Sentence examples for platelet function phenotypes from inspiring English sources

Heritability studies of agonist-induced platelet function phenotypes suggest that genetic variation may be responsible for ASA responsiveness.

To date only specific agonists or single pathway platelet function phenotypes have been examined offering little insight into the potentially complex interplay among platelet function cascades.

Clinical data on 37 agonist-induced platelet function phenotypes were evaluated before and after a 2-week trial of ASA (81 mg/day) in 1231 European American and 846 African American healthy subjects with a family history of premature CAD.

Previously, we have found evidence of moderate to high heritability of platelet function phenotypes, in both the presence [ 10] and absence of aspirin [ 11], suggesting that genetic variants contribute to differences among individuals in platelet activation and response to aspirin therapy.

The results of applying the methods on the four phenotypes of platelet function can be found in the Supplementary Tables S8 S11.

Clinical data on agonist-induced platelet function, PFA, and Tx-M phenotypes were evaluated in healthy subjects with a family history of premature CAD before and after a 2-week trial of ASA (81 mg/day).

While the PCA-derived phenotypic values are not in and of themselves intuitively informative, they enable the identification of possibly important loci for more integrated platelet phenotypes that represent baseline platelet function or true global responses to aspirin.

However, these cases also displayed abnormal platelet function indicating that the PV only partially explained the phenotype.

Previously reported collections have comprised BPD cases without prior investigation [ 4, 5] and collections linked by similar phenotypes such as abnormal platelet number [ 38], platelet function [ 33] or von Willebrand disease [ 21, 39].

Although a compensatory up-regulation of PP1cα and PP1cβ isoforms was not particularly evident in PP1cγ−/− platelets, a potential redundancy between the individual PP1c isoforms in PP1cγ−/− platelet function is to be expected and may underlie the mild platelet phenotype seen in PP1cγ−/− mice.

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.