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https://www.selleckchem.com/products/sn-011-gun35901.html 65-0.98), but not in those without SAC (RR 1.17; 95% CI, 0.82-1.67) nor in the whole study population (RR 0.88; 95% CI, 0.74-1.04). There was no significant difference in major bleeding between rhsTM and controls in the whole population (RR 1.25; 95% CI, 0.80-1.96), patients with SAC (RR 0.94; 95% CI, 0.45-1.95), and those without SAC (RR 2.26; 95% CI, 0.95-5.35). CONCLUSIONS In patients with sepsis, SAC is associated with higher 28-day mortality. The administration of rhsTM reduced 28-day mortality in patients with SAC, but not in those without SAC. This article is protected by copyright. All rights reserved.BACKGROUND Heparin induced thrombocytopenia (HIT) is likely a misdirected bacterial host defense mechanism. Platelet factor 4 (PF4) binds to polyanions on bacterial surfaces exposing neo-epitopes to which HIT-antibodies bind. Platelets are activated by the resulting immune complexes via FcγRIIA, release bactericidal substances and kill Gram-negative Escherichia coli. OBJECTIVES To assess the role of PF4, anti-PF4/H antibodies and FcγRIIa in killing of Gram-positive bacteria by platelets. METHODS Binding of PF4 to protein-A deficient Staphylococcus aureus (SA113Δspa) and non-encapsulated Streptococcus pneumoniae (D39Δcps) and its conformational change were assessed by flow cytometry using monoclonal (KKO,5B9) and patient derived anti-PF4/H antibodies. Killing of bacteria was quantified by counting colony forming units (cfu) after incubation with platelets or platelet releasate. Using flow cytometry, platelet activation (CD62P-expression, PAC-1 binding) and phosphatidylserine (PS)-exposure were analyzed. RESULTS Monoclonal and patient-derived anti-PF4/H antibodies bound in the presence of PF4 to both S.aureus and S.pneumoniae (1.6-fold increased fluorescence signal for human anti-PF4/H antibodies to 24.0-fold increase for KKO). S.aureus (5.5×104 cfu/ml) was efficiently killed by platelets (2.7×104 cfu/ml)

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