ライフサイエンスコーパス: platelet activation

1 from AMI patients, accounting for increased platelet activation.

2 on whereas hyperglycemic conditions increase platelet activation.

3 rombotic endothelial phenotype that promoted platelet activation.

4 with the ability of its ligands to modulate platelet activation.

5 mation and anti-PF4/heparin antibody-induced platelet activation.

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

7 structures with distinct areas of differing platelet activation.

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

9 th functions beyond inhibiting ITAM-mediated platelet activation.

10 3, which plays a negative role in regulating platelet activation.

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

12 eted strategies that counter cooling-induced platelet activation.

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

14 of PAR4 internalization reduces integrin and platelet activation.

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

16 complications associated with shear-mediated platelet activation.

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

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

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

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

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

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

23 SK9 as a mechanism potentially implicated in platelet activation.

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

25 ons initiating and progressing GPVI-mediated platelet activation.

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

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

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

29 olymerization and sickling, coagulation, and platelet activation.

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

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

32 y on the blood coagulation cascade including platelet activation.

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

34 ous in patients with increased intravascular platelet activation.

35 at contribute to its effective inhibition of platelet activation.

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

37 0 Hematology System as a marker surrogate of platelet activation.

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

39 lammation and upregulation of podoplanin and platelet activation.

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

41 platelet surface GPCR P2Y12 and thus inhibit platelet activation.

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

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

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

45 ment of FcgammaRIIA in the course of SLE and platelet activation.

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

47 the experimental dynamics of CLEC-2-induced platelet activation.

48 es, and biochemical markers of mast cell and platelet activation.

49 to correlate with any measured indicators of platelet activation.

50 ti-atherothrombotic effect via inhibition of platelet activation.

51 g the rate-limiting steps of CLEC-2-mediated platelet activation.

52 with SLE, levels of ICs are associated with platelet activation.

53 V-activated human MCs led to increased human platelet activation.

54 ellitus (T1DM) have increased thrombosis and platelet activation.

55 ceptor in a Sia-dependent manner to suppress platelet activation.

56 was also unable to induce heparin-dependent platelet activation.

57 ty was detected as inhibition of ADP-induced platelet activation.

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

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

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

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

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

63 st, NSML mouse platelets exhibited increased platelet activation after GPVI and CLEC-2 stimulation an

64 uced exaggerated acute lung inflammation and platelet activation after intratracheal LPS or Pseudomon

65 preventative strategy for stroke by reducing platelet activation, aggregate formation, and cerebral t

66 ection, MCs release serotonin, which prompts platelet activation, aggregation, and enhanced phagocyto

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

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

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

70 The increase in platelet activation and aggregation could partially be a

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

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

73 was incubated with TIMP-GLIA, and hemolysis, platelet activation and aggregation, and complement acti

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

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

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

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

78 s (SFKs) Src, Lyn, and Fyn are essential for platelet activation and also involved in megakaryocyte (

79 periodontal infection promotes pathological platelet activation and amplifies shape change.

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

81 Here, we studied platelet activation and arterial thrombus formation in A

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

83 r potential cation channel 6 (TRPC6) reduced platelet activation and calcium flux, and reduced lung i

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

85 mediated red blood cell (RBC) agglutination, platelet activation and clumping, but not platelet sprea

86 tivation, extracellular matrix organization, platelet activation and degranulation, or post-translati

87 We hypothesized that platelet activation and depletion occur during intestina

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

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

90 amaged vessel wall, with a greater extent of platelet activation and fibrin accumulation on the outsi

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

92 esults reveal striking spatial regulation of platelet activation and fibrin formation that could not

93 alters serotonergic signaling and influences platelet activation and hemostasis.

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

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

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

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

98 patients with AERD who had greater baseline platelet activation and milder upper respiratory symptom

99 Platelet activation and monocyte TF expression were asso

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

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

102 critical role of NOX1 in collagen-dependent platelet activation and pathological arterial thrombosis

103 Here, we show that platelet number, platelet activation and platelet aggregation are increas

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

105 ght on new pathological mechanisms involving platelet activation and platelet-dependent monocyte TF e

106 This report demonstrates that increased platelet activation and platelet-monocyte aggregate form

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

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

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

110 viable strategy to control collagen-induced platelet activation and reduce thrombosis without delete

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

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

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

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

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

116 on and also provide a potential link between platelet activation and the progression of fibrosing dis

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

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

119 Whereas chronic platelet activation and thrombosis are well-recognized f

120 Here we show that Slc44a2 controls platelet activation and thrombosis by regulating mitocho

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

122 metabolism in vivo contributes to increased platelet activation and thrombosis in a model of T1DM.

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

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

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

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

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

128 (protease-activated receptor 1), leading to platelet activation and thrombus formation, which can be

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

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

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

132 itiates an early ADP secretion, potentiating platelet activation, and a secondary wave of ADP secreti

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

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

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

136 to dysregulation of coagulation, complement, platelet activation, and leukocyte recruitment in the mi

137 Fibrinogen levels, fibrin polymerization, platelet activation, and microparticle release were incr

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

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

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

141 he importance of mitochondrial metabolism to platelet activation, and reveal a mechanism by which Slc

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

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

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

145 hich participate in acute phase response and platelet activation (APMAP [adipocyte plasma membrane-as

146 s, the rate-limiting steps of CLEC-2-induced platelet activation are not clear.

147 us studies have been performed, gradients of platelet activation are readily apparent, as is an asymm

148 lexes, and anti-PF4/heparin antibody-induced platelet activation as a result of PF4/heparin complex d

149 Our study illuminates platelet activation as an efficacious target of aspirin,

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

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

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

153 Platelet activation assays that use "washed" platelets a

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

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

156 Platelet activation at sites of vascular injury is essen

157 Surprisingly, platelet activation began in our model 3 h after TNBS ad

158 The model described platelet activation beginning with CLEC-2 receptor clust

159 Platelet cargo, platelet adhesion and platelet activation but not platelet aggregation were id

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

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

162 nase-1 (PDK1) is required for Ca2+-dependent platelet activation, but its role in MK development and

163 t with these predictions, the CLEC-2-induced platelet activation, but not activation mediated by G-pr

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

165 In the bloodstream, podoplanin induces platelet activation by binding to CLEC-2 and facilitates

166 her treatment with prasugrel, which inhibits platelet activation by blocking the type 12 purinergic (

167 Platelet activation by CAP-PEs includes assembly of TLR2

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

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

170 le protein major basic protein, which causes platelet activation by eosinophils.

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

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

173 increased within five minutes in response to platelet activation by PAR1-AP, PAR4-AP or CRP-XL.

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

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

176 with that of aspirin-tolerant patients, and platelet activation can contribute to aspirin-induced re

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

178 experimental evidence that infection-induced platelet activation compromises protective host immunity

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

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

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

182 TMEM16F is widely expressed and has roles in platelet activation during blood clotting, bone formatio

183 -1 (PAR1) couples the coagulation cascade to platelet activation during myocardial infarction and to

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

185 PVI resulted in decreased Abeta40-stimulated platelet activation, factor secretion, and platelet aggr

186 Platelet activation following bacterial-fibrinogen inter

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

188 Tempering platelet activation genetically reduced TGF-beta signali

189 We then investigated C. albicans actions on platelet activation, granule release, and aggregation.

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

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

192 d standard functional assay (heparin-induced platelet activation [HIPA]).

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

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

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

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

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

198 we assessed markers of endothelial cell and platelet activation in critically and non-critically ill

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

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

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

202 This study investigates platelet activation in patients with NS and NSML and in

203 Platelet activation in response to the ligand for collag

204 f human SLE, the exact mechanisms underlying platelet activation in SLE remain unknown.

205 s a role for FcgammaRIIA in nephritis and in platelet activation in SLE.

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

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

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

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

210 appears to be largely inadequate in reducing platelet activation in the vast majority of patients wit

211 lts establish BIN2 as a central regulator of platelet activation in thrombosis and thrombo-inflammato

212 o overcome the effects of drugs that inhibit platelet activation in vitro and to restore thrombocytop

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

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

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

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

217 ERCA3-dependent stores was required for full platelet activation in weak stimulation conditions.

218 We assessed markers of endothelial cell and platelet activation, including von Willebrand Factor (VW

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

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

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

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

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

224 Upon platelet activation, inside-out signaling pathways incre

225 Our findings show that platelet activation is an important pathophysiological e

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

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

228 Since CLEC-2 mediated platelet activation is independent of major haemostatic

229 Overall, our data demonstrate that platelet activation is not largely influenced by any of

230 Platelet activation is persistently enhanced, and its in

231 us aspirin to reduce thromboxane A2-mediated platelet activation is superior to aspirin or rivaroxaba

232 hrombosis, where a pivotal role is played by platelet activation, it would be arguable that diets wit

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

234 LPS(EC) did not affect platelet activation markers such as inside-out signallin

235 no effect on platelet-leukocyte aggregates, platelet activation markers, or plasma cytokines in eith

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

237 9, and the inhibition of pathways related to platelet activation may improve the outcomes during COVI

238 hermore, circulating serotonin, derived from platelet activation, may play a role in the polarization

239 thelial cells-a marker of which is increased platelet activation.Objectives: This study compared whol

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

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

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

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

244 iplatelet agents and genetic manipulation of platelet activation pathways.

245 Because the MV signature mirrors platelet activation, patients with a high MV score could

246 let aggregates and a distinct neutrophil and platelet activation pattern in blood, which changes with

247 Thrombosis and platelet activation play a central role in stroke pathog

248 However, after collagen-induced platelet activation, PN-1 deficiency in F8-/-mice or PN-

249 Platelet-derived MVs may be biomarkers of platelet activation, possibly reflecting pathogenesis ev

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

251 Among them are a platelet activation receptor, C-type lectin-like recepto

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

253 ived metabolite, PAGln, was shown to enhance platelet activation-related phenotypes and thrombosis po

254 -induced pulmonary embolism model of in vivo platelet activation relative to nondiabetic controls.

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

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

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

258 des, the model predicted that CLEC-2-induced platelet activation results in cytosolic calcium spiking

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

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

261 However, the extent to which platelet activation shapes the immunosuppressive tumor m

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

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

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

265 in-coupled receptor kinase 5 (GRK5) promotes platelet activation specifically via PAR4 receptor signa

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

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

268 by cyclooxygenase-1 (COX-1) turnover during platelet activation that can stimulate human neutrophil

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

270 Because of its modulating effect on platelet activation, this NAADP-SERCA3 pathway may be a

271 and upregulation of macrophage, complement, platelet activation, thrombosis, and proinflammatory mar

272 que, in which we assessed platelet adhesion, platelet activation, thrombus structure and fibrin clot

273 Kinetics of platelet activation, thrombus structure and fibrin forma

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

275 Thrombopoietin (TPO) enhances platelet activation through activation of the tyrosine k

276 ived antimicrobial components and inhibiting platelet activation through engagement of inhibitory Sig

277 ceptor for collagen and fibrin that triggers platelet activation through immunoreceptor tyrosine-base

278 ease liver damage by inducing macrophage and platelet activation through the TLR4 pathway.

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

280 latelet glucose utilization, which increases platelet activation to promote thrombosis.

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

282 blood whereas LPS(SM) and LPS(RS) inhibited platelet activation under specific conditions at supraph

283 d thrombus formation following intravascular platelet activation via FcgammaRIIA.

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

285 tion of genes involved in blood coagulation, platelet activation was characteristic of the rapid resp

286 The in vivo platelet activation was determined by quantification of

287 Platelet activation was minimally sufficient to elicit e

288 Platelet activation was triggered by thrombin, which, in

289 obing the consequence of biased signaling on platelet activation, we found that a peptide that cannot

290 Hence, to determine the impact of LPS on platelet activation, we used ultrapure preparations of L

291 tryptase, platelet-leukocyte aggregates, and platelet activation were also recorded.

292 croparticle (EMP) numbers and phenotype, and platelet activation were evaluated by flow cytometry.

293 Markers of endothelial cell and platelet activation were significantly elevated in ICU p

294 en though the degree of thrombocytopenia and platelet activation were similar between dengue-infected

295 atelets revealed that normal glucose reduces platelet activation whereas hyperglycemic conditions inc

296 vealed MIN(DTE) calf surviving well with low platelet activation, whereas the MAX(DTE) animal sustain

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

298 platelets produces aberrant TRPC6-dependent platelet activation, which is a major driver of CF lung

299 -coupled receptors are critical mediators of platelet activation whose signaling can be modulated by

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