ライフサイエンスコーパス: platelet activation

1 was found to inhibit both FGF2 signaling and platelet activation.

2 y on the blood coagulation cascade including platelet activation.

3 migration, effects on blood coagulation, and platelet activation.

4 ous in patients with increased intravascular platelet activation.

5 th functions beyond inhibiting ITAM-mediated platelet activation.

6 at contribute to its effective inhibition of platelet activation.

7 R2) may represent a more global mechanism of platelet activation.

8 0 Hematology System as a marker surrogate of platelet activation.

9 tion risk during HFRS, which could be due to platelet activation.

10 lammation and upregulation of podoplanin and platelet activation.

11 c reticulum protein 5 (ERp5), is involved in platelet activation.

12 platelet surface GPCR P2Y12 and thus inhibit platelet activation.

13 and that they may be targeted independent of platelet activation.

14 alpha-granule secretion, a key component of platelet activation.

15 cal glycoprotein VI-mediated (GPVI-mediated) platelet activation.

16 on, even in the absence of thrombin-mediated platelet activation.

17 3, which plays a negative role in regulating platelet activation.

18 a negative regulator of FcgammaRIIA-mediated platelet activation.

19 te, and therefore extent, of GPVI-stimulated platelet activation.

20 ide galactosaminogalactan potently triggered platelet activation.

21 he potential use of miRNAs as biomarkers for platelet activation.

22 y cells, and blood samples were assessed for platelet activation.

23 (ADP) secreted from dense granules, trigger platelet activation.

24 NO is formed by red blood cells and inhibits platelet activation.

25 eted strategies that counter cooling-induced platelet activation.

26 phoinositide 3-kinase (PI3K) activity during platelet activation.

27 thrombin activity, and appears prior to full platelet activation.

28 rylated and is rapidly dephosphorylated upon platelet activation.

29 ectively propagate the signal and coordinate platelet activation.

30 of lysosomal enzymes that are released upon platelet activation.

31 (IgG) to form immune complexes that promote platelet activation.

32 of PAR4 internalization reduces integrin and platelet activation.

33 assessed their contribution in H1N1-induced platelet activation.

34 n tumor growth/metastasis and thrombocytosis/platelet activation.

35 h a dose-dependent inhibition of ADP-induced platelet activation.

36 ation inhibitory factor (MIF) is released on platelet activation.

37 It is unclear how these interactions lead to platelet activation.

38 ype lectin-like receptor 2 (CLEC-2)-mediated platelet activation.

39 in coupled receptors play important roles in platelet activation.

40 Thus, creatine kinase reduces ADP-induced platelet activation.

41 (PAR) 1 and PAR4 have differential roles in platelet activation.

42 the major signaling pathways responsible for platelet activation.

43 pal target for prevention of immune-mediated platelet activation.

44 of a new receptor-ligand pair that inhibits platelet activation.

45 ncubation with LTA, an effect which inhibits platelet activation.

46 gulation, anticoagulation, and initiation of platelet activation.

47 role in the regulation of vascular tone and platelet activation.

48 complications associated with shear-mediated platelet activation.

49 bserved, for instance, at the onset of blood platelet activation.

50 so performed to explore the effect of LPS on platelet activation.

51 y proposed numerical model of shear-mediated platelet activation.

52 rinogen, and acts as a positive regulator of platelet activation.

53 al lipopolysaccharide (LPS) is implicated in platelet activation.

54 wn that TRAF2 plays a role in CD40L-mediated platelet activation.

55 and an 80% reduction in IP3 generation upon platelet activation.

56 SK9 as a mechanism potentially implicated in platelet activation.

57 dro-thromboxane B2 (11-dh-TxB2), a marker of platelet activation.

58 ng that loss of SERTs causes a deficiency in platelet activation.

59 et agents, leading to impaired inhibition of platelet activation.

60 ion, acting convergently to increase AKT and platelet activation.

61 olymerization and sickling, coagulation, and platelet activation.

62 structures with distinct areas of differing platelet activation.

63 y to inhibit thrombin- and collagen-mediated platelet activation.

64 nsors were adopted to monitor the process of platelet activation.

65 ced NETs formation in an indirect manner via platelets activation.

66 thematical model of a key initiating step in platelet activation, a central process in the prevention

67 signaling, or genetic inhibition of maternal platelet activation abolishes the PE-like phenotype.

68 Inhibiting platelet activation abrogated the ability of platelets t

69 et dependent, yet the role of purines in the platelet activation accompanying inflammation is unknown

70 endothelial regeneration, and inhibition of platelet activation after coronary interventions.

71 a significant relative increase of 23.1% in platelet activation after PT transfusion (42.2+/-23.6% v

72 Plaque rupture or erosion stimulates platelet activation, aggregation, and thrombosis, whilst

73 e of BAMBI had no effect on platelet counts, platelet activation, aggregation, or platelet procoagula

74 in (Efb) from Staphylococcus aureus inhibits platelet activation, although its mechanism of action ha

75 ining intrathrombus agonist distribution and platelet activation and (2) define a novel role for inte

76 all aspects of thrombus formation, including platelet activation and adhesion, and activation of the

77 Inappropriate platelet activation and adhesion, however, can lead to t

78 SbO4L prevented thrombin-mediated platelet activation and aggregation as expected on the b

79 RBC transfusion increases in vitro platelet activation and aggregation in healthy volunteer

80 ssed the effect of ex vivo and in vivo PT on platelet activation and aggregation in patients on dual

81 Interestingly, platelet activation and aggregation in response to agoni

82 Pharmacologic inhibitors of ERK5 blunted platelet activation and aggregation in response to oxLDL

83 bility of quercetin and apigenin to modulate platelet activation and aggregation, and compared the ob

84 ed von Willebrand factor (VWF), factor VIII, platelet activation and aggregation, platelet-dependent

85 hetic compounds modulated significantly both platelet activation and aggregation, thus turning out to

86 -activating peptide (PAR4-AP), which induced platelet activation and aggregation, was successful in d

87 minescent detection of NO, and inhibition of platelet activation and aggregation.

88 mboxane (TX) A2 production and TXA2-mediated platelet activation and aggregation.

89 ion by MKs and as an unexpected regulator of platelet activation and arterial thrombus formation dyna

90 cally phagocytose PMPs generated at sites of platelet activation and as a way to effect endothelial r

91 o viral analogs and intact virus, leading to platelet activation and binding to various leukocyte sub

92 ned leukocytes, as well as the potential for platelet activation and clogging, are significant drawba

93 Platelet activation and cytoskeleton reorganization were

94 g/ml], and this was associated with impaired platelet activation and enhanced inflammatory responses.

95 ficant prolonged bleeding time by inhibiting platelet activation and extracellular mitochondrial DNA

96 ement factors make distinct contributions to platelet activation and fibrin deposition.

97 This dysfunction correlates with platelet activation and hemolysis in vivo and can be rec

98 alters serotonergic signaling and influences platelet activation and hemostasis.

99 d positively with markers of endothelial and platelet activation and histidine-rich protein-2 levels,

100 Undesired Fc-mediated functions, such as platelet activation and IL-8 release induced by the porc

101 Thus, TRAF3 plays a negative role in platelet activation and in thrombus formation in vivo.

102 PE is associated with coagulation and platelet activation and increased extracellular vesicle

103 leukocytes and endothelial cells, suppresses platelet activation and leukocyte infiltration by phosph

104 reduced expression of RASA3 led to premature platelet activation and markedly reduced the life span o

105 ammation mediates its effects via increasing platelet activation and microvascular coagulation in the

106 a combination of direct FcgammaRIIA-mediated platelet activation and monocyte-derived thrombin contri

107 ion injury was accompanied by neutrophil and platelet activation and neutrophil-platelet aggregate fo

108 n and inhibits KKO and human HIT IgG-induced platelet activation and platelet aggregation in vitro, a

109 ain interaction with FcgammaRs in modulating platelet activation and potential for TE.

110 LPS may be responsible for platelet activation and potentially contributes to throm

111 cus aureus alpha-toxin simultaneously alters platelet activation and promotes neutrophil inflammatory

112 ovide evidence that the GAP, RASA3, inhibits platelet activation and provides a link between P2Y12 an

113 illation significantly reduces the increased platelet activation and reactivity associated with the p

114 Platelet activation and reactivity were assessed by flow

115 via multiple pathways, including inhibiting platelet activation and reducing the pathologic expressi

116 of pneumonia and is associated with in vivo platelet activation and serum TxB2 overproduction; aspir

117 CD36 axis and cyclooxygenase 1 in subsequent platelet activation and stable thrombus formation.

118 ut not without platelet S1P, suggesting that platelet activation and stimulus-response coupling is ne

119 ses play a crucial role in the regulation of platelet activation and Syk phosphorylation downstream o

120 CLEC-2-mediated, but not GPVI-mediated, platelet activation and Syk phosphorylation were abolish

121 Both of these processes involve platelet activation and the coagulation cascade, forming

122 effectively resolved the correlation between platelet activation and the various frequency components

123 by adenosine 5'-diphosphate (ADP) to induce platelet activation and thereby serves as an important a

124 ly accepted as a major negative regulator of platelet activation and thrombosis for many years, but m

125 The mechanisms by which CD36 promotes platelet activation and thrombosis remain incompletely d

126 le platelet signaling pathways and regulates platelet activation and thrombosis.

127 , our findings demonstrate that LOX enhances platelet activation and thrombosis.

128 it RASA3 and enable sustained RAP1-dependent platelet activation and thrombus formation at sites of v

129 - and C-type lectin-like receptor 2-mediated platelet activation and thrombus formation in vivo.

130 (2+)-dependent focal adhesion kinase Pyk2 in platelet activation and thrombus formation in vivo.

131 P2Y12R regulates platelet activation and thrombus formation, and several

132 CD40L has been shown to potentiate platelet activation and thrombus formation, involving bo

133 newly discovered Eph kinase in platelets) in platelet activation and thrombus formation.

134 The small GTPase RAP1 is critical for platelet activation and thrombus formation.

135 ntly activate inhibitory pathways that limit platelet activation and thrombus size.

136 ion 40 ligand and p-selectin (two markers of platelet activation), and zonulin (a marker of gut perme

137 egulator of thrombopoiesis, Ca(2+)-dependent platelet activation, and arterial thrombosis in vivo.

138 alance; increases proinflammatory responses, platelet activation, and coagulation biomarkers; and red

139 e, ex vivo thrombus formation, fibrinolysis, platelet activation, and forearm blood flow in response

140 Thus, dampening platelet activation, and in turn PMC formation, with ant

141 tolic pressure and RV hypertrophy, decreased platelet activation, and less pulmonary vascular remodel

142 erial stiffness, cardiac autonomic function, platelet activation, and NADPH oxidase gene expression a

143 esults have implications on the mechanism of platelet activation, and on the pathophysiology of von W

144 GP1 complex binds to the thrombus, enhancing platelet activation, and platelet secretion leads to enh

145 pleted mice showed reduced platelet numbers, platelet activation, and platelet-leukocyte complex form

146 , leading to defective actin polymerization, platelet activation, and shape change.

147 Mechanically labile ligands dampen platelet activation, and the onset of piconewton integri

148 plement activation, endothelial cell damage, platelet activation, and thrombosis.

149 ent, would increase platelet counts, improve platelet activation, and/or reduce bleeding in WAS/XLT p

150 Perhaps most importantly, this platelet activation appears absolutely essential for hos

151 ons with myocardial infarction (MI) and with platelet activation are still undefined.

152 describe a model that provides insights into platelet activation as it occurs in vivo.

153 Fc domain with FcgammaRs is responsible for platelet activation, as measured by induction of PAC-1 a

154 er substrates also leads to higher levels of platelet activation, as measured by integrin alphaIIbbet

155 subacute HIT; for this situation, a negative platelet activation assay (eg, platelet serotonin-releas

156 This dissociation between the platelet activation assay and a PF4-dependent immunoassa

157 eparin reexposure should be tested by serial platelet activation assays even when their EIAs remain s

158 Platelet activation assays suggested that PavB and PspC

159 high concentrations of thrombin, and maximal platelet activation at high concentrations of thrombin r

160 PAR1 is required for platelet activation at low but not high concentrations o

161 gen receptor GPVI is the primary trigger for platelet activation at sites of injury.

162 Platelet activation at sites of vascular injury is essen

163 Thus platelet activation at sites of vascular injury results

164 y severely impaired glycoprotein VI-mediated platelet activation because of defective stabilization o

165 brand factor (VWF)-GPIb adhesive function or platelet activation, but instead associated with reduced

166 hate (polyP) is released from platelets upon platelet activation, but it is not clear if it contribut

167 dependent signaling molecule, Sema4D, delays platelet activation, but not the emergence of the low tr

168 h cirrhosis may display impaired or enhanced platelet activation, but the reasons for these equivocal

169 a3 in resting platelets and dissociates upon platelet activation by agonists.

170 Platelet activation by CAP-PEs includes assembly of TLR2

171 Platelet activation by CLEC-2 and GPVI is abolished in S

172 ents that are highly effective at inhibiting platelet activation by decreasing the release of free mt

173 ts such as thrombin, affecting the extent of platelet activation by establishing agonist-specific con

174 nding of the N-terminal SH2 domain of Syk on platelet activation by GPVI, CLEC-2, and integrin alphaI

175 The combination of direct platelet activation by HIT immune complexes through Fcga

176 n circulation in hyperlipidemia and inducing platelet activation by promoting cross-talk between inna

177 Ibbeta3, and Src and Syk tyrosine kinases in platelet activation by Staphylococcus aureus, Streptococ

178 of critical importance for the mechanism of platelet activation by thrombin.

179 Platelet activation by TLR9 ligands induces IRAK1 and AK

180 Adenosine diphosphate (ADP) enhances platelet activation by virtually any other stimulant to

181 ix HA through the activity of HYAL2 and that platelet activation causes the immediate translocation o

182 cyte (CD3, CD4, CD8, CD19, CD22, & CD56) and platelets activation (CD41, CD42 & CD62P (P- selectins))

183 and stable glycemic control display enhanced platelet activation correlating with female sex and micr

184 Platelet activation did not improve in 3 WAS/XLT patient

185 )-mediated inflammation of mesenteric veins, platelet activation drives the rapid mobilization of Ly6

186 t P2Y(1)(2), represents a clear dichotomy in platelet activation during allergic inflammation versus

187 ies performed in vivo have demonstrated that platelet activation during hemostasis and thrombosis is

188 ia models and are dependent on the timing of platelet activation during infection.

189 This suggests a dichotomy exists in platelet activation during inflammation compared to haem

190 -1 (PAR1) couples the coagulation cascade to platelet activation during myocardial infarction and to

191 During platelet activation, dynein slides microtubules apart, l

192 in IgG antibodies that cause strong in vitro platelet activation even in the absence of heparin.

193 et receptor for thrombin that is crucial for platelet activation, exacerbated influenza-induced acute

194 Platelet activation following bacterial-fibrinogen inter

195 TMAO enhanced sub-maximal stimulus-dependent platelet activation from multiple agonists through augme

196 vealed that HMGB1 is critical for regulating platelet activation, granule secretion, adhesion, and sp

197 by a coagulation factor cascade coupled with platelet activation has been increasingly challenged by

198 lying mechanisms of platelet aggregation and platelet activation heterogeneity during thrombus format

199 Following platelet activation, however, c-Src was co-immunoprecipi

200 ic tail of this Eph kinase regulates initial platelet activation in a contact-independent manner in t

201 ing the release of free mtDNA, which induces platelet activation in a DC-SIGN-dependent manner.

202 physiologically modulates thrombin-dependent platelet activation in a manner that is required for suc

203 n human platelets, participates in sustained platelet activation in a P2Y12-dependent manner; however

204 prevent bacterial proliferation and prevent platelet activation in blood-contacting applications.

205 Radiofrequency ablation induced platelet activation in both groups, which persisted afte

206 increased along with circulating markers of platelet activation in Cd39+/-Apoe-/- mice fed a high-fa

207 mild and severe forms of dengue, the role of platelet activation in dengue pathogenesis has not been

208 ns, less attention is given to mechanisms of platelet activation in diseased states.

209 ity lipoprotein (oxLDL) promotes unregulated platelet activation in dyslipidemic disorders.

210 we observed significantly increased in vivo platelet activation in HFRS patients with intravascular

211 In comparison with platelet activation in normal healthy conditions, less a

212 These findings imply that measuring platelet activation in patients might be an interesting

213 Despite significant platelet activation in patients with allergic diseases,

214 Clinical studies reveal platelet activation in patients with asthma, allergic rh

215 Platelet activation in response to the ligand for collag

216 secondary mediators regulate CLEC-2-mediated platelet activation in terms of signaling is not clearly

217 C- and ADP-dependent pathways allow residual platelet activation in the absence of functional CalDAG-

218 en troponin elevation and in vivo markers of platelet activation in the early phase of hospitalizatio

219 beneficial effects on platelet count but not platelet activation in the majority of WAS/XLT patients.

220 ed platelet production, leading to increased platelet activation in the setting of hypercholesterolem

221 odeling, a decrease in thrombin activity and platelet activation in the thrombus core.

222 deletion of TRAF3, suggesting that increased platelet activation in the TRAF3 knockout mice was not d

223 cynomolgus monkey platelets, and cynomolgus platelet activation in vitro These experiments demonstra

224 C5-deficient mice had no apparent defect in platelet activation in vitro, and vessel wall platelet d

225 The Gi protein Galpha(i2) mediates platelet activation in vitro, but its in vivo role in he

226 form nitric oxide (NO) and potently inhibits platelet activation in vitro, to a greater extent than h

227 e ligated inferior vena cava, and diminished platelet activation in vitro.

228 so translated into fewer side effects due to platelet activation in vivo.

229 Western diet feeding resulted in increased platelet activation, increased thrombin/antithrombin com

230 ts delineate that C3 plays specific roles in platelet activation independent of formation of the term

231 dicating a role for Vps34 kinase activity in platelet activation, independent from its role in MKs.

232 e of Blood, Estevez et al propose a model of platelet activation induced by low levels of thrombin an

233 ssessed whether remote IPC has any effect on platelet activation induced by radiofrequency ablation o

234 We show that active MMP-2 enhances platelet activation induced by weak stimuli by cleaving

235 Upon platelet activation, inside-out signaling pathways incre

236 Platelet activation is associated with significant chang

237 receptor for IgG IIA (FcgammaRIIA)-mediated platelet activation is essential in heparin-induced thro

238 binding of PS-modified oligonucleotides, and platelet activation is fully abolished.

239 nding of the molecular mechanisms leading to platelet activation is important for the development of

240 Platelet activation is persistently enhanced, and its in

241 One major pathway of platelet activation is triggered by 2 receptors that sig

242 barrier dysfunction, graft-vs-host disease, platelet activation, ischemia, and reperfusion injury or

243 he patients possessed a significantly higher platelets activation marker; CD62P (P-selectins) and hig

244 in patients with acute coronary syndrome and platelet activation markers in the general population.

245 At admission, platelet activation markers such as plasma soluble P-sel

246 miR-126 accounted for a rise in circulating platelet activation markers.

247 Platelet activation may play a key role in graft occlusi

248 These results present a new view of the platelet activation mechanism and reveal principal mecha

249 Anti-beta2GP1 autoantibodies enhanced platelet activation, monitored by calcium mobilization,

250 (1) the reduced platelet activation observed in WAS/XLT is primarily due

251 e (SCD) patients, a population with aberrant platelet activation of an unknown mechanism and in which

252 FcgammaRIIa in prostate cancer cell-induced platelet activation opening the opportunity to develop n

253 ar blood recirculating devices as to overall platelet activation over time.

254 c studies, including vascular disruption and platelet activation, oxidation and inflammation, endothe

255 , it is not known whether coagulation-driven platelet activation participates in APAP hepatotoxicity.

256 Those studies indicate that distinct platelet activation pathways are not merely redundant, b

257 haemostasis, and that hitherto undiscovered platelet activation pathways might be exploited to creat

258 iplatelet agents and genetic manipulation of platelet activation pathways.

259 Platelet activation promoted influenza A virus pathogene

260 Together with increased myelopoiesis, platelet activation promotes prothrombotic and proathero

261 cers, and together with LPA generated during platelet activation promotes skeletal metastasis of brea

262 t platelet-specific ERK5(-/-) mice have less platelet activation, reduced MI size, and improved post-

263 rved and the mechanistic relevance of EV and platelet activation remains unknown.

264 Twf2a-controlled actin rearrangements dampen platelet activation responses in a n-cofilin- and profil

265 Enhanced platelet activation responses in aged mice were also pre

266 telet-derived FV/Va (7% of normal) following platelet activation resulted in robust thrombin generati

267 Platelet activation results in profound morphologic chan

268 sonator sensors in monitoring the process of platelet activation, revealing an effective method to me

269 ith thrombin-mediated signaling pathways and platelet activation, secretion, and aggregation, but not

270 GPIIbIIIa antibodies, induces Fc-independent platelet activation, sialidase neuraminidase-1 transloca

271 igonucleotides to platelets eliciting strong platelet activation, signaling, reactive oxygen species

272 n-like receptor-2 (CLEC-2), elicits powerful platelet activation signals in conjunction with Src fami

273 ing the hydrophobin protein induced stronger platelet activation than wild-type conidia.

274 ceptor 2 (CLEC2) are receptors implicated in platelet activation that both signal via an immunorecept

275 mbosis is a process mediated by dysregulated platelet activation that can cause life-threatening comp

276 studies unravel a novel mechanism regulating platelet activation that involves the binding of MMP-2 t

277 s study also demonstrated that mtDNA induces platelet activation through a DC-SIGN dependent pathway.

278 C-type lectin-like receptor CLEC-2 mediates platelet activation through a hem-immunoreceptor tyrosin

279 inlike receptor 2 (CLEC-2) mediates powerful platelet activation through a Src- and spleen tyrosine k

280 h RBCs also reduce nitrite to NO and inhibit platelet activation to a greater extent than human RBCs,

281 plate-based assay of 7 distinct pathways of platelet activation to characterize inherited platelet d

282 Prostacyclin (PGI2) modulates platelet activation to regulate haemostasis.

283 The platelet activation triggers during H1N1 infection remai

284 isseminated intravascular coagulation due to platelet activation via CLEC-2.

285 Platelet activation via FcgammaRIIa, the sine qua non of

286 d thrombus formation following intravascular platelet activation via FcgammaRIIA.

287 and the relationship to the requirement for platelet activation via fragment crystallizable (Fc)gamm

288 that platelet ERK5 has an adverse effect on platelet activation via selective receptor-dependent and

289 patients and 8 age-matched healthy controls, platelet activation was assessed by whole blood flow cyt

290 The in vivo platelet activation was determined by quantification of

291 riven by hepatocyte growth factor (HGF), and platelet activation was followed by HMGB1/TLR-4-dependen

292 Platelet activation was inhibited with aspirin, and NETs

293 Platelet activation was minimally sufficient to elicit e

294 Defective thrombus formation and platelet activation were confirmed in vitro by studying

295 ates local thrombin accumulation and greater platelet activation, whereas faster transport rates with

296 S patients have increased thrombopoiesis and platelet activation, which contributes to intravascular

297 mmaRIIA and integrin alphaIIbbeta3 to induce platelet activation, which is further facilitated by pla

298 ied that showed minimal FcgammaR binding and platelet activation while maintaining full binding to CD

299 particles during megakaryocyte maturation or platelet activation, while retaining the capacity for cr

300 nucleated cells and their ability to promote platelet activation with resultant thrombosis and thromb