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Mouse platelets do not contain S1P but they contain and release DHS1P upon stimulation [ 14].
More recent studies have failed to clear up the controversy; although eNOS is reportedly present in bovine platelets (11), other groups have concluded that human and mouse platelets do not express either eNOS or inducible NOS and that some platelet agonists directly affect the soluble guanylyl cyclase, resulting in an NO-independent activation of the cyclic GMP signaling pathway (13).
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Although the lack of an identified role for Rif in mouse platelets does not preclude a role for the protein in human platelets, the question of which Rho GTPase(s) regulate platelet filopodia formation remains open.
Even the loss of the core SNARE STX11 in FHL4 patients [62] or the knockout of VAMP8 coupled with tetanus neurotoxin (TnT-LC) treatment in mouse platelets [69], does not lead to full ablation of secretion, suggesting ranked redundancy and compensation mechanisms [69].
It should be stressed that mouse platelets, in contrast to human and non-human primate platelets, do not express FcRs and, therefore, these published studies suggest that blocking CD40L alone would not contribute to an increased incidence of thrombosis and possibly would even suppress thrombosis under certain conditions.
HBO-treated young mice exhibited an increase in lymphocyte and monocyte counts relative to control air-breathing mice (p < 0.05), but blood counts of total white blood cells, basophils, eosinophils, red blood cells and platelets did not differ.
Platelets did not differ between groups.
WT platelets did not bind to III-01c.
Their interaction with platelets did not augment their invasive capabilities.
WBCs and platelets did not differ among groups.
CD82 was present on the surface of both human and mouse platelets, and its levels did not change upon platelet activation or degranulation.
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