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@ARTICLE{Rack:838893,
      author       = {Rack, Kathrin and Huck, Volker and Hoore, Masoud and
                      Fedosov, Dmitry A. and Schneider, Stefan W. and Gompper,
                      Gerhard},
      title        = {{M}argination and stretching of von {W}illebrand factor in
                      the blood stream enable adhesion},
      journal      = {Scientific reports},
      volume       = {7},
      number       = {1},
      issn         = {2045-2322},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {FZJ-2017-07399},
      pages        = {14278},
      year         = {2017},
      abstract     = {The protein von Willebrand factor (VWF) is essential in
                      primary hemostasis, as it mediates platelet adhesion to
                      vessel walls. VWF retains its compact (globule-like) shape
                      in equilibrium due to internal molecular associations, but
                      is able to stretch when a high enough shear stress is
                      applied. Even though the shear-flow sensitivity of VWF
                      conformation is well accepted, the behavior of VWF under
                      realistic blood flow conditions remains poorly understood.
                      We perform mesoscopic numerical simulations together with
                      microfluidic experiments in order to characterize VWF
                      behavior in blood flow for a wide range of flow-rate and
                      hematocrit conditions. In particular, our results
                      demonstrate that the compact shape of VWF is important for
                      its migration (or margination) toward vessel walls and that
                      VWF stretches primarily in a near-wall region in blood flow
                      making its adhesion possible. Our results show that VWF is a
                      highly optimized protein in terms of its size and internal
                      associations which are necessary to achieve its vital
                      function. A better understanding of the relevant mechanisms
                      for VWF behavior in microcirculation provides a further step
                      toward the elucidation of the role of mutations in various
                      VWF-related diseases.},
      cin          = {ICS-2 / JARA-HPC},
      ddc          = {000},
      cid          = {I:(DE-Juel1)ICS-2-20110106 / $I:(DE-82)080012_20140620$},
      pnm          = {553 - Physical Basis of Diseases (POF3-553) / Margination
                      and Adhesion of Particles and Cells in Blood Flow
                      $(jiff44_20140501)$},
      pid          = {G:(DE-HGF)POF3-553 / $G:(DE-Juel1)jiff44_20140501$},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29079767},
      UT           = {WOS:000413907000101},
      doi          = {10.1038/s41598-017-14346-4},
      url          = {https://juser.fz-juelich.de/record/838893},
}