コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 in was potentiated by ADP acting through the P2Y12 receptor.
2 y active, and its activity is potentiated by P2Y12 receptors.
3 ATP release, and microglial response through P2Y12 receptors.
4 d an autocrine ADP-mediated response through P2Y12 receptors.
5 addition to that derived from antagonism of P2Y12 receptors.
6 CysLT1R and CysLT2R but not in mice lacking P2Y12 receptors.
7 d in the initiation of platelet aggregation, P2Y12 receptor activation appears to account for the bul
8 process outgrowth to damaged tissue requires P2Y12 receptor activation but is unaffected by blocking
10 of a local thrombus, dual inhibition of the P2Y12 receptor and calcium mobilization result in a comp
11 is dependent on both the G(alpha)(i)-coupled P2Y12 receptor and the G(alpha)(q)-coupled P2Y1 receptor
12 mole inhibit platelet function by inhibiting P2Y12 receptors and platelet phosphodiesterase, respecti
14 s a potent, highly selective, and reversible P2Y12 receptor antagonist and by far the most potent inh
15 ubstituents on the ribose and base conferred P2Y12 receptor antagonist properties to these molecules
21 on of platelets with aspirin, but not with a P2Y12 receptor antagonist, caused a marked reduction in
22 d by either the integrin inhibitor RGDS or a P2Y12 receptor antagonist, indicating a requirement for
24 heral arterial disease, or following a brief P2Y12-receptor antagonist interruption, whereas clopidog
25 Platelet inhibitory effects induced by oral P2Y12 receptor antagonists are delayed in patients with
26 lar patients who smoke benefit from platelet P2Y12 receptor antagonists more than their nonsmoking pe
27 ntagonists), cyclopentyltriazolopyrimidines (P2Y12 receptor antagonists), anti-von Willebrand factor
28 al study, consisting of the thienopyridines (P2Y12 receptor antagonists), cyclopentyltriazolopyrimidi
29 morphine and its potential interactions with P2Y12 receptor antagonists, as well as on the central is
31 As head-to-head comparative trials between P2Y12-receptor antagonists are lacking, selection of a s
32 r and inside-out signaling from the P2Y1 and P2Y12 receptors are necessary for phospholipase A(2) act
36 P did not require Gi signaling or functional P2Y12 receptors but was mediated through activation of a
39 rful synergism is explained by blockade of a P2Y12 receptor-dependent, NO/cGMP-insensitive phosphatid
40 epinephrine (alpha(2A)-adrenergic) and ADP (P2Y12) receptors display strong preferences among G(i) f
41 thus reduces surveillance, whereas blocking P2Y12 receptors does not affect membrane potential, rami
46 ently identified functional effector for the P2Y12 receptor, in the regulation of ADP-induced TXA2 ge
48 stenting and treatment strategies to improve P2Y12 receptor inhibition in patients with high post-tre
49 phoprotein phosphorylation levels to measure P2Y12 receptor inhibition were determined (n = 20) and c
54 me (ACS) patients are not pre-treated with a P2Y12 receptor inhibitor, and percutaneous coronary inte
57 after discharge for beta-blockers, platelet P2Y12 receptor inhibitors, statins, and angiotensin-conv
62 osine diphosphate (ADP)-reactive purinergic (P2Y12) receptor is required for LTE4-mediated pulmonary
63 Because clopidogrel antagonizes the platelet P2Y12 receptor, it is widely prescribed for patients wit
66 ntial signalling and cell activation through P2Y12 receptor or receptor heterodimers but no specific
69 Ticagrelor is a potent antagonist of the P2Y12 receptor (P2Y12R) and consequently an inhibitor of
70 ed BSM contraction is blocked by a selective P2Y12 receptor (P2Y12R) antagonist, PSB 0739 (25 muM), b
73 th tests measuring the adenosine diphosphate-P2Y12 receptor pathway, without significant variations i
75 elated factors (higher on-treatment platelet P2Y12 receptor reactivity and premature thienopyridine d
76 ene adenosine 5'-triphosphate (AR-C67085), a P2Y12 receptor-selective antagonist, and adenosine-2'-ph
77 inhibited in the presence of AR-C69931MX, a P2Y12 receptor-selective antagonist, or GF 109203X, a pr
78 or that abolishes secretion, or AR-C66096, a P2Y12 receptor-selective antagonist; alpha-thrombin-indu
82 in undergoes synergy with ADP acting via the P2Y12 receptor whereas there is no synergy via the P2Y1
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。