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10.1182/blood-2014-01-550335 http://scihub22266oqcxt.onion/10.1182/blood-2014-01-550335 C4162110!4162110 !24951424     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24951424 &cmd=llinks): Failed to open stream: HTTP request failed! 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A systems approach to hemostasis: 1 The interdependence of thrombus architecture and agonist movements in the gaps between platelets |pdf=|usr=}}{{24951424 }} gab.com Text A systems approach to hemostasis: 1 The interdependence of thrombus architecture and agonist movements in the gaps between platelets JO: Blood http://www.kidney.de/pget.php?&tw=1&pmid=24951424 #FOAvip Hemostatic thrombi develop a characteristic architecture in which a core of highly activated platelets is covered by a shell of less-activated platelets. Here we have used a systems biology approach to examine the interrelationship of this architecture with transport rates and agonist distribution in the gaps between platelets. Studies were performed in mice using probes for platelet accumulation, packing density, and activation plus recently developed transport and thrombin activity probes. The results show that intrathrombus transport within the core is much slower than within the shell. The region of slowest transport coincides with the region of greatest packing density and thrombin activity, and appears prior to full platelet activation. Deleting the contact-dependent signaling molecule, Sema4D, delays platelet activation, but not the emergence of the low transport region. Collectively, these results suggest a timeline in which initial platelet accumulation and the narrowing gaps between platelets create a region of reduced transport that facilitates local thrombin accumulation and greater platelet activation, whereas faster transport rates within the shell help to limit thrombin accumulation and growth of the core. Thus, from a systems perspective, platelet accumulation produces an altered microenvironment that shapes thrombus architecture, which in turn affects agonist distribution and subsequent thrombus growth. Twit Text FOAVip A systems approach to hemostasis: 1 The interdependence of thrombus architecture and agonist movements in the gaps between platelets ????Blood http://www.kidney.de/pget.php?&tw=1&pmid=24951424 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24951424 #FOAvip English Wikipedia <ref>{{Cite pmid|24951424 }}</ref> A systems approach to hemostasis: 1 The interdependence of thrombus architecture and agonist movements in the gaps between platelets #MMPMID24951424 Welsh JD ; Stalker TJ ; Voronov R ; Muthard RW ; Tomaiuolo M ; Diamond SL ; Brass LF Blood 2014[Sep]; 124 (11 ): 1808-15 PMID24951424 show ga Hemostatic thrombi develop a characteristic architecture in which a core of highly activated platelets is covered by a shell of less-activated platelets. Here we have used a systems biology approach to examine the interrelationship of this architecture with transport rates and agonist distribution in the gaps between platelets. Studies were performed in mice using probes for platelet accumulation, packing density, and activation plus recently developed transport and thrombin activity probes. The results show that intrathrombus transport within the core is much slower than within the shell. The region of slowest transport coincides with the region of greatest packing density and thrombin activity, and appears prior to full platelet activation. Deleting the contact-dependent signaling molecule, Sema4D, delays platelet activation, but not the emergence of the low transport region. Collectively, these results suggest a timeline in which initial platelet accumulation and the narrowing gaps between platelets create a region of reduced transport that facilitates local thrombin accumulation and greater platelet activation, whereas faster transport rates within the shell help to limit thrombin accumulation and growth of the core. Thus, from a systems perspective, platelet accumulation produces an altered microenvironment that shapes thrombus architecture, which in turn affects agonist distribution and subsequent thrombus growth. |*Blood Coagulation [MESH] |*Models, Cardiovascular [MESH] |*Platelet Activation [MESH] |Animals [MESH] |Humans [MESH] |Mice [MESH] |Protein Transport [MESH]A systems approach to hemostasis: 1 The interdependence of thrombus a(epmc).pdf DeepDyve Pubget Overpricing