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10.3389/fimmu.2018.00393

http://scihub22266oqcxt.onion/10.3389/fimmu.2018.00393
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suck abstract from ncbi


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pmid29616016
      Front+Immunol 2018 ; 9 (ä): 393
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  • Heparan Sulfate Induces Necroptosis in Murine Cardiomyocytes: A Medical-In silico Approach Combining In vitro Experiments and Machine Learning #MMPMID29616016
  • Zechendorf E ; Vaßen P ; Zhang J ; Hallawa A ; Martincuks A ; Krenkel O ; Müller-Newen G ; Schuerholz T ; Simon TP ; Marx G ; Ascheid G ; Schmeink A ; Dartmann G ; Thiemermann C ; Martin L
  • Front Immunol 2018[]; 9 (ä): 393 PMID29616016 show ga
  • Life-threatening cardiomyopathy is a severe, but common, complication associated with severe trauma or sepsis. Several signaling pathways involved in apoptosis and necroptosis are linked to trauma- or sepsis-associated cardiomyopathy. However, the underling causative factors are still debatable. Heparan sulfate (HS) fragments belong to the class of danger/damage-associated molecular patterns liberated from endothelial-bound proteoglycans by heparanase during tissue injury associated with trauma or sepsis. We hypothesized that HS induces apoptosis or necroptosis in murine cardiomyocytes. By using a novel Medical-In silico approach that combines conventional cell culture experiments with machine learning algorithms, we aimed to reduce a significant part of the expensive and time-consuming cell culture experiments and data generation by using computational intelligence (refinement and replacement). Cardiomyocytes exposed to HS showed an activation of the intrinsic apoptosis signal pathway via cytochrome C and the activation of caspase 3 (both p?
  • |*Machine Learning [MESH]
  • |Algorithms [MESH]
  • |Animals [MESH]
  • |Apoptosis [MESH]
  • |Cardiomyopathies/*metabolism/pathology [MESH]
  • |Caspase 3/metabolism [MESH]
  • |Cell Culture Techniques/*methods [MESH]
  • |Cells, Cultured [MESH]
  • |Cytochromes c/metabolism [MESH]
  • |Heparitin Sulfate/*metabolism [MESH]
  • |Humans [MESH]
  • |Mice [MESH]
  • |Myocytes, Cardiac/*physiology [MESH]
  • |Necrosis [MESH]
  • |Receptor-Interacting Protein Serine-Threonine Kinases/metabolism [MESH]
  • |Sepsis/*metabolism/pathology [MESH]
  • |Signal Transduction [MESH]


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