ライフサイエンスコーパス: platelet

1 m) used to first deplete red blood cells and platelets.

2 n enlists PP1c to modulate GPCR signaling in platelets.

3 as most pronounced in, but not exclusive to, platelets.

4 s also abrogated by lack of CD40 on injected platelets.

5 sed collagen at damaged vessels and captures platelets.

6 d aggregation were abrogated in ck2beta(-/-) platelets.

7 patients with brain cancer and may activate platelets.

8 ating soluble EGF bioactivity from activated platelets.

9 s were abrogated by lack of CD40 on injected platelets.

10 s, 10 of 10 (100%) recipients accepted donor platelets.

11 , this effect was reduced in the presence of platelets.

12 munoprecipitated with Gbeta1 in unstimulated platelets.

13 of HE, we explored the regulatory effect of platelets.

14 uced generation of factor Xa and thrombin on platelets.

15 hemo-component with a high concentration of platelets.

16 role of PAR1 activation on cells other than platelets.

17 This assigns platelets a central role in innate immune responses and

18 BCs promote arterial thrombosis by enhancing platelet accumulation at the site of vessel injury.

19 13-Series resolvins mediate the leukocyte-platelet actions of atorvastatin and pravastatin in infl

20 th Kindlin-2 siRNA showed enhanced basal and platelet-activating factor (PAF) or lipopolysaccharide-s

21 Platelet-activating factor acetylhydrolase 1B1 (LIS1), a

22 nvolved in immune responses include CD36 and platelet-activating factor receptor (PAFR).

23 Anaphylaxis was inhibited by platelet-activating factor receptor or histamine recepto

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

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

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

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

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

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

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

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

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

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

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

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

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

37 structures with distinct areas of differing platelet activation.

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

39 th functions beyond inhibiting ITAM-mediated platelet activation.

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

41 ntithrombotic drug development and assessing platelet activity in health and disease.

42 e blood von Willebrand factor (VWF) mediates platelet adhesion to injured vessels by sequestering pla

43 oprotein ligand 1 axis, followed by (2) firm platelet adhesion to the endothelium via interaction of

44 We propose a shear-dependent platelet adhesive model based on the Morse potential tha

45 Static platelet aggregate formation on extracellular matrix was

46 Circulating platelets, aggregates of monocytes and platelets, and ac

47 (GPIIb/IIIa) is the key receptor involved in platelet aggregation and is a validated target for thera

48 Thrombin- or collagen-induced platelet aggregation and secretion are increased in TRAF

49 Platelet aggregation at the site of vascular injury is e

50 Further, we couple the calibrated platelet aggregation model with a tissue-factor/contact

51 One mystery in the mechanism of platelet aggregation pertains to how resting platelets i

52 of intravascular thrombin activity, reduced platelet aggregation, and improved microvascular perfusi

53 ies against, for example, Rhesus D (RhD) and platelet Ags frequently have reduced fucosylation that e

54 alidated ICH prediction risk score PANWARDS (platelets, albumin, no congestive heart failure, warfari

55 PF4 is stored in platelet alpha-granules bound to the glycosaminoglycan (

56 hesion to the endothelium via interaction of platelet alphaIIbbeta3 with endothelial alphavbeta3 and

57 nduce formation of CD36/TLR2/TLR6 complex in platelets and activate downstream signaling via TIRAP (T

58 ame size distribution as infused human donor platelets and are preferentially incorporated into clots

59 rious length scales creates oriented mineral platelets and chiral vaterite suprastructures.

60 te thrombotic events involving activation of platelets and coagulation proteins.

61 eukocyte adhesion to P-selectin on activated platelets and endothelial cells induces shedding of the

62 a chemokine abundantly produced by activated platelets and immune cells.

63 ation was decreased in PP1calpha(-/-) murine platelets and in human platelets treated with a small-mo

64 We conclude that platelets and Meg-01 cells express the MS cation channel

65 induce the production of IL-1beta, activate platelets and neutrophils and elevate blood pressure in

66 Using DREAM-null platelets and PI3K isoform-specific inhibitors, we obser

67 icant independent factors were the number of platelets and regular need for pain medication.

68 ch imply a single subpopulation of versatile platelets and thus suggest that their commonality requir

69 duced association of disseminated cells with platelets and white blood cells.

70 building blocks, the aragonite lamellae (or platelets), and (ii) the imbricated, or staggered, arran

71 ating platelets, aggregates of monocytes and platelets, and activation of microglial cells were measu

72 t monocyte phagocytosis of cynomolgus monkey platelets, and cynomolgus platelet activation in vitro T

73 It incorporates leukocytes, platelets, and growth factors within the dense fibrin ma

74 s; older age (especially >/=50 years), lower platelets, and liver stiffness >/=12 kPa at year 5 repre

75 BCs, and between RBCs and white blood cells, platelets, and the endothelium.

76 Increased levels of leukocytes, platelets, and tissue factor-positive (TF(+)) microvesic

77 HLA-B12, and 9% of 66 HLA-B35 donors showed platelet antigen expression that was not or only minimal

78 These results indicate that platelet APP limits venous thromboembolism through a neg

79 Platelets are anucleate cytoplasmic fragments that lack

80 During this process, platelets are bridged by soluble fibrinogen that binds s

81 Platelets are the sole source of EGF in circulation, yet

82 targeted MB exhibited increased adhesion to platelets as compared to MBControl.

83 sis or hemostasis, VAMP-3(-/-) mice had less platelet-associated Fg, indicating a defect in Fg uptake

84 Human platelets at a physiologic ratio of 1 platelet to 9 red

85 Older age, lower platelets at baseline and year 5, and liver stiffness >/

86 immobile fibrinogen on the surface of other platelets at the primary injury site.

87 nal pulling causes shortening and bending of platelet-attached fibers, resulting in formation of fibe

88 mproving endothelial coverage and minimizing platelet attachment while enhancing the mechanical prope

89 impact of the CK2 regulatory beta-subunit on platelet biogenesis and activation.

90 d sphingosine synthesis pathways in skin and platelet biology.

91 uired for the activation of human and murine platelets by oxPCCD36.

92 Platelet C-type lectin-like receptor 2 (CLEC-2) is known

93 agonist, Yoda1, potentiated shear-dependent platelet Ca(2+) transients by 170%.

94 rombocytopenia due to a markedly accelerated platelet clearance in the spleen.

95 This trial assessed the hypothesis that platelets collected from donors with highly responsive p

96 In addition, platelet concentrates prepared from F-LR + MPR whole blo

97 , with increased circulating neutrophils and platelets, consistent with increased cardiac inflammatio

98 ombosis at sites of arterial injury and that platelets contribute to venous thrombosis has prompted t

99 he best new expanded classification rule was platelet count >110 x 10(9) cells/L and LSM <25 kPa.

100 trombopag or placebo, stratified by baseline platelet count (<10 x 10(9) platelets per L vs >/=10 x 1

101 azards ratio, 0.98; p = 0.002) and decreased platelet count (hazards ratio, 1.19; p = 0.03) were asso

102 hite blood cell count (HR, 1.910; P = .017), platelet count (HR, 7.437; P = .005), and Ph-like ALL (H

103 rom low-responder donors, resulting in lower platelet count increments following transfusion.

104 atelet transfusion, symptomatic bleeding, or platelet count of less than 10 x 10(9) per L.

105 Patients with a stable platelet count of lower than 30 x 10(9) platelets per L,

106 bocytopenia, a disorder characterized by low platelet count.

107 tent immune thrombocytopenia (ITP) increased platelet counts and reduced bleeding.

108 telets from healthy donors in vitro, raising platelet counts by 0% (unsupplemented control), 25%, 50%

109 Platelet counts had a nadir at day 3 followed by a rebou

110 Median platelet counts increased to 50 x 10(9)/L or more by wee

111 Deceased CFLD patients had lower platelet counts than those alive with CFLD (143 versus 2

112 poietic TFs in the pathobiology of inherited platelet defects.

113 When attached to multiple fibers, platelets densify the fibrin network by pulling on fiber

114 latelet activation in vitro, and vessel wall platelet deposition and initial hemostasis in vivo.

115 hrombus incidence, thrombus size, fibrin and platelet deposition in the ligated inferior vena cava, a

116 in murine platelets prevented oxLDL-induced platelet deposition on immobilized collagen in response

117 clotted wound by a concentration gradient of platelet-derived growth factor (PDGF), together with oth

118 Platelet-derived growth factor (PDGF)-BB belongs to a fa

119 d quiescent mesenchymal cell activation in a platelet-derived growth factor (PDGF)-dependent manner.

120 r receptor alpha (PDGFRalpha) and its ligand platelet-derived growth factor A (PDGF-A) are co-express

121 s (angiopoietin 2; hepatocyte growth factor; platelet-derived growth factor AA and BB; placental grow

122 tor, vascular endothelial growth factor, and platelet-derived growth factor AB) before and after comp

123 odeling linked to maximal thrombospondin and platelet-derived growth factor D expression.

124 We find that platelet-derived growth factor evokes transient oxidatio

125 Platelet-derived growth factor receptor (PDGFR) senses e

126 isib also inhibited ALL proliferation in ABL/platelet-derived growth factor receptor (PDGFR)-mutant m

127 -oncogene receptor tyrosine kinase (KIT) and platelet-derived growth factor receptor alpha (PDGFRA) m

128 errations in FLT3, tyrosine kinase 2 (TYK2), platelet-derived growth factor receptor alpha (PDGFRA),

129 Here we report that platelet-derived growth factor receptor alpha (PDGFRalph

130 Platelet-derived growth factor receptor alpha (PDGFRalph

131 many different signaling pathways, including platelet-derived growth factor receptor alpha (PDGFRalph

132 Here, we show that platelet-derived growth factor receptor alpha (PDGFRalph

133 (NOXs), and oxidized SHP2 co-localizes with platelet-derived growth factor receptor and NOX1/4.

134 Connective tissue progenitor cells, platelet-derived growth factor receptor-alpha-positive c

135 e Boyden chamber and show that a gradient of platelet-derived growth factor-AB (PDGF-AB) expedites mi

136 rom the culture of fat with ROS or PGZ on i) platelet-derived growth factor-BB (PDGF-BB)-stimulated p

137 tor-2, transforming growth factor-beta1, and platelet-derived growth factor-BB at 2 weeks compared wi

138 ein oxidation within cells, and suggest that platelet-derived growth factor-dependent "redoxosomes,"

139 Platelet-derived proteins incorporated into the coacerva

140 and functionally intact, and transfer of WT platelets did not restore arthritis susceptibility.

141 In fact, we found platelets did not store EGF, synthesized as a single 6-k

142 nrelated families in the BRIDGE Bleeding and Platelet Disorders (BPD) collection who carry a TPM4 var

143 es in pedigrees with unexplained bleeding or platelet disorders to data from 5422 controls.

144 Platelets displayed reduced aggregation in response to a

145 These findings collectively indicate platelets do not kill bloodstage Plasmodium at physiolog

146 support the current policy of not selecting platelet donors on the basis of platelet function for pr

147 eriments further indicated the importance of platelet DREAM in thrombogenesis.

148 soform-specific inhibitors, we observed that platelet DREAM is important for alpha-granule secretion,

149 Platelet-driven reduction in blood clot volume (clot con

150 sting that the ITS force map can report anti-platelet drug efficacy.

151 hich is sensitive to treatment with the anti-platelet drug tirofiban, suggesting that the ITS force m

152 ge of Plasmodium-infected (iRBCs) with bound platelets during the ascending parasitemia in Plasmodium

153 unction, culminating in thrombocytopenia and platelet dysfunction.

154 Platelets effectively killed two different strains of S.

155 blood endothelial markers (CD34, endomucin, platelet endothelial cell adhesion molecule 1, and plasm

156 VEGF-A165 b restores the expression of platelet endothelial cell adhesion molecule in glomerula

157 There is increasing evidence that platelet-endothelial interactions also contribute to ear

158 This review provides insight into the platelet-endothelial interface, based on in vitro flow c

159 The median time to platelet engraftment was 27 days.

160 and, second, we tested the possibility that platelets enhance macrophage phagocytosis and intracellu

161 Similar to Vps34-deficient platelets, ex vivo treatment of wild-type mouse or human

162 Although not required for normal platelet exocytosis or hemostasis, VAMP-3(-/-) mice had

163 y antibodies against complexes between human platelet factor 4 (hPF4) and heparin.

164 hole blood or blood's hemostatic components (platelets, fibrinogen, and coagulation factors).

165 We found that platelet force distribution has strong polarization whic

166 Measuring and mapping single platelet forces are desired in both research and clinica

167 utrophils were stimulated to produce NETs in platelet-free plasma (PFP) or in buffer using phorbol my

168 adhesion to injured vessels by sequestering platelets from blood flow and depositing them to collage

169 samples were supplemented with concentrated platelets from healthy donors in vitro, raising platelet

170 DS AND Using in vitro approaches, as well as platelets from mice with genetic deletion of MyD88 (myel

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

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

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

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

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

176 in modulating thrombopoiesis, the process of platelet generation.

177 pass (1) platelet rolling via interaction of platelet glycoprotein Ib-IX-V with endothelial-released

178 Strong TR peptide ligands from platelet GP1balpha and G-protein-coupled receptor MAS ef

179 to the endothelium, and Mac-1 engagement of platelet GPIbalpha is required for injury responses in d

180 vestigate this, we infected mice depleted of platelet GPVI or CLEC2 by antibody treatment or GPVI(-/-

181 as associated with microthrombocytopenia and platelet granule abnormalities.

182 ed blood cells, mammalian erythroblasts, and platelets have a peripheral ring of microtubules, called

183 noikis and succeed in the metastatic process.Platelets have been associated with increased tumor grow

184 Although it was shown that platelets help maintain hemostasis in the ischemic brain

185 , a higher Gleason score, a higher number of platelets, higher C-reactive protein, regular need for p

186 h ITIM-containing receptor in the context of platelet homeostasis.

187 reased thrombin generation in the absence of platelets; however, this effect was reduced in the prese

188 RATIONALE: Platelet hyperreactivity, which is common in many pathol

189 en interrelated variables that contribute to platelet hyperreactivity-high blood glucose, oxidative s

190 platelet aggregation pertains to how resting platelets ignore soluble fibrinogen, the third most abun

191 tion of Akt activity significantly abolished platelet-induced EOMA cell proliferation in vitro and tu

192 Moreover, injection of wild-type platelets inhibited endothelial recovery in wire-injured

193 ard Therapy to Achieve Optimal Management of Platelet Inhibition (CHAMPION PCI, CHAMPION PLATFORM, an

194 ard Therapy to Achieve Optimal Management of Platelet Inhibition [PLATFORM]: NCT00385138; A Clinical

195 d 30 days, supporting the use of intensified platelet inhibition during the first year after STEMI.

196 ard therapy to achieve optimal management of platelet inhibition) PHOENIX randomized 11 145 patients

197 ard Therapy to Achieve Optimal Management of Platelet Inhibition) trials analyzed all randomized pati

198 n the current article, we tested whether the platelet innate immune system contributes to responses t

199 The main mechanisms of platelet interaction with the activated endothelium enco

200 Metoprolol inhibits neutrophil-platelet interactions in AMI patients by targeting neutr

201 PSGL-1, the receptor involved in neutrophil-platelet interactions, fully abrogated metoprolol's infa

202 The i.v. injection of thrombin-activated platelets into CD40(-/-)apoE(-/-) mice was performed eve

203 Transfusion of wild-type platelets into platelet-specific CLEC-2 knockout mice re

204 evolutionarily critical roles, the anucleate platelet is uniquely mammalian.

205 sitive (MS) Ca(2+)-permeable ion channels in platelets is unclear, despite the importance of shear st

206 Here, we demonstrate that PFK1 platelet isoform (PFKP) is the predominant PFK1 isoform

207 recessive bleeding disorder characterized by platelets lacking alpha-granules and progressive marrow

208 , intravascular hemolysis, and activation of platelets leading to a procoagulative state, formation o

209 ice presented a higher number of circulating platelet-leukocyte aggregates, and neutrophils displayed

210 ECs resulted in a corresponding decrease in platelet-leukocyte complex formation and markedly reduce

211 Swelling cases presented low platelet levels and increased transcript abundance of pa

212 a mouse model with Vps34 deletion in the MK/platelet lineage (Pf4-Cre/Vps34(lox/lox)).

213 ITS is a powerful biosensor for the study of platelet mechanobiology, and holds great potential in an

214 nositol between organelles, is essential for platelet-mediated tumor metastasis.

215 Circulating PMPs transfer platelet microRNAs (miRNAs) to vascular cells.

216 The locomotion capacity and platelet-mimicking biological function of the biomimetic

217 This study indicates that platelet miR-223 is a potential therapeutic target for p

218 Platelet MPs (3.5-fold; P < .01) and basophil MPs (2.5-f

219 n molecule [EpCAM](+)MPs, E-cadherin(+)MPs), platelet MPs (CD31(+)CD41(+)MPs), eosinophil MPs (EGF-li

220 Our data suggest that the decay of platelet mRNAs is slowed by the natural loss of the mRNA

221 luding cytotoxicity, viral response, B cell, platelet, neutrophil, and mast cell/basophil activity.

222 It thus appears that platelets not only serve in concert as building blocks o

223 g often reveals a range of changes affecting platelet numbers and function, procoagulant or anticoagu

224 Platelets participate in many important physiological pr

225 the impact of CK2-dependent signaling on MK/platelet (patho-)physiology has remained elusive.

226 h analytical rheology, we quantify real-time platelet pause times and translocation velocities across

227 Higher platelet PCTP expression is associated with increased pl

228 Little is known about the regulation of platelet PCTP.

229 fied by baseline platelet count (<10 x 10(9) platelets per L vs >/=10 x 10(9) platelets per L) and di

230 <10 x 10(9) platelets per L vs >/=10 x 10(9) platelets per L) and disease (MDS vs AML).

231 able platelet count of lower than 30 x 10(9) platelets per L, aged at least 18 years, with refractori

232 Platelets play a key role in the physiological hemostasi

233 Platelets play a role in DVT, but the impact of specific

234 Recent studies have shown that platelets prevent inflammatory bleeding through (hem) im

235 targeted genetic deletion of ERK5 in murine platelets prevented oxLDL-induced platelet deposition on

236 iverse aspects of megakaryocyte biology, and platelet production and function, culminating in thrombo

237 in cytoskeleton is a prerequisite for proper platelet production and function.

238 es megakaryocyte proliferation and increased platelet production.

239 ncertain daily demand, and short shelf life, platelet products are frequently wasted due to expiratio

240 anisms underpinning variant association with platelet quantitative traits using cell type-matched epi

241 HPR was defined as on-clopidogrel P2Y12 platelet reaction units >208 as measured by the VerifyNo

242 hin SVG, and the relative importance of high platelet reactivity (HPR) in SVG PCI versus native lesio

243 Platelet reactivity in hyperlipidemic conditions is enha

244 on of PECAM-1, several other ITIM-containing platelet receptors have been discovered.

245 ay a role in DVT, but the impact of specific platelet receptors remains unclear.

246 ten (4%) complete remission with incomplete platelet recovery, 46 (18%) complete remission with inco

247 rophil recovery, 88% v 93%, P = .07; 100-day platelet recovery, 88% v 85%, P = .33).

248 RIS study (Patterns of Non-Adherence to Anti-Platelet Regimens in Stented Patients Registry), 4222 pa

249 rd an SDF1alpha gradient, leading to ectopic platelet release within the bone marrow.

250 We conclude that activated platelets release ADAMDEC1, which hydrolyzes pro-EGF to

251 sessile arginyl residue and found stimulated platelets released soluble activity that cleaved this pr

252 Furthermore, platelet removal by ECs resulted in a corresponding decr

253 PCTP expression is associated with increased platelet responses on activation of protease-activated r

254 Platelet-rich fibrin (PRF) is an autologous non-transfus

255 ysiologically relevant conditions such as in platelet-rich plasma and whole blood.

256 cient selection of RNA biomarker panels from platelet RNA-sequencing libraries (n = 779).

257 with the activated endothelium encompass (1) platelet rolling via interaction of platelet glycoprotei

258 n hyperlipidemic conditions is enhanced when platelet scavenger receptor CD36 recognizes oxidized lip

259 This study revealed that platelet serglycin is decorated with chondroitin/dermata

260 aining receptors are versatile regulators of platelet signal transduction, with functions beyond inhi

261 Transfusion of wild-type platelets into platelet-specific CLEC-2 knockout mice restored thrombos

262 with general inducible deletion of CLEC-2 or platelet-specific deficiency in CLEC-2 are protected aga

263 Here we show that platelet-specific deletion of CLEC-2 but not GPVI leads

264 We found that platelets stimulated EOMA proliferation but did not miti

265 Moreover, highly contractile platelet subpopulations present in healthy controls are

266 The platelet surface target of MMP-2 and the mechanism throu

267 affolding protein Nbeal2, are causal of gray platelet syndrome (GPS), a rare recessive bleeding disor

268 eporter mice and induce sr39tk expression in platelets, T lymphocytes or cardiomyocytes.

269 inase 2 (CK2) is readily detected in MKs and platelets, the impact of CK2-dependent signaling on MK/p

270 Human platelets at a physiologic ratio of 1 platelet to 9 red blood cells (RBCs) did not inhibit the

271 collected from donors with highly responsive platelets to agonists in vitro assessed by flow cytometr

272 results indicate that cancer cells depend on platelets to avoid anoikis and succeed in the metastatic

273 First, we determined the ability of platelets to kill S. aureus directly; and, second, we te

274 -2 and the mechanism through which it primes platelets to respond to subsequent stimuli are still unk

275 of von Willebrand factor and recruitment of platelets to the inferior vena cava wall after DVT induc

276 vidence that thrombin may be as important as platelets to thrombosis at sites of arterial injury and

277 Fresh frozen plasma-to-packed RBCs and platelets-to-packed RBCs ratios were not associated with

278 ne Guidelines (the use of leukoreduction and platelet transfusion in solid tumors or chronic, stable

279 wing within the screening period of 4 weeks: platelet transfusion, symptomatic bleeding, or platelet

280 bone marrow failure, requiring prophylactic platelet transfusion.

281 basis of platelet function for prophylactic platelet transfusion.

282 nic hematology/oncology patients in spite of platelet transfusions.

283 PP1calpha(-/-) murine platelets and in human platelets treated with a small-molecule inhibitor of Gbe

284 or the dramatic morphological transformation platelets undergo when becoming procoagulant.

285 urface is resistant to adhesion of activated platelets unlike planar control titania and smooth PDMS

286 statistical formulation, we have found that platelet usage is highly dependent on weekday/weekend pa

287 investigate this model, we interrogate human platelets using approaches that include the supported li

288 gordonii and Streptococcus sanguinis, binds platelets via terminal sialic acid.

289 3-kinase (PI3K), in megakaryocytes (MKs) and platelets, we created a mouse model with Vps34 deletion

290 all these inflammatory actions by activated platelets were abrogated by lack of CD40 on injected pla

291 In KitW/Wv mice, platelets were present in numbers similar to those in WT

292 at are composed of von Willebrand factor and platelets, which account for the thrombocytopenia, hemol

293 aps in the reported characteristics of these platelets, which imply a single subpopulation of versati

294 that a substantial proportion of donors have platelets with consistently low expression of specific H

295 ciation of host cells such as leukocytes and platelets with endothelia under vascular shear stress re

296 The coculture of platelets with lymphocytes in the presence of stimulatio

297 cess and we found that treatment of adherent platelets with PGI2 caused inhibitory phosphorylation of

298 x vivo treatment of wild-type mouse or human platelets with the Vps34-specific inhibitors, SAR405 and

299 ed cytotoxicity and showed strong binding to platelets within thrombi in infected mouse lungs.

300 FV(+) HG/CD42b(+) MKs, leading to increased platelet yield in vivo, but not in vitro.