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@ARTICLE{Huisman:837998,
      author       = {Huisman, Brooke and Hoore, Masoud and Gompper, Gerhard and
                      Fedosov, Dmitry A.},
      title        = {{M}odeling the cleavage of von {W}illebrand factor by
                      {ADAMTS}13 protease in shear flow},
      journal      = {Medical engineering $\&$ physics},
      volume       = {48},
      issn         = {1350-4533},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2017-06746},
      pages        = {14 - 22},
      year         = {2017},
      abstract     = {Von Willebrand factor (VWF) is a key protein in hemostasis
                      as it mediates adhesion of blood platelets to a site of
                      vascular injury. A proper distribution of VWF lengths is
                      important for normal functioning of hemostatic processes,
                      because a diminished number of long VWF chains may
                      significantly limit blood clotting and lead to bleeding,
                      while an abundant number of long VWFs may result in
                      undesired thrombotic events. VWF size distribution is
                      controlled by ADAMTS13 protease, which can cleave VWF chains
                      beyond a critical shear rate when the chains are stretched
                      enough such that cleavage sites become accessible. To better
                      understand the cleavage process, we model VWF cleavage in
                      shear flow using mesoscopic hydrodynamic simulations. Two
                      cleavage models are proposed, a geometrical model based on
                      the degree of local stretching of VWF, and a tension-force
                      model based on instantaneous tension force within VWF bonds.
                      Both models capture the susceptibility of VWF to cleavage at
                      high shear rates; however, the geometrical model appears to
                      be much more robust than the force model. Our simulations
                      show that VWF susceptibility to cleavage in shear flow
                      becomes a universal function of shear rate, independent of
                      VWF length for long enough chains. Furthermore, VWF is
                      cleaved with a higher probability close to its ends in
                      comparison to cleaving in the middle, which results into
                      longer circulation lifetimes of VWF multimers. Simulations
                      of dynamic cleavage of VWF show an exponential distribution
                      of chain lengths, consistently with available in vitro
                      experiments. The proposed cleavage models can be used in
                      realistic simulations of hemostatic processes in blood
                      flow.},
      cin          = {ICS-2 / JARA-HPC},
      ddc          = {610},
      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
                      $(jiff44_20140501)$ / Blood Flow Resistance in Microvascular
                      Networks $(jics21_20131101)$},
      pid          = {G:(DE-HGF)POF3-553 / $G:(DE-Juel1)jiff44_20140501$ /
                      $G:(DE-Juel1)jics21_20131101$},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28734872},
      UT           = {WOS:000413177800003},
      doi          = {10.1016/j.medengphy.2017.06.044},
      url          = {https://juser.fz-juelich.de/record/837998},
}