ライフサイエンスコーパス: platelet function

1 ategy for patients with diseases that affect platelet function.

2 ism in SCD as well as a modulator of healthy platelet function.

3 entional and microfluidic assays to evaluate platelet function.

4 le-associated membrane protein-3 (VAMP-3) in platelet function.

5 elets to a number of well-accepted models of platelet function.

6 ), but little is known how JAK2V617F affects platelet function.

7 ts Cu,Zn-superoxide dismutase (Cu,Zn-SOD) in platelet function.

8 , abnormal platelet morphology, and impaired platelet function.

9 th current literature linking the disease to platelet function.

10 ich the cAMP-PKA signaling pathway regulates platelet function.

11 gh heteromeric interactions in regulation of platelet function.

12 roles for hemichannels and gap junctions in platelet function.

13 ded for clinically meaningful restoration in platelet function.

14 n, baroreflex sensitivity, inflammation, and platelet function.

15 -leukocyte aggregate formation, and improved platelet function.

16 lets functions as an endogenous inhibitor of platelet function.

17 y used to demonstrate the role of P2Y(12) in platelet function.

18 gic receptors (P2Y1, P2Y12), and thus normal platelet function.

19 erized by macrothrombocytopenia and impaired platelet function.

20 for </= 15% of total phenotypic variation in platelet function.

21 platelet production and had a mild effect on platelet function.

22 oskeletal and adhesion machinery critical to platelet function.

23 prevailing concept that No and cGMP inhibits platelet function.

24 ITAM-like-containing receptor signaling and platelet function.

25 reduced ceramide levels in skin and impaired platelet function.

26 duce significant thrombocytopenia or inhibit platelet function.

27 amining the impact of ectodomain shedding on platelet function.

28 sues as well, including a role in regulating platelet function.

29 that stimulates cAMP-mediated inhibition of platelet function.

30 e and the role of dense granule secretion in platelet function.

31 r whether plasma miRNA levels correlate with platelet function.

32 et size, is a potential biological marker of platelet function.

33 denafil, potentiates NO signaling to inhibit platelet function.

34 the platelet-enriched miRNA, miR-223, affect platelet function.

35 host physiology, modulating GI motility and platelet function.

36 tases have emerged as critical regulators of platelet function.

37 g the facilitation of alphaIIbbeta3-mediated platelet functions.

38 uggesting distinct roles of PDI and ERp57 in platelet functions.

39 atopoietic stem cell (HSC) and megakaryocyte/platelet functions.

40 n important role in controlling archetypical platelet functions.

41 clin (PGI2) and nitric oxide (NO) to inhibit platelet functions.

42 ltitude of physiological activities in which platelets function.

43 ome who had undergone detailed assessment of platelet function 30 days after the acute event.

44 study demonstrates that PGI2 can reverse key platelet functions after their initial activation and id

45 Platelet-function analysis (PFA) of closure times (CT) o

46 a and leukocyte-platelet aggregates; and (3) platelet function analyzer (PFA)-100 collagen-epinephrin

47 Closure times in the shear-dependent platelet function analyzer (PFA)-100 were measured on he

48 Platelet function analyzer closure times were lower with

49 osine diphosphate, collagen and epinephrine, Platelet Function Analyzer-100 (Siemens Healthcare Diagn

50 endent platelet hyper-reactivity measured by Platelet Function Analyzer-100 CADP CT are novel indepen

51 ood flow, (2) a bedside point-of-care assay (platelet function analyzer-closure time adenine DI-phosp

52 that aimed to find the genetic structure of platelet function and body mass index, respectively.

53 mining the relation of CYP2C19*2 genotype to platelet function and cardiovascular outcomes in an inde

54 e effects of pharmacogenetic determinants on platelet function and cardiovascular outcomes in type DM

55 status of the P2Y12 promoter has effects on platelet function and clinical ischemic events.

56 ic substrates provides devices for measuring platelet function and coagulation with low blood volumes

57 -terminal CGHC motif of PDI is important for platelet function and coagulation.

58 ysregulation leads to significant defects in platelet function and disease.

59 orter localization and expression can affect platelet function and drug sensitivity.

60 light onto the mechanistic underpinnings of platelet function and dysfunction.

61 bition may be an effective way of preserving platelet function and eventually decelerating atherothro

62 or 12-LOX in regulating FcgammaRIIa-mediated platelet function and identifies 12-LOX as a potential t

63 beta3, Leu33Pro is associated with enhanced platelet function and increased risk for coronary thromb

64 r, despite the importance of shear stress in platelet function and life-threatening thrombus formatio

65 Platelet function and mechanisms of activation in ischem

66 tic TFs implicated in patients with impaired platelet function and number include runt-related transc

67 nnection between the influence of statins on platelet function and PECAM-1 signaling.

68 inhibition of platelet mitochondria disrupts platelet function and platelet-activated blood coagulati

69 tic variant in PEAR1 associated with altered platelet function and provide a plausible biologic mecha

70 thrombopoietin receptor agonist (TPO-RA), on platelet function and reactivity.

71 Widespread monitoring of platelet function and the effect of antiplatelet drugs w

72 The inhibition of platelet function and the prevention of thrombus formati

73 ly developed a genetic mouse model to assess platelet function and thrombosis in the setting of GPx-3

74 including TLR9; however, the role of TLR in platelet function and thrombosis is poorly understood.

75 To address the role of LPA in regulating platelet function and thrombosis, we investigated the ef

76 The effects of Slit2 on platelet function and thrombus formation have never been

77 sin displayed a 4-fold greater inhibition of platelet function and thrombus formation in vitro than c

78 at Slit2 is a powerful negative regulator of platelet function and thrombus formation.

79 amic forces that contribute significantly to platelet function and thrombus formation.

80 ncy have insulin hypersensitivity, defective platelet function, and abnormal mast cell development.

81 the association between PPI use, measures of platelet function, and clinical outcomes for patients tr

82 hat participates in both of these aspects of platelet function, and it is the only one to signal thro

83 the insulin receptor substrate (IRS)-1 gene, platelet function, and long-term outcomes in patients wi

84 r E2 in regulating the platelet proteome and platelet function, and point to new potential antithromb

85 association between IRS-1 genetic variants, platelet function, and the risk of major adverse cardiac

86 ranule secretion plays a significant role in platelet function, and they also indicate that abnormal

87 en specific dietary nutrients, gut microbes, platelet function, and thrombosis risk.

88 c regimens on cerebral microembolization and platelet function are equivalent.

89 Important regulators of platelet function are G proteins controlled by seven tra

90 ts and mechanisms that contribute to altered platelet function are poorly defined.

91 plethora of factors released on activation, platelet functions are also connected to tumor growth, n

92 In this work, a broad range of platelet functions are quantitatively assessed by levera

93 inogenversusfibrin to alphaIIbbeta3-mediated platelet functions are unknown.

94 ss variable, and more complete inhibition of platelet function - are in various phases of development

95 rtantly, GSK3 phosphorylation contributes to platelet function as knock-in mice where GSK3alpha Ser(2

96 shed surface proteins, potentially modifying platelet function as well as providing a source of bioac

97 Medications to disrupt platelet function as well as the coagulation system are

98 Thus, our data reveal that platelets function as mediators of tumor-bone communicat

99 Thus, our data reveal that platelets function as mediators of tumor-bone communicat

100 Here we show that JAM-A in resting platelets functions as an endogenous inhibitor of platel

101 spectively whether COX-1-dependent and other platelet function assays correlate with clinical outcome

102 ponse to clopidogrel as measured by in-vitro platelet function assays is associated with a poor clini

103 chanism that is not detected by conventional platelet function assays.

104 assessed by standardized bleeding score) and platelet function (assessed by whole blood flow cytometr

105 th cancer may be correlated with the altered platelet functions associated with malignancy.

106 h increasingly novel methods of manipulating platelet function at our disposal, we highlight avenues

107 osphate (cAMP)-dependent signaling modulates platelet function at sites of vascular injury.

108 There was no significant difference in platelet function between groups.

109 a useful tool for predicting differences in platelet function between mice and humans.

110 strate that alpha-granule deficiency impairs platelet function beyond their purely hemostatic role an

111 g the role of these phosphatases not only on platelet function but also on megakaryocyte development

112 Mg(2+) plays a vital role in platelet function, but despite implications for life-thr

113 at GSK3 functions as a negative regulator of platelet function, but how GSK3 is regulated in platelet

114 as Rac, RhoA, and Cdc42 are vital for normal platelet function, but the role of RhoG in platelets has

115 el is associated with a further reduction in platelet function by 1 week using prasugrel MD or within

116 There was full recovery of platelet function by 24 hours.

117 N85 complex in supporting integrin-dependent platelet function by dampening the phosphatase activity.

118 Ticagrelor and dipyridamole inhibit platelet function by inhibiting P2Y12 receptors and plat

119 orphisms, which exert a cumulative effect on platelet function by modifying basic platelet parameters

120 s demonstrate that PKCalpha and Akt modulate platelet function by phosphorylating and inhibiting GSK3

121 model of thrombus formation, coagulation and platelet function can be accurately measured in vitro in

122 Thus, the basic scientist studying platelet function can think beyond the traditional hemos

123 Loss of VAMP-3 also affected some acute platelet functions, causing enhanced spreading on Fg and

124 Impaired platelet function coincided with reduced thrombus growth

125 ith significant changes in blood pressure or platelet function compared with CF-free controls in norm

126 rolled patients, 2796 (99.98%) had evaluable platelet function data.

127 asma prostacyclin and NO leading to acquired platelet function defects and thrombosis delay.

128 In vitro and in vivo assays reveal platelet function defects in KO mice.

129 lood from healthy subjects and patients with platelet function deficiencies.

130 this issue of Blood, Stritt et al show that platelet functions dependent on integrin activation are

131 le for Fc gammareceptor IIa (FcgammaRIIa) in platelet functions dependent on integrin alpha(IIb)beta(

132 We analyzed candidate platelet function disorder genes in 13 index cases with

133 Heritable platelet function disorders (PFDs) are genetically heter

134 worldwide for the investigation of heritable platelet function disorders (PFDs), but interpretation o

135 clinically efficacious in patients with mild platelet function disorders but it is not known which me

136 eta3, the ligand-receptor pair essential for platelet function during hemostasis and thrombosis.

137 proteinases, have been linked to the loss of platelet function during storage before transfusion, but

138 effect of proteases on protein activity and platelet function during storage.

139 ervations unravel SGK1 as novel regulator of platelet function, effective at least in part by NF-kapp

140 ed inflammation and that the absence of this platelet function elicits vascular injuries by tumor-inf

141 Decades of research and knowledge of platelet function exist and the same is true for inflamm

142 had a normal coagulation profile and normal platelet function, fibrin accumulated in their tissues d

143 ts, 2 new assays were developed to determine platelet function: first, the microaggregation test, mea

144 ot selecting platelet donors on the basis of platelet function for prophylactic platelet transfusion.

145 honey and passionflower on the modulation of platelet function, haemostasis and thrombosis.

146 A variety of changes in platelet function have been observed in patients with as

147 t studies have suggested a role for SR-BI in platelet function; however, its role in hemostasis is un

148 n is thought to contribute to variability in platelet function; however, the specific variants and me

149 lood, in a departure from studies of classic platelet function, Huang et al turn their attention to e

150 cancer, infection, and neuroscience, and how platelet function impacts the pathophysiology of each cl

151 1000 platelets/nL, are widely used to assess platelet function in (patho-)physiology, but also in thi

152 y used whole blood flow cytometry to examine platelet function in 20 patients receiving eltrombopag t

153 at are associated with phenotypic changes in platelet function in a large group of whites and blacks.

154 normal healthy conditions is different from platelet function in chronic ischemic and inflammatory c

155 alizing platelet miRNA processing as well as platelet function in diabetes mellitus.

156 g the observed association between PEAR1 and platelet function in genome-wide association studies.

157 his review examines our current knowledge of platelet function in haemostasis, possible mechanisms fo

158 pography of platelet mRNA and how it impacts platelet function in health and disease.

159 hisms) that have small individual effects on platelet function in humans, but can cumulatively lead t

160 bopag, a thrombopoietin-receptor agonist, on platelet function in immune thrombocytopenia (ITP) are n

161 There are few data on platelet function in intracerebral hemorrhage (ICH).

162 To determine if differences in platelet function in ITP patients account for this varia

163 This demonstrates that platelet function in normal healthy conditions is differ

164 unctional tests that allow for evaluation of platelet function in patients with extremely low platele

165 The effect of variation in platelet function in platelet donors on patient outcome

166 vent a complete mechanistic understanding of platelet function in these other diseases.

167 establish RhoA as an important regulator of platelet function in thrombosis and hemostasis.

168 ting granule release from platelets and thus platelet function in thrombosis and hemostasis.

169 ate-depleted beetroot juice) on vascular and platelet function in untreated hypercholesterolemics.

170 Notably, these effects of statins on platelet function in vitro and in vivo were diminished i

171 opment of arterial atheroma, their effect on platelet function in vivo remains unclear.

172 eans for evaluating human thrombopoiesis and platelet function in vivo using immunodeficient mice.

173 gnificance of these distinct interactions on platelet function in vivo, we generated knock-in mice ex

174 RP4, or ABCC4), a nucleotide transporter, in platelet functions in vivo and in vitro by investigating

175 lls, RhoG orchestrates processes integral to platelet function, including actin cytoskeletal rearrang

176 rs1354034) and affects a module enriched for platelet function, independent of platelet counts.

177 although PIP5KIgamma is essential for normal platelet function, individual isoforms of PIP5KIgamma fu

178 ts roles in vasodilation, cell permeability, platelet function, inflammation, and other vascular proc

179 als and investigated whether polyP-dependent platelet function is altered in IP6K1 knockout (Ip6k1(-/

180 Testing of platelet function is central to the cardiovascular pheno

181 Normal platelet function is critical to blood hemostasis and ma

182 While platelet function is dynamic in individual patients beca

183 Analysis of platelet function is limited by currently available devi

184 These tests show that platelet function is related to bleeding phenotype in ch

185 NO is synthesized by platelets and regulates platelet function is still controversial.

186 e Wiskott-Aldrich syndrome protein (WASp) in platelet function is unclear because platelets that lack

187 eins, but the importance of glycosylation to platelet functions is poorly understood.

188 to create an NO deficiency which can augment platelet function leading to a prothrombotic state.

189 ized by defective neutrophil trafficking and platelet function, leading to recurrent bacterial infect

190 e warranted to clarify whether assessment of platelet function may help tailoring antithrombotic ther

191 serum thromboxane B(2) and COX-1-independent platelet function measured by PFA-100 collagen-ADP CT, b

192 e reasonable to consider both genotyping and platelet function measurement to assess ischemic risk an

193 Platelet function mediates both beneficial and harmful e

194 mount and intake duration on blood pressure, platelet function, metabolic variables, and potential ad

195 This article reviews platelet function, molecular targets of antiplatelet age

196 ed before coronary stenting to a strategy of platelet function monitoring (VerifyNow P2Y12/aspirin po

197 icant improvements in clinical outcomes with platelet-function monitoring and treatment adjustment fo

198 nary stenting at 38 centers to a strategy of platelet-function monitoring, with drug adjustment in pa

199 th bleeding symptoms, and detects changes in platelet function more readily than LTA.

200 ough physiologically relevant measurement of platelet function now is more important than ever, a cri

201 Objective measures of platelet function on admission are associated with intra

202 y enrolled 69 patients with ICH and measured platelet function on admission.

203 Routine platelet function or genetic testing is currently not re

204 for the relation between the PEAR1 gene and platelet function phenotype.

205 tion between variation in the PEAR1 gene and platelet function phenotype.

206 iently reverse the effects of ibrutinib, and platelet functions recovered after treatment interruptio

207 the molecular characterization of the first platelet function-related CpG-SNP, a genetic predisposit

208 Eph kinase or ephrin signaling in regulating platelet function remained unidentified.

209 cessing machinery, but their contribution to platelet function remains incompletely understood.

210 ria, the role of bioenergetics in regulating platelet function remains unclear.

211 t Module, related to collagen catabolism and platelet function respectively.

212 ficient platelet production and/or defective platelet function results in bleeding disorders resultin

213 Patients with at least 2 platelet function results on the same maintenance dose o

214 Normal platelet function results were particularly predictive (

215 Platelet function was assessed using the platelet function score (PFS) in HV1 and HV2 and the Ver

216 ors contribute to a substantial variation in platelet function seen among normal persons.

217 Primary outcomes were blood pressure and platelet function, select metabolic variables, and the o

218 ed, unblinded investigation (Timing Based on Platelet Function Strategy to Reduce Clopidogrel-Associa

219 We undertook platelet function studies and linkage analyses in a pedi

220 Platelet function studies in patients are difficult to i

221 prasugrel LD in 149 patients with evaluable platelet function studies.

222 zed, single-center, open, 2-period crossover platelet function study conducted in 30 healthy voluntee

223 9326 participants, 27.5% were included in a platelet function substudy: 1286 treated with prasugrel

224 among participants >/=75 years of age in the platelet-function substudy (P=0.06).

225 l platelet reactivity unit measurements in a platelet-function substudy.

226 much is known about extrinsic regulators of platelet function such as nitric oxide and prostaglandin

227 ocetin inhibited a range of collagen-induced platelet functions such as fibrinogen binding, calcium m

228 If so, should results of a platelet function test be used to guide the dose or type

229 Because regular platelet function test cannot be performed in patients w

230 of antiplatelet therapies based on a single platelet function test is beneficial.

231 Platelet function test results (vasodilator-stimulated p

232 eening tests, coagulation factor assays, and platelet function test results were within normal limits

233 iables identified in univariate analysis and platelet function test results.

234 ction units according to the VerifyNow P2Y12 platelet function test.

235 Three randomized trials examined the role of platelet function testing (PFT) in clopidogrel-treated p

236 sis And Safety) trial screened patients with platelet function testing after PCI and randomly assigne

237 Thus, treatment adjustment according to platelet function testing at a single time point might n

238 in the genetics cohort; of these, 2,236 had platelet function testing data.

239 Individualizing antiplatelet therapy after platelet function testing did not improve outcome after

240 These results do not support platelet function testing for MACE risk evaluation in st

241 We evaluated the role of platelet function testing in clopidogrel-treated patient

242 Detection of platelet hyper-reactivity by platelet function testing in patients undergoing coronar

243 el and high-dose clopidogrel on the basis of platelet function testing in patients with acute coronar

244 ove outcomes in cardiovascular patients, but platelet function testing is not routine in clinical pra

245 The relationship of platelet function testing measurements with outcomes in

246 lowing clopidogrel loading was determined by platelet function testing on a Multiplate analyzer (Veru

247 among intervention arm patients who received platelet function testing than untested usual care arm (

248 A strategy based on preoperative platelet function testing to determine the timing of CAB

249 Little is known about how clinicians use platelet function testing to guide choice and dosing of

250 ry intervention with drug-eluting stents and platelet function testing using the VerifyNow assay.

251 00 hospitals were assigned access to no-cost platelet function testing versus usual care for acute my

252 Platelet function testing was performed in 66.9% of pati

253 In patients with high OTR identified by platelet function testing, the CYP2C19 genotype provides

254 PS found that when clinicians routinely used platelet function testing, they were more likely to adju

255 tion was obtained at 24.8+/-0.3 months after platelet function testing.

256 ions in the past decade on the usefulness of platelet function tests (PFTs) in clinical cardiology, i

257 Several platelet function tests have been developed for use in t

258 Traditional platelet function tests have been developed primarily fo

259 lated plasma miRNAs and YRNAs correlate with platelet function tests in patients with acute coronary

260 Thus, platelet function tests related to platelet age (IPF, FS

261 t of changing clopidogrel treatment based on platelet function tests, single-nucleotide polymorphisms

262 ry, and clopidogrel effects were measured by platelet function tests.

263 latelet inhibition by clopidogrel on ex vivo platelet function tests.

264 elated miRNAs and YRNAs were correlated with platelet function tests.

265 tivation, indicate a genomic contribution to platelet function that differs by race and emphasize a n

266 ultiple connexins are involved in regulating platelet function, thereby contributing to haemostasis a

267 monstrate that 2MeSAMP and Cangrelor inhibit platelet function through the P2Y(12)-dependent mechanis

268 During studies of platelet function under shear flow, we discovered that A

269 cetylsalicylate (L-ASA; 1-300 mumol/L) on 1) platelet function under shear stress; 2) aggregation ind

270 Baseline fibrinogen and platelet function using the VerifyNow P2Y12 assay (Accum

271 ect programmed cell death, female fertility, platelet function, vasculature inflammation, and diet-in

272 CD36 modulates platelet function via binding to oxidized LDL (oxLDL), c

273 In this study, the platelet function was assessed in a well-defined cohort

274 Platelet function was assessed using the platelet functi

275 Platelet function was assessed using VerifyNow P2Y12 Rea

276 Platelet function was assessed with a Multiplate analyze

277 Platelet function was compared by varying levels of RPs,

278 Platelet function was evaluated at 2 h, 24 h, 7 days, an

279 Platelet function was evaluated at baseline, 30 minutes,

280 Platelet function was intact in RIAM-deficient animals.

281 The role of WIP in platelet function was investigated using mice that lack

282 Platelet function was measured 12 to 36 h after PCI with

283 Platelet function was measured by aggregometry.

284 Impaired Nbeal2(-/-) platelet function was shown by flow cytometry, platelet

285 Platelet function was tested by (1) serum thromboxane B(

286 Together with the defect in platelet function we previously observed in SPL(-/-) mic

287 ms by which this sequence variation modifies platelet function, we produced transgenic knockin mice e

288 Preoperative demographics and baseline platelet function were equivalent in both groups.

289 sised and their effects on the modulation of platelet function were evaluated.

290 The effects of albumin on platelet function were investigated in vitro.

291 pidogrel active metabolite and inhibition of platelet function were reduced less by the coadministrat

292 anine aminotransferase, LDL cholesterol, and platelet function) were made at baseline and at 3 and 6

293 ean platelet volume, which indirectly affect platelet function, were the subjects of GWAS.

294 atelet surfaces that play essential roles in platelet functions, were partially proteolyzed in EHC Co

295 f SLAP or SLAP2 had only moderate effects on platelet function, whereas double deficiency of both ada

296 e plasma are reduced following inhibition of platelet function, while others have shown a correlation

297 ansfer was explored as a strategy to improve platelet function within a canine model for GT.

298 rate that EphB2 signaling not only modulates platelet function within a thrombus but is also involved

299 sight into the role of LOX in thrombosis and platelet function without compounding the influences of

300 To examine whether altered platelet function would compensate for the lack of TFPI