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Nature Medicine 14, 606 - 608 (2008)
doi:10.1038/nm0608-606

Keeping blood clots at bay in sepsis

Cornelis van 't Veer1 & Tom van der Poll1

  1. Cornelis van 't Veer and Tom van der Poll are at the Centre for Infection and Immunity Amsterdam and the Centre for Experimental and Molecular Medicine, Academic Medical Centre, University of Amsterdam, Meibergdreef 9, Room G2-129, 1105 AZ Amsterdam, The Netherlands. e-mail: c.vantveer@amc.uva.nl or e-mail: t.vanderpoll@amc.uva.nl


Clearance of platelets by the liver can help counteract the dangerous blood coagulation that can occur during sepsis. The mechanism involves clearance of platelets through the liver's Ashwell receptor, which binds to platelet glycoproteins altered by sepsis-causing bacteria (pages 648–655).


The glycan branches of the body's ubiquitous glycoproteins, which decorate many cell types, are not naked. They often sprout sialic acid (N-acetylneuraminic acid) at their termini in a process named sialylation.

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