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However, firm evidence that these receptors mediate platelet stimulation by LPA and plaque lipid-rich core is lacking: The LPA response of platelets did not match with the pharmacological properties of the heterologously expressed LPA4 and LPA5 receptors, and the pharmacological receptor agonists and antagonists used were not selective for LPA5.
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In our previous studies, the identification of the functional LPA receptor(s) in platelets was carried out by using a pharmacological approach, and firm evidence that the LPA5 receptor mediates platelet stimulation by LPA and plaque lipid-rich core was lacking.
Although Vav1 is phosphorylated in platelets by thrombin stimulation [ 121], the phenotype of Vav1/Vav3−/− mice suggests Vav proteins do not mediate platelet function following PAR activation.
These glycoproteins mediate platelet adhesion and adherence.
Mean platelet volume (MPV) indicates average size of platelet; it could reflect the rate of platelet stimulation and production.
This evidence of platelet stimulation of neutrophils and neutrophil stimulation of platelets suggests a positive feedback loop leading to further stimulation and amplification of tissue injury [ 38].
Platelets also express a lower number of α5β1 and αvβ3 receptors on their surface, which mediate platelet adhesion [ 45].
The lag-time is the time between platelet stimulation and the initiation of aggregation.
In an ex vivo setting, solutions of hydroxyethyl starches impair coagulation and provoke platelet stimulation.
The small GTPase Rac is activated in the early stages of platelet stimulation.
Platelet stimulation with thrombin-plus-CRP rapidly triggers a sustained increase in [Ca2+]i.
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