ライフサイエンスコーパス: glycoprotein IIb

1 This protein does not appear to be glycoprotein IIb.

2 The platelet glycoprotein IIb (alpha(IIb); CD41) constitutes the alph

3 cific promoters platelet factor 4 (PF4), and glycoprotein IIb (GPIIb) as model systems to explore the

4 reviously, we have shown that, when bound to glycoprotein IIb (GPIIb), calcium- and integrin-binding

5 have cloned zebrafish CD41 cDNA (alpha(IIb), glycoprotein IIb [GPIIb]) and its promoter and have gene

6 P patients, 2E7, specific for human platelet glycoprotein IIb heavy chain, and 5E5, specific for a ne

7 The Platelet Glycoprotein IIb-IIIa in Unstable Angina: Receptor Suppr

8 Although clinical trial data suggest that glycoprotein IIb-IIIa inhibition benefits moderate-risk

9 ns consisting of aspirin, clopidogrel, and a glycoprotein IIb-IIIa inhibitor provide substantial bene

10 t therapy--including aspirin, clopidogrel, a glycoprotein IIb-IIIa inhibitor, and an anticoagulant--m

11 g important questions regarding the value of glycoprotein IIb-IIIa inhibitors as accompaniments of hi

12 oronary syndromes--aspirin, clopidogrel, and glycoprotein IIb-IIIa inhibitors for the majority of pat

13 ed surfaces, and suggest that currently used glycoprotein IIb-IIIa inhibitors may be effective inhibi

14 rprets the role of oral antiplatelet agents, glycoprotein IIb-IIIa inhibitors, and bivalirudin in the

15 agents such as aspirin, thienopyridines and glycoprotein IIb-IIIa inhibitors.

16 The major platelet integrin glycoprotein IIb-IIIa plays a primary role in platelet a

17 The integrin alpha(IIb)beta3 (glycoprotein IIb-IIIa) is a major platelet glycoprotein

18 s of the main aggregation receptor-activated glycoprotein IIb-IIIa, which might indicate a defect in

19 elet surface proteins, particularly platelet glycoprotein IIb/IIIa (alpha(IIb)beta(3)).

20 The expression of the glycoprotein IIb/IIIa (alphaIIb/beta3 integrin) receptor

21 al of this study was to test: 1) if platelet glycoprotein IIb/IIIa (GP IIb/IIIa) blockade with abcixi

22 PLACE)-2 trial, bivalirudin with provisional glycoprotein IIb/IIIa (Gp IIb/IIIa) inhibition was found

23 delines recommend administration of platelet glycoprotein IIb/IIIa (Gp IIb/IIIa) inhibitors, either u

24 Glycoprotein IIb/IIIa (Gp IIb/IIIa) receptor antagonists

25 Glycoprotein IIb/IIIa (GPIIb/IIIa) blockade was associat

26 precipitation analyses indicate that CIB and glycoprotein IIb/IIIa (GPIIb/IIIa) interact with each ot

27 Glycoprotein IIb/IIIa (GPIIb/IIIa) is the key receptor i

28 argeting another platelet adhesion receptor, glycoprotein IIb/IIIa (GPIIb/IIIa), also reduced EAE sev

29 and-induced binding site (LIBS) on activated glycoprotein IIb/IIIa (LIBS-MPIOs).

30 (5 and 20 micromol/L ADP), the activation of glycoprotein IIb/IIIa (PAC-1 antibody), and the expressi

31 urface receptors P-selectin, CD11b/CD18, and glycoprotein IIb/IIIa abrogated the changes in neutrophi

32 Markers of platelet activation, including glycoprotein IIb/IIIa activation and P-selectin expressi

33 received daily aspirin, thienopyridine, and glycoprotein IIb/IIIa agents during the procedure.

34 Targeting of scuPA to activated glycoprotein IIb/IIIa allows effective thrombolysis and

35 ed platelet surface P-selectin and activated glycoprotein IIb/IIIa and leukocyte-platelet aggregates;

36 ng a single-chain antibody against activated glycoprotein IIb/IIIa and the extracellular domain of CD

37 s with the recommended dose of heparins or a glycoprotein IIb/IIIa antagonist (safety), and its assoc

38 Pharmacodynamic effects of the platelet glycoprotein IIb/IIIa antagonist eptifibatide have been

39 els of platelet receptor occupancy (RO) by a glycoprotein IIb/IIIa antagonist in ST-elevation MI (STE

40 presence or absence of norepinephrine or the glycoprotein IIb/IIIa antagonist tirofiban.

41 ruses, and treating the mice with a specific glycoprotein IIb/IIIa antagonist, eptifibatide, had the

42 potent platelet inhibition from intravenous glycoprotein IIb/IIIa antagonists has reduced the rate o

43 bo-controlled, randomized trials of the oral glycoprotein IIb/IIIa antagonists have failed to provide

44 ntrolled trials testing intravenous platelet glycoprotein IIb/IIIa antagonists in the setting of perc

45 ide-in signaling are incompletely understood.Glycoprotein IIb/IIIa antagonists were developed under t

46 esized that long-term administration of oral glycoprotein IIb/IIIa antagonists, which block the aggre

47 Adjunctive angioplasty and use of glycoprotein IIb/IIIa antiplatelet agents at the time of

48 rction, stroke, urgent revascularization, or glycoprotein IIb/IIIa bailout through 7 days from random

49 coprotein IIb/IIIa inhibitor rescue therapy (glycoprotein IIb/IIIa bailout) through day 7, did not di

50 similar in those procedures with and without glycoprotein IIb/IIIa blockade (p = 0.94).

51 The effect of glycoprotein IIb/IIIa blockade on heparin rebound is unk

52 Platelet glycoprotein IIb/IIIa blockade with abciximab (ReoPro) i

53 py and enhance the selection of patients for glycoprotein IIb/IIIa blockade.

54 Lotrafiban, an orally administered platelet glycoprotein IIb/IIIa blocker, induced a 33% increase in

55 n and early catheterization; clopidogrel and glycoprotein IIb/IIIa blockers were encouraged.

56 onses to new pharmacological agents, such as glycoprotein IIb/IIIa blockers, in patients with acute m

57 had higher use of preprocedural aspirin and glycoprotein IIb/IIIa blockers, lower use of postprocedu

58 1:20 000) IgG antibody that reacted with the glycoprotein IIb/IIIa complex only in the presence of th

59 Whereas antagonists to P-selectin and glycoprotein IIb/IIIa had no effects on LPS-mediated ALI

60 Glycoprotein IIb/IIIa has low affinity for its soluble l

61 lving broader use of the early inhibition of glycoprotein IIb/IIIa in combination with an early invas

62 Inhibitor for STENTing (EPISTENT), Platelet glycoprotein IIb/IIIa in Unstable angina Receptor Suppre

63 e economic substudy of the PURSUIT (Platelet Glycoprotein IIB/IIIA In Unstable Angina: Receptor Suppr

64 for Occluded Arteries (GUSTO)-IIb, Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppr

65 ry Arteries (GUSTO) IIb, GUSTO-III, Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppr

66 429 patients from 153 sites in the Platelet glycoprotein IIb/IIIa in unstable angina: Receptor Suppr

67 egation in patients enrolled in the Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppr

68 We assessed the effect of glycoprotein IIb/IIIa inhibition (GPI) on microvascular

69 heparin (unfractionated or enoxaparin) plus glycoprotein IIb/IIIa inhibition (GPI), bivalirudin plus

70 heparin (unfractionated or enoxaparin) plus glycoprotein IIb/IIIa inhibition (GPI), bivalirudin plus

71 e care of patients with UA/NSTEMI, including glycoprotein IIb/IIIa inhibition and stenting, were asso

72 f combined fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition for improving reperfusi

73 esults from these and other recent trials of glycoprotein IIb/IIIa inhibition in acute coronary syndr

74 y intervention (PCI) in the EARLY ACS (Early Glycoprotein IIb/IIIa Inhibition in Non-ST-Segment Eleva

75 Patients from the EARLY-ACS (Early Glycoprotein IIb/IIIa Inhibition in Non-ST-Segment Eleva

76 Using data from the Early Glycoprotein IIb/IIIa Inhibition in Non-ST-Segment Eleva

77 al among 9211 patients enrolled in the Early Glycoprotein IIb/IIIa Inhibition in NSTE ACS (EARLY ACS)

78 syndromes (NSTEACS) in the EARLY ACS (Early Glycoprotein IIb/IIIa Inhibition in Patients With Non-ST

79 (EARLY ACS: Early Glycoprotein IIb/IIIa Inhibition in Patients With Non-ST

80 In the Early Glycoprotein IIb/IIIa Inhibition in Patients with Non-ST

81 have established the benefits of intravenous glycoprotein IIb/IIIa inhibition in the management of co

82 t criteria and designs, except that upstream glycoprotein IIb/IIIa inhibition was mandated and corona

83 The goal of this study was to evaluate glycoprotein IIb/IIIa inhibition with eptifibatide when

84 This rebound is attenuated by glycoprotein IIb/IIIa inhibition with eptifibatide.

85 cute coronary syndromes enrolled in the Oral Glycoprotein IIb/IIIa Inhibition with Orbofiban in Patie

86 ent revascularization was observed with oral glycoprotein IIb/IIIa inhibition, pooled analysis favore

87 tine radial artery access, and only bail-out glycoprotein IIb/IIIa inhibition.

88 inical outcomes after coronary stenting with glycoprotein IIb/IIIa inhibition.

89 udin (switch group, n = 1,178) or UFH plus a glycoprotein IIb/IIIa inhibitor (control group, n = 1,17

90 ention who were randomized to heparin plus a glycoprotein IIb/IIIa inhibitor (GPI) (n=1802) versus bi

91 ) versus unfractionated heparin (UFH) plus a glycoprotein IIb/IIIa inhibitor (GPI) (UFH+GPI; n = 1,80

92 safety of bivalirudin versus heparin plus a glycoprotein IIb/IIIa inhibitor (GPI) in patients with n

93 s in outcomes were because of differences in glycoprotein IIb/IIIa inhibitor (GPI) use, a test of med

94 assigned randomly to receive heparin plus a glycoprotein IIb/IIIa inhibitor (GPI), bivalirudin plus

95 than did patients assigned to heparin plus a glycoprotein IIb/IIIa inhibitor (GPI).

96 domized to either bivalirudin or heparin+/-a glycoprotein IIb/IIIa inhibitor (GPI).

97 t thrombosis rates compared with heparin + a glycoprotein IIb/IIIa inhibitor (GPI).

98 1:1 to receive bivalirudin or heparin plus a glycoprotein IIb/IIIa inhibitor (GPI; pharmacological ra

99 (n = 1,800) or unfractionated heparin plus a glycoprotein IIb/IIIa inhibitor (n = 1,802).

100 compared with unfractionated heparin plus a glycoprotein IIb/IIIa inhibitor (UFH+GPI) can be fully a

101 antithrombotic treatments (anticoagulant +/- glycoprotein IIb/IIIa inhibitor [GPI]).

102 Both stenting and the glycoprotein IIb/IIIa inhibitor abciximab improve outcom

103 istent across 4 trials with 3 different oral glycoprotein IIb/IIIa inhibitor agents, this was associa

104 ization to bivalirudin versus heparin plus a glycoprotein IIb/IIIa inhibitor and use of drug-eluting

105 e-Type Plasminogen Activator With or Without Glycoprotein IIb/IIIa Inhibitor as Reperfusion Strategy

106 platelet activation with either aspirin or a glycoprotein IIb/IIIa inhibitor decreased NET formation

107 ars, white race, and use of bivalirudin or a glycoprotein IIb/IIIa inhibitor during coronary interven

108 upporting the benefits of enoxaparin and the glycoprotein IIb/IIIa inhibitor eptifibatide evolved in

109 bivalirudin alone rather than heparin plus a glycoprotein IIb/IIIa inhibitor for nearly all patients.

110 primary PCI to treatment with heparin plus a glycoprotein IIb/IIIa inhibitor or to treatment with biv

111 eatment-related variable (use of heparin + a glycoprotein IIb/IIIa inhibitor rather than bivalirudin

112 rction, stroke, urgent revascularization, or glycoprotein IIb/IIIa inhibitor rescue therapy (glycopro

113 Glycoprotein IIb/IIIa inhibitor therapy appears to be un

114 el revascularization, and thrombotic bailout glycoprotein IIb/IIIa inhibitor therapy at 48 h) was act

115 Although PI > or = 95% measured 10 min after glycoprotein IIb/IIIa inhibitor therapy is associated wi

116 vo study of combination intravenous platelet glycoprotein IIb/IIIa inhibitor therapy.

117 Enoxaparin or the combination of glycoprotein IIb/IIIa inhibitor tirofiban with unfractio

118 -segment elevation who were treated with the glycoprotein IIb/IIIa inhibitor tirofiban, the use of an

119 were treated with aspirin, heparin, and the glycoprotein IIb/IIIa inhibitor tirofiban.

120 Until recently, the selection of which glycoprotein IIb/IIIa inhibitor to use for patients with

121 riate subgroup analyses performed across the glycoprotein IIb/IIIa inhibitor trials.

122 s (P<0.01), increasing patient age (P<0.01), glycoprotein IIb/IIIa inhibitor use (P=0.02), and curren

123 rction, urgent revascularisation, or bailout glycoprotein IIb/IIIa inhibitor use up to 7 days.

124 de of the reduction depending on concomitant glycoprotein IIb/IIIa inhibitor use.

125 tment with bivalirudin versus heparin plus a glycoprotein IIb/IIIa inhibitor was associated with a no

126 An intravenous glycoprotein IIb/IIIa inhibitor was used in 48.2% of the

127 lopidogrel; and 1.82 [95% CI, 1.43-2.32] for glycoprotein IIb/IIIa inhibitor); however, an early inva

128 ngioguard, or double-blind use of a platelet glycoprotein IIb/IIIa inhibitor, abciximab, in a 2x2 fac

129 , 35% with early clopidogrel, 14% with early glycoprotein IIb/IIIa inhibitor, and 36% with early inva

130 Bivalirudin plus a glycoprotein IIb/IIIa inhibitor, as compared with hepari

131 Compared with unfractionated heparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin monotherapy

132 th acute coronary syndrome to heparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glyc

133 1 of 3 antithrombin regimens (heparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glyc

134 unfractionated heparin or enoxaparin plus a glycoprotein IIb/IIIa inhibitor, bivalirudin plus a glyc

135 h either bivalirudin alone or a heparin plus glycoprotein IIb/IIIa inhibitor, bleeding complications

136 f serious bleeding were female sex, use of a glycoprotein IIb/IIIa inhibitor, duration of interventio

137 Eptifibatide, a small-molecule glycoprotein IIb/IIIa inhibitor, is conventionally admin

138 cytopenia, catheter thrombus, bailout use of glycoprotein IIb/IIIa inhibitor, or any bleeding through

139 otein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin alone.

140 otein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin alone.

141 otein IIb/IIIa inhibitor, bivalirudin plus a glycoprotein IIb/IIIa inhibitor, or bivalirudin monother

142 rudin alone, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with a n

143 a inhibitor, as compared with heparin plus a glycoprotein IIb/IIIa inhibitor, was associated with non

144 utrophil receptor CD11b/CD18, and a platelet glycoprotein IIb/IIIa inhibitor, were incubated with cel

145 ndication, with or without the addition of a glycoprotein IIb/IIIa inhibitor.

146 imilar efficacy compared with heparin plus a glycoprotein IIb/IIIa inhibitor.

147 welve patients (86%) received an intravenous glycoprotein IIb/IIIa inhibitor; none underwent atherect

148 4% versus 1.4%; P=1.00) or with heparin plus glycoprotein IIb/IIIa inhibitors (1.1%) compared with bi

149 e primary outcome compared with heparin plus glycoprotein IIb/IIIa inhibitors (2.7% versus 7.3%, adju

150 in alone and those who received heparin plus glycoprotein IIb/IIIa inhibitors (230 [9%] patients vs 2

151 ith bivalirudin (28,378) or with heparin and glycoprotein IIb/IIIa inhibitors (35,674).

152 e than among those who received heparin plus glycoprotein IIb/IIIa inhibitors (92 [4%] patients vs 17

153 ive coronary revascularization, aspirin, and glycoprotein IIb/IIIa inhibitors (all P<0.0001) may have

154 hibitors and those who received heparin plus glycoprotein IIb/IIIa inhibitors (composite ischaemia: 2

155 r low-molecular-weight heparin with optional glycoprotein IIb/IIIa inhibitors (control group).

156 ischemic and bleeding risks associated with glycoprotein IIb/IIIa inhibitors (GPIs) and a potent P2Y

157 as to investigate the efficacy and safety of glycoprotein IIb/IIIa inhibitors (GPIs) during elective

158 with heparin with routine or optional use of glycoprotein IIb/IIIa inhibitors (GPIs) in patients with

159 el in subgroups that did and did not receive glycoprotein IIb/IIIa inhibitors (GPIs).

160 f mortality or reinfarction with intravenous glycoprotein IIb/IIIa inhibitors (P=0.17, 0.70, and 0.50

161 rategy of Enoxaparin, Revascularization, and Glycoprotein IIb/IIIa Inhibitors (SYNERGY) trial were an

162 erhaps more importantly, the combined use of glycoprotein IIb/IIIa inhibitors and intracoronary stent

163 rmed prior to the widespread use of platelet glycoprotein IIb/IIIa inhibitors and intracoronary stent

164 Concomitant administration of intravenous glycoprotein IIb/IIIa inhibitors and ischemic time did n

165 ngiotensin-converting enzyme inhibitors, and glycoprotein IIb/IIIa inhibitors and less commonly recei

166 ailability of stents, and more recent use of glycoprotein IIb/IIIa inhibitors and low-molecular-weigh

167 Antithrombotic effects of glycoprotein IIb/IIIa inhibitors and magnesium are known

168 tal initiation of treatment, optional use of glycoprotein IIb/IIIa inhibitors and novel P2Y12 inhibit

169 he older elderly were less likely to receive glycoprotein IIb/IIIa inhibitors and statins during the

170 between those who received bivalirudin plus glycoprotein IIb/IIIa inhibitors and those who received

171 first device with consequently higher use of glycoprotein IIb/IIIa inhibitors and thrombus aspiration

172 In particular, use of glycoprotein IIb/IIIa inhibitors and/or low-molecular-we

173 Although intravenous glycoprotein IIb/IIIa inhibitors are beneficial in patie

174 Glycoprotein IIb/IIIa inhibitors are indicated in patien

175 Trials of platelet glycoprotein IIb/IIIa inhibitors as adjuncts to primary

176 clopidogrel before randomization, and use of glycoprotein IIb/IIIa inhibitors at randomization.

177 produced by treatment with platelet-specific glycoprotein IIb/IIIa inhibitors demonstrating a detrime

178 Adjustment for the use of glycoprotein IIb/IIIa inhibitors did not change the resu

179 lopidogrel, prasugrel, or aspirin along with glycoprotein IIb/IIIa inhibitors during the procedure.

180 Glycoprotein IIb/IIIa inhibitors enhance thrombolysis.

181 a roll-in group (n=2) treated with REG1 plus glycoprotein IIb/IIIa inhibitors followed by 2 groups ra

182 therapy with reduced-dose fibrinolytics and glycoprotein IIb/IIIa inhibitors for ST-segment elevatio

183 e-receptor antagonists, the need for routine glycoprotein IIb/IIIa inhibitors has diminished.

184 ents including aspirin, thienopyridines, and glycoprotein IIb/IIIa inhibitors has led to a major redu

185 Although glycoprotein IIb/IIIa inhibitors have been shown to redu

186 Glycoprotein IIb/IIIa inhibitors have improved outcomes

187 ation, agents in the class known as platelet glycoprotein IIb/IIIa inhibitors have significantly redu

188 unctive use of embolic protection devices or glycoprotein IIb/IIIa inhibitors improves renal function

189 ty compared with unfractionated heparin plus glycoprotein IIb/IIIa inhibitors in patients in the uppe

190 more appropriate alternative, to heparin and glycoprotein IIb/IIIa inhibitors in patients with chroni

191 n in clopidogrel maintenance dose and use of glycoprotein IIb/IIIa inhibitors in selected patients.

192 in compared with unfractionated heparin plus glycoprotein IIb/IIIa inhibitors in the Harmonizing Outc

193 h-risk acute coronary syndromes treated with glycoprotein IIb/IIIa inhibitors in whom percutaneous co

194 It is not clear if combining enoxaparin with glycoprotein IIb/IIIa inhibitors is as safe or as effect

195 on with PTCA, coronary stenting and platelet glycoprotein IIb/IIIa inhibitors may further improve out

196 New data regarding the use of glycoprotein IIb/IIIa inhibitors now exist and low molec

197 ter anticoagulation with either heparin plus glycoprotein IIb/IIIa inhibitors or bivalirudin with or

198 at in persons with acute coronary syndromes, glycoprotein IIb/IIIa inhibitors or clopidogrel plus sta

199 It is unclear whether intravenous glycoprotein IIb/IIIa inhibitors or ischemic time might

200 compared with those treated with heparin and glycoprotein IIb/IIIa inhibitors overall and in the PCI

201 Bivalirudin use compared with glycoprotein IIb/IIIa inhibitors plus heparin as an anti

202 monstrated the superiority of bivalirudin to glycoprotein IIb/IIIa inhibitors plus heparin in patient

203 The value of prehospital initiation of glycoprotein IIb/IIIa inhibitors remains a controversial

204 Although many believe that platelet glycoprotein IIb/IIIa inhibitors should be used only in

205 Treatment with bivalirudin glycoprotein IIb/IIIa inhibitors significantly reduced m

206 to compare the antithrombotic effects of the glycoprotein IIb/IIIa inhibitors tirofiban and eptifibat

207 cebo-controlled, randomized trials with oral glycoprotein IIb/IIIa inhibitors were calculated and com

208 Stents were used in 12 trials, and platelet glycoprotein IIb/IIIa inhibitors were used in eight.

209 Glycoprotein IIb/IIIa inhibitors were used more frequent

210 ried greatly (p<0.0001) depending on whether glycoprotein IIb/IIIa inhibitors were used predominantly

211 ss (OR, 0.89; 95% CI, 0.57-1.41) and planned glycoprotein IIb/IIIa inhibitors were used with bivaliru

212 of aspirin and clopidogrel (with or without glycoprotein IIb/IIIa inhibitors) in percutaneous corona

213 trategy of Enoxaparin, Revascularization and Glycoprotein IIb/IIIa Inhibitors) studies and to study t

214 trategy of Enoxaparin, Revascularization and GlYcoprotein IIb/IIIa inhibitors) study treated with PCI

215 rategy of Enoxaparin, Revascularization, and Glycoprotein IIb/IIIa Inhibitors) trial.

216 ylic acid, thienopyridines, thianopyridines, glycoprotein IIb/IIIa inhibitors), and antithrombotic ag

217 nhibitors; P=0.0002 versus 4.4% heparin with glycoprotein IIb/IIIa inhibitors).

218 ary intervention, 2561 received heparin plus glycoprotein IIb/IIIa inhibitors, 2609 received bivaliru

219 tein IIb/IIIa inhibitors, 9.7%; heparin plus glycoprotein IIb/IIIa inhibitors, 9.1%).

220 alirudin monotherapy, 9.6%; bivalirudin plus glycoprotein IIb/IIIa inhibitors, 9.7%; heparin plus gly

221 In patients not receiving planned glycoprotein IIb/IIIa inhibitors, a significant increase

222 receive newer ACS therapies, including acute glycoprotein IIb/IIIa inhibitors, acute and discharge cl

223 a inhibitors, 2609 received bivalirudin plus glycoprotein IIb/IIIa inhibitors, and 2619 received biva

224 received bivalirudin, 699 patients received glycoprotein IIb/IIIa inhibitors, and 676 patients recei

225 ng 3 types of platelet antagonists, aspirin, glycoprotein IIb/IIIa inhibitors, and adenosine diphosph

226 icrovascular dysfunction, including platelet glycoprotein IIb/IIIa inhibitors, and agents designed to

227 ments such as low-molecular-weight heparins, glycoprotein IIb/IIIa inhibitors, and an early invasive

228 erapies, such as thrombolysis, vasodilators, glycoprotein IIb/IIIa inhibitors, and anti-inflammatory

229 Transradial access, adjunctive glycoprotein IIb/IIIa inhibitors, and potent P2Y12 inhib

230 ation, concurrent administration of platelet glycoprotein IIb/IIIa inhibitors, and the exact mechanis

231 heparin (unfractionated or enoxaparin) plus glycoprotein IIb/IIIa inhibitors, bivalirudin plus glyco

232 who were undergoing invasive treatment with glycoprotein IIb/IIIa inhibitors, bivalirudin was associ

233 lowing: age, sex, intra-aortic balloon pump, glycoprotein IIb/IIIa inhibitors, chronic kidney disease

234 d with drug-induced thrombocytopenia include glycoprotein IIb/IIIa inhibitors, cinchona alkaloids, an

235 acute coronary syndrome who are treated with glycoprotein IIb/IIIa inhibitors, even small elevations

236 Bivalirudin, as compared with heparin and glycoprotein IIb/IIIa inhibitors, has been shown to redu

237 ut percutaneous coronary intervention [PCI], glycoprotein IIb/IIIa inhibitors, low-molecular-weight h

238 rotein IIb/IIIa inhibitors, bivalirudin plus glycoprotein IIb/IIIa inhibitors, or bivalirudin alone.

239 between RPH and arterial sheath size, use of glycoprotein IIb/IIIa inhibitors, or deployment of a vas

240 lirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, resulted in a reduced

241 lirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, resulted in significan

242 lirudin alone, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, results in significant

243 r bivalirudin, as compared with heparin plus glycoprotein IIb/IIIa inhibitors, results in similar sup

244 nts to a similar extent as does heparin plus glycoprotein IIb/IIIa inhibitors, while significantly lo

245 ractionated heparin (85 U/kg or 60 U/kg with glycoprotein IIb/IIIa inhibitors, with ACT guidance).

246 P2Y12 inhibitors without the planned use of glycoprotein IIb/IIIa inhibitors.

247 el, or cangrelor) without the planned use of glycoprotein IIb/IIIa inhibitors.

248 were preloaded with clopidogrel and received glycoprotein IIb/IIIa inhibitors.

249 ionated or low-molecular-weight heparin, and glycoprotein IIb/IIIa inhibitors.

250 d combination of unfractionated heparin with glycoprotein IIb/IIIa inhibitors.

251 th prior trials performed without the use of glycoprotein IIb/IIIa inhibitors.

252 n the setting of PCI and in conjunction with glycoprotein IIb/IIIa inhibitors.

253 ations for the cost-effective utilization of glycoprotein IIb/IIIa inhibitors.

254 parin and aspirin, and in high-risk patients glycoprotein IIb/IIIa inhibitors.

255 ng in the era before routine use of platelet glycoprotein IIb/IIIa inhibitors.

256 ic complications in patients with or without glycoprotein IIb/IIIa inhibitors.

257 leeding compared with heparins plus optional glycoprotein IIb/IIIa inhibitors.

258 monotherapy; P=0.005, 2.0% bivalirudin plus glycoprotein IIb/IIIa inhibitors; P=0.0002 versus 4.4% h

259 ractions using antagonists to P-selectin and glycoprotein IIb/IIIa or a small peptide antagonist disr

260 ir respective receptors (eg, fibrinogen with glycoprotein IIb/IIIa or factor V with phosphatidylserin

261 y thrombus with a compound that binds to the glycoprotein IIb/IIIa present on activated platelets (DM

262 combination of a fibrin-specific agent and a glycoprotein IIb/IIIa receptor antagonist in patients >7

263 el of embolic stroke treated with rtPA and a glycoprotein IIb/IIIa receptor antagonist, 7E3 F(ab')2,

264 ory effects of currently prescribed platelet glycoprotein IIb/IIIa receptor antagonists during and af

265 The role of glycoprotein IIb/IIIa receptor antagonists for the treat

266 h gender differences in response to platelet glycoprotein IIb/IIIa receptor blockade have been descri

267 Previous work has suggested that platelet glycoprotein IIb/IIIa receptor blockade may confer benef

268 preprocedural aspirin or clopidogrel, use of glycoprotein IIb/IIIa receptor blockers and postprocedur

269 The use of platelet glycoprotein IIb/IIIa receptor blockers did not appear t

270 Clinical benefit was seen even when platelet glycoprotein IIb/IIIa receptor blockers were administere

271 ), antiplatelet drugs (aspirin, P2Y(12), and glycoprotein IIb/IIIa receptor blockers), and anticoagul

272 mended drug regimens to inhibit the platelet glycoprotein IIb/IIIa receptor have distinct pharmacodyn

273 eding predictors among patients treated with glycoprotein IIb/IIIa receptor inhibition might aid in t

274 bination reperfusion therapy with a platelet glycoprotein IIb/IIIa receptor inhibitor (abciximab) and

275 AST when either bivalirudin or heparin plus glycoprotein IIb/IIIa receptor inhibitor (GPI) is used.

276 nd less bleeding than regimens incorporating glycoprotein IIb/IIIa receptor inhibitors (GPI) for mode

277 s designed to evaluate the safety profile of glycoprotein IIb/IIIa receptor inhibitors (GPI) in octog

278 post-PCI cTFC rank score was the first bolus glycoprotein IIb/IIIa receptor occupancy (P<0.001).

279 nt resolution with higher levels of platelet glycoprotein IIb/IIIa receptor occupancy after therapy w

280 tide may result in higher levels of platelet glycoprotein IIb/IIIa receptor occupancy in the local co

281 The primary end point was the local glycoprotein IIb/IIIa receptor occupancy measured in the

282 Platelet glycoprotein IIb/IIIa receptor occupancy was significant

283 y syndromes results in higher local platelet glycoprotein IIb/IIIa receptor occupancy, which is assoc

284 om Bitis arietans venom, binds avidly to the glycoprotein IIb/IIIa receptor on platelets.

285 The absolute number of glycoprotein IIb/IIIa receptors available for cross-link

286 bleeding and mortality observed in the oral glycoprotein IIb/IIIa studies indicate the consequences

287 increase in mortality was observed with oral glycoprotein IIb/IIIa therapy (OR, 1.37; 95% CI, 1.13 to

288 itional insight into therapeutic efficacy of glycoprotein IIb/IIIa therapy similar to that demonstrat

289 single-chain antibody specific for activated glycoprotein IIb/IIIa via binding to a Ligand-Induced Bi

290 on the ability of integrin alpha IIb beta 3 (glycoprotein IIb/IIIa) to interact with components of th

291 rins, alpha(V)beta(3) and alpha(IIb)beta(3) (glycoprotein IIb/IIIa), and leukocytes have been implica

292 a cyclic heptapeptide antagonist of platelet glycoprotein IIb/IIIa, are substantially altered by anti

293 By virtue of its cross-reactivity with the glycoprotein IIb/IIIa, avbeta3, and alphaMbeta2 receptor

294 Glycoprotein IIb/IIIa-blocking therapy is safe, and with

295 We demonstrate that glycoprotein IIb/IIIa-targeted MBs specifically bind to

296 the activated form of the platelet-integrin glycoprotein IIb/IIIa.

297 elet transcripts, including clusterin (CLU), glycoproteins IIb/IIIa (ITGA2B/3), lipocalin (LCN2), lac

298 The addition of glycoprotein IIb or IIIa inhibitors to fibrinolytic ther

299 The addition of glycoprotein IIb or IIIa inhibitors to fibrinolytic ther

300 s deficient in the platelet integrin subunit glycoprotein IIb or in embryos in which platelet alpha-g