TL;DR: In this paper, the authors identified a homozygote for a loss-of-function variant, in which leucine replaces proline 376 (P376L), in SCARB1, the gene encoding SR-BI.
Abstract: Scavenger receptor BI (SR-BI) is the major receptor for high-density lipoprotein (HDL) cholesterol (HDL-C). In humans, high amounts of HDL-C in plasma are associated with a lower risk of coronary heart disease (CHD). Mice that have depleted Scarb1 (SR-BI knockout mice) have markedly elevated HDL-C levels but, paradoxically, increased atherosclerosis. The impact of SR-BI on HDL metabolism and CHD risk in humans remains unclear. Through targeted sequencing of coding regions of lipid-modifying genes in 328 individuals with extremely high plasma HDL-C levels, we identified a homozygote for a loss-of-function variant, in which leucine replaces proline 376 (P376L), in SCARB1, the gene encoding SR-BI. The P376L variant impairs posttranslational processing of SR-BI and abrogates selective HDL cholesterol uptake in transfected cells, in hepatocyte-like cells derived from induced pluripotent stem cells from the homozygous subject, and in mice. Large population-based studies revealed that subjects who are heterozygous carriers of the P376L variant have significantly increased levels of plasma HDL-C. P376L carriers have a profound HDL-related phenotype and an increased risk of CHD (odds ratio = 1.79, which is statistically significant).
417 citations
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TL;DR: The strong correlation between elevated uPA and/or PAI-1 values in primary cancer tissues and the tumor invasion/ metastasis capacity of cancer cells, proteolytic factors have been selected as targets for therapy.
Abstract: Extravasation and intravasation of solid malignant tumors is controlled by attachment of tumor cells to components of the basement membrane and the extracellular matrix, by local proteolysis and tumor cell migration. Strong clinical and experimental evidence has accumulated that the tumor-associated serine protease plasmin, its activator uPA (urokinase-type plasminogen activator), the receptor uPA-R (CD87), and the inhibitors PAI-1 and PAI-2 are linked to cancer invasion and metastasis. In cancer, increase of uPA, uPA-R, and/or PAI-1 is associated with tumor progression and with shortened disease-free and/or overall survival in patients afflicted with malignant solid tumors. uPA and/or its inhibitor PAI-1 appear to be one of the strongest prognostic markers so far described. Strong prognostic value to predict disease recurrence and overall survival has been documented for patients with cancer of the breast, ovary, cervix, endometrium, stomach, colon, lung, bladder, kidney, brain, and soft-tissue. Due to the strong correlation between elevated uPA and/or PAI-1 values in primary cancer tissues and the tumor invasion/ metastasis capacity of cancer cells, proteolytic factors have been selected as targets for therapy. Various very different approaches to interfere with the expression or reactivity of uPA or CD87 at the gene or protein level were successfully tested including antisense oligonucleotides, antibodies, enzyme inhibitors, and recombinant or synthetic uPA and uPA-R analogues.
417 citations
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A. Abramowski1, Felix Aharonian2, Faical Ait Benkhali2, A. G. Akhperjanian +226 more•Institutions (28)
TL;DR: Deep γ-ray observations with arcminute angular resolution of the region surrounding the Galactic Centre are reported, which show the expected tracer of the presence of petaelectronvolt protons within the central 10 parsecs of the Galaxy, and it is proposed that the supermassive black hole Sagittarius A* is linked to this PeVatron.
Abstract: Galactic cosmic rays reach energies of at least a few petaelectronvolts(1) (of the order of 1015 electronvolts). This implies that our Galaxy contains petaelectronvolt accelerators ('PeVatrons'), b ...
417 citations
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TL;DR: The structure reveals the mechanism of native TbCatB inhibition and demonstrates that new biomolecular information can be obtained by the “diffraction-before-destruction” approach of x-ray free-electron lasers from hundreds of thousands of individual microcrystals.
Abstract: The Trypanosoma brucei cysteine protease cathepsin B (TbCatB), which is involved in host protein degradation, is a promising target to develop new treatments against sleeping sickness, a fatal disease caused by this protozoan parasite. The structure of the mature, active form of TbCatB has so far not provided sufficient information for the design of a safe and specific drug against T. brucei. By combining two recent innovations, in vivo crystallization and serial femtosecond crystallography, we obtained the room-temperature 2.1 angstrom resolution structure of the fully glycosylated precursor complex of TbCatB. The structure reveals the mechanism of native TbCatB inhibition and demonstrates that new biomolecular information can be obtained by the “diffraction-before-destruction” approach of x-ray free-electron lasers from hundreds of thousands of individual microcrystals.
417 citations
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TL;DR: Although histologically similar, GBMs arising with and without IDH1(R132MUT) appear to represent distinct disease entities that arise from separate cell types of origin as the result of largely nonoverlapping sets of molecular events.
Abstract: Purpose Mutation in isocitrate dehydrogenase 1 (IDH1) at R132 (IDH1 R132MUT ) is frequent in low-grade diffuse gliomas and, within glioblastoma (GBM), has been proposed as a marker for GBMs that arise by transformation from lower-grade gliomas, regardless of clinical history. To determine how GBMs arising with IDH1 R132MUT differ from other GBMs, we undertook a comprehensive comparison of patients presenting clinically with primary GBM as a function of IDH1 R132 mutation status.
417 citations
Authors
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Name | H-index | Papers | Citations |
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Rudolf Jaenisch | 206 | 606 | 178436 |
Bruce M. Psaty | 181 | 1205 | 138244 |
Stefan Schreiber | 178 | 1233 | 138528 |
Chris Sander | 178 | 713 | 233287 |
Dennis J. Selkoe | 177 | 607 | 145825 |
Daniel R. Weinberger | 177 | 879 | 128450 |
Ramachandran S. Vasan | 172 | 1100 | 138108 |
Bradley Cox | 169 | 2150 | 156200 |
Anders Björklund | 165 | 769 | 84268 |
J. S. Lange | 160 | 2083 | 145919 |
Hannes Jung | 159 | 2069 | 125069 |
Andrew D. Hamilton | 151 | 1334 | 105439 |
Jongmin Lee | 150 | 2257 | 134772 |
Teresa Lenz | 150 | 1718 | 114725 |
Stefanie Dimmeler | 147 | 574 | 81658 |