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Institution

University of Münster

EducationMünster, Germany
About: University of Münster is a education organization based out in Münster, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 35609 authors who have published 69059 publications receiving 2278534 citations. The organization is also known as: University of Munster & University of Muenster.


Papers
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Journal ArticleDOI
TL;DR: This review of the literature supports the concept that ROS are not only deleterious agents involved in cartilage degradation, but that they also act as integral factors of intracellular signaling mechanisms.

676 citations

Journal ArticleDOI
01 Feb 2007-Elements
TL;DR: In both aqueous fluids and melts, replacement of zircon with undamaged structure by a coupled dissolution-reprecipitation process can produce similar textures as discussed by the authors.
Abstract: Natural zircon crystals often show complex secondary textures that cut across primary growth zones. In zircon showing structural damage caused by self-irradiation, such textures are the result of a diffusion-reaction process in which a hydrous species diffuses inwards and “catalyzes” structural recovery. Nanoscale pores develop, solvent elements such as Ca, Al and Fe are gained, and radiogenic Pb is lost. In both aqueous fluids and melts, replacement of zircon with undamaged structure by a coupled dissolution-reprecipitation process can produce similar textures. The reacted domains usually have lower trace element contents and may contain micrometer-sized pores and inclusions of uranium, thorium and/or yttrium phases, originally in solid solution. Both processes have considerable implications for zircon geochronology.

675 citations

Journal ArticleDOI
01 Nov 1987-Nature
TL;DR: Macrophages act prominently in the inflammatory response and it is reported here that they express two calcium-binding proteins, referred to as MRP-8 and MRp-14, which are specific for cells of myeloid origin and are observed in blood granulocytes and monocytes but not in normal tissue macrophages.
Abstract: The aetiology and cellular mechanism of chronic inflammatory processes are poorly understood. Macrophages act prominently in the inflammatory response and we report here that they express two calcium-binding proteins. The expression of these proteins, referred to as MRP-8 and MRP-14, is specific for cells of myeloid origin, namely granulocytes, monocytes and macrophages, and is observed in blood granulocytes and monocytes but not in normal tissue macrophages. In acutely inflamed tissues, macrophages can express MRP-14 but not MRP-8, and in chronic inflammations, such as primary chronic polyarthritis, infiltrate macrophages express both MRP-8 and MRP-14. Characterization of MRP-8 and MRP-14 could therefore be useful to the understanding of cellular processes induced in chronic inflammation.

670 citations

Journal ArticleDOI
TL;DR: Digital holographic microscopy enables a quantitative phase contrast metrology that is suitable for the investigation of reflective surfaces as well as for the marker-free analysis of living cells.
Abstract: Digital holographic microscopy enables a quantitative phase contrast metrology that is suitable for the investigation of reflective surfaces as well as for the marker-free analysis of living cells. The digital holographic feature of (subsequent) numerical focus adjustment makes possible applications for multifocus imaging. An overview of digital holographic microscopy methods is described. Applications of digital holographic microscopy are demonstrated by results obtained from livings cells and engineered surfaces.

668 citations

Journal ArticleDOI
20 Mar 2014-Nature
TL;DR: It is concluded that skeletal defects in endothelial-cell-specific Notch pathway mutants involved defective angiocrine release of Noggin from endothelial cells, which is positively regulated by Notch.
Abstract: Blood vessel growth in the skeletal system and osteogenesis seem to be coupled, suggesting the existence of molecular crosstalk between endothelial and osteoblastic cells. Understanding the nature of the mechanisms linking angiogenesis and bone formation should be of great relevance for improved fracture healing or prevention of bone mass loss. Here we show that vascular growth in bone involves a specialized, tissue-specific form of angiogenesis. Notch signalling promotes endothelial cell proliferation and vessel growth in postnatal long bone, which is the opposite of the well-established function of Notch and its ligand Dll4 in the endothelium of other organs and tumours. Endothelial-cell-specific and inducible genetic disruption of Notch signalling in mice not only impaired bone vessel morphology and growth, but also led to reduced osteogenesis, shortening of long bones, chondrocyte defects, loss of trabeculae and decreased bone mass. On the basis of a series of genetic experiments, we conclude that skeletal defects in these mutants involved defective angiocrine release of Noggin from endothelial cells, which is positively regulated by Notch. Administration of recombinant Noggin, a secreted antagonist of bone morphogenetic proteins, restored bone growth and mineralization, chondrocyte maturation, the formation of trabeculae and osteoprogenitor numbers in endothelial-cell-specific Notch pathway mutants. These findings establish a molecular framework coupling angiogenesis, angiocrine signals and osteogenesis, which may prove significant for the development of future therapeutic applications.

667 citations


Authors

Showing all 36075 results

NameH-indexPapersCitations
Hyun-Chul Kim1764076183227
Klaus Müllen1642125140748
Giacomo Bruno1581687124368
Anders M. Dale156823133891
Holger J. Schünemann141810113169
Joachim Heinrich136130976887
Markus Merschmeyer132118884975
Klaus Ley12949557964
Robert W. Mahley12836360774
Robert J. Kurman12739760277
Bart Barlogie12677957803
Thomas Schwarz12370154560
Carlos Caldas12254773840
Klaus Weber12152460346
Andrey L. Rogach11757646820
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023253
2022831
20213,683
20203,499
20193,236
20182,918