Sentence examples for binding to platelets and from inspiring English sources

Centocor's Reopro, for instance, prevents blood clots by binding to platelets and preventing the platelets from clumping together.

Our observation that platelet-Fg weakly correlates with d-dimer levels suggests that fibrinogen binding to platelets and the activation of coagulation could be driven by the same factors.

Using this compound, along with highly selective second-generation inhibitors of AADACL1, metabolomics, and RNA interference, we show that AADACL1 regulates platelet aggregation, thrombus growth, RAP1 and PKC activation, lipid metabolism, and fibrinogen binding to platelets and megakaryocytes.

Our previous findings support the concept that CS chains promote survival in the circulation and tumor cell extravasation via P-selectin-mediated binding to platelets and endothelial cells.

Holly et al. also discovered that KIAA1363 regulates platelet aggregation, thrombus growth, RAP1 and PKC activation, ether lipid metabolism, and fibrinogen binding to platelets and megakaryocytes.

These patients had a higher SOFA score at admission; levels of fibrinogen binding to platelets (platelet-Fg) and of D-dimers were also significantly increased compared to the other patients.

To test this we examined the relationship between surface expression of PECAM-1 on unactivated platelets and its association with P-selectin exposure and fibrinogen binding to platelets in response to CRP-XL, ADP and TRAP, in 89 healthy subjects [20].

In ischemic stroke, two studies showed increased expression of platelet P-selectin and fibrinogen binding to platelets as compared to controls [25, 29].

When considering laboratory tests and flow cytometry parameters recorded within 24 h of admission to ICU (Table 2), d-dimers and fibrinogen binding to platelets (platelet-Fg expressed as MFI or %) were markedly higher (P < 0.001) in patients who later developed sepsis.

CD147, which is a platelet receptor that is upregulated on activated platelets, is a critical mediator of the positive regulators that are implicated in platelet activation, and its binding to platelets fosters platelet degranulation.

These mutants have also been shown to have impaired binding to platelets, resulting in increased complement-mediated platelet activation and release of tissue factor expressing microvesicles.