ライフサイエンスコーパス: platelet

1 was partially rescued in Src and Fyn in TKO platelets.

2 ting blood progressively fragments them into platelets.

3 h activated alpha(IIb)beta(3) and VWF-primed platelets.

4 instability determines the size of the final platelets.

5 tected by messenger RNA (mRNA) or protein in platelets.

6 d, in part, by the presence of intra-tumoral platelets.

7 s compared to those produced by unstimulated platelets.

8 dation products (D-dimer) and consumption of platelets.

9 (SOCE) is the major route of Ca2+ influx in platelets.

10 n mice with conditional knockout of PDGFB in platelets.

11 calcium ionophore (A23187)-stimulated murine platelets.

12 ct lipid-signaling pathways such as in human platelets.

13 cking for most primary cell types, including platelets.

14 erexpress PD-L1 to produce immunosuppressive platelets.

15 RGS10 and RGS18 have complementary roles in platelets.

16 d to an antibody against the ENaC present on platelets.

17 1-overexpressing platelets (designated PD-L1 platelets) accumulate in the inflamed pancreas and may s

18 perties of the yoghurts PL fractions against platelet-activating factor (PAF) and thrombin-induced pl

19 ults in the production of the lipid mediator platelet-activating factor (PAF).

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

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

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

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

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

25 Platelet activation and monocyte TF expression were asso

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 rombotic endothelial phenotype that promoted platelet activation.

43 ti-atherothrombotic effect via inhibition of platelet activation.

44 ons initiating and progressing GPVI-mediated platelet activation.

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

46 ed eosinophilic inflammation; recruitment of platelet-adherent eosinophils; and increases in IL-33, I

47 orted that mouse, as well as human GPVI, had platelet adhesion to colon and breast cancer cells.

48 rospot-based technique, in which we assessed platelet adhesion, platelet activation, thrombus structu

49 be avoided and long-term medication of anti-platelet agent is not needed.

50 ctors (such as anti-hypertensive drugs, anti-platelet agents and statins) seem to have little or no e

51 s with COVID-19 also present with neutrophil-platelet aggregates and a distinct neutrophil and platel

52 Platelet aggregation and activation were assessed by agg

53 urs postinfection, had significantly reduced platelet aggregation and NET release.

54 for e.g. learning, memory, mood regulation, platelet aggregation and vasoconstriction, but its invol

55 Both agents inhibit human platelet aggregation but preserve clot retraction.

56 s: This study compared whole-blood impedance platelet aggregation in children with clinically diagnos

57 Integrin activation and platelet aggregation in mice whose platelets express onl

58 Platelet aggregation responses, as well as thrombus form

59 sults: Children with SDB exhibited increased platelet aggregation to TRAP (thrombin receptor-activati

60 ting blood sample was taken, and whole-blood platelet aggregation was measured.Measurements and Main

61 tegrate the initiation of a thrombus through platelet aggregation with its subsequent viscoelastic re

62 imum amplitude, a follow-up study evaluating platelet aggregation would be instructive.

63 PEL-negative individuals showed an impaired platelet aggregation, confirming a role for ABCC4 in pla

64 lbicans can also exert inhibitory effects on platelet aggregation.

65 activating factor (PAF) and thrombin-induced platelet aggregation.

66 ng in mammals, where ADP plays a key role in platelet aggregation.

67 Point-of-care tests (thrombelastometry/platelet aggregometry), conventional coagulation tests,

68 iplatelet agents, nearly normal responses to platelet agonists, and normal platelet survival.

69 se and Ca2+ influx in response to all tested platelet agonists.

70 Binding of platelet alpha(IIb)beta(3) to SLC44A2 on neutrophils lea

71 terized by bleeding symptoms, the absence of platelet alpha-granules, splenomegaly, and bone marrow (

72 Platelets also promote cancer cell growth, survival in c

73 ize new lines of evidence that point to both platelet and endothelial dysfunction as essential compon

74 s of intermediate severity show an exhausted platelet and hyporeactive neutrophil phenotype, patients

75 with COVID-19 are characterized by excessive platelet and neutrophil activation in comparison with he

76 the consequences of the interactions between platelets and a tumor may promote or prevent cancer prog

77 reduced amyloid fibril formation in cultured platelets and decreased the adhesion of Abeta-activated

78 galectin-3 uses ITAM-signaling components in platelets and favors the extravasation of tumor cells.

79 for the accurate measurement of coagulation, platelets and fibrin content.

80 utrophil extracellular traps associated with platelets and fibrin.

81 id profiles linked to inhibition of COX-1 in platelets and in the remainder of the cardiovascular sys

82 stream, iMPs activated endothelial cells and platelets and induced epithelial-to-mesenchymal transiti

83 Pf4, which had been considered specific for platelets and megakaryocytes, is also prominently expres

84 o map integrin receptor forces in live human platelets and mouse embryonic fibroblasts.

85 dy, including in the gastrointestinal tract, platelets and the nervous system.

86 ndividual variations in ABO(H) expression on platelets and/or VWF (particularly HXP and LXP) impact u

87 rombosis or analyzed biomarkers of clotting, platelet, and fibrinolysis activation in human; furtherm

88 hrombosis potential in whole blood, isolated platelets, and animal models of arterial injury.

89 marker-based phenotyping of neutrophils and platelets, and functional assays for platelet, neutrophi

90 measures: hemoglobin, alkaline phosphatase, platelets, and lymphocytes.

91 derived from erythrocytes, rather than from platelets, and that it was abolished by MP PS capping us

92 acid (HETE), and 15-HETE was absent in both platelet- and global-COX-1-ko mice.

93 Platelets are blood cells responsible for vascular integ

94 Platelets are chief effector cells of hemostasis and pat

95 The study persuasively suggests that platelets are critical thromboinflammatory effector cell

96 Blood platelets are formed by fragmentation of long membrane e

97 How platelets are produced by megakaryocytes in vivo remains

98 tients with sepsis have increased amounts of platelet-associated histones (PAHs), which appear to be

99 Deletion of platelet BIN2 (Bin2fl/fl,Pf4-Cre mice) resulted in reduc

100 1 negative tumors and that interference with platelet binding to PD-L1 negative cancer cells promotes

101 entation explains the strong acceleration of platelet biogenesis in the presence of an external flow,

102 ulation of platelet size in flow-accelerated platelet biogenesis.

103 elet formation, supplies the majority of the platelet biomass.

104 epithelial sodium channel (ENaC) in membrane platelets can be related with the presence of HTN and th

105 e results illustrate for the first time that platelets can directly kill C. albicans through release

106 the atomically thick triangle-shaped vacancy platelets can directly produce <c> dislocation loops.

107 data from humans and mice demonstrating that platelet CLEC-2 influences the hepatic sterile inflammat

108 Our data demonstrate that blocking platelet CLEC-2 signalling enhances liver recovery from

109 y comparing all three aspects of hemostasis (platelets, coagulation, and fibrinolysis) in patients wi

110 ation (18 patients), and PPV plus autologous platelet concentrate (22 patients).

111 derivative, platelet-derived growth factor, platelet concentrates, and fibroblast-growth factor-2.

112 complement system along with neutrophils and platelets contributes to COVID-19, the authors present e

113 ve intent chemotherapy), laboratory-related (platelet count < 50 x 109/L, albumin below normal, LDH a

114 e (10.82 [1.49-78.69] per 1 mg/dL increase), platelet count <250 x 103/muL (1.92 [1.02-3.60]), lower

115 while a weak correlation was found with the platelet count (r = 0.257).

116 enhanced response to agonists in vitro, but platelet count and survival are normal.

117 ecause current treatment guidelines based on platelet count are confounded by variable bleeding pheno

118 Poor platelet recovery was defined as a platelet count of <=20 000/muL on Day 2.

119 RGS18-/- mice have a 15% reduction in platelet count that is not affected by antiplatelet agen

120 , the impact of C-reactive protein (CRP) and platelet count was also analysed.

121 Platelet count was normal in Chk knockout (KO) mice, red

122 e derived neutrophil-to-lymphocyte ratio and platelet count were significantly associated with HPD st

123 tes of paroxysmal atrial fibrillation, lower platelet count.

124 tive study of 49 patients with ITP and nadir platelet counts <30 x 109/L and 18 aged-matched healthy

125 ary or secondary immune thrombocytopenia and platelet counts less than 100 x 10(9) cells per L before

126 In addition, higher platelet counts were observed among recipients who achie

127 itters had significant reductions in WBC and platelet counts whereas five non-remitters did not.

128 rombocytopenia showing a marked reduction in platelet counts, and dengue hemorrhagic fever.

129 tively show declining fibrinogen, increasing platelet counts, and lower white blood cell counts.

130 aryocytes (MKs) deficient in miRs have lower platelet counts, but information about the role of miRs

131 PO(a)-L(Rx) dose and placebo with respect to platelet counts, liver and renal measures, or influenza-

132 between blood dose and dose rate, RIFs, and platelet counts.

133 ose adjustments were allowed weekly based on platelet counts.

134 mboxane B2 (sTXB2), a validated biomarker of platelet COX-1 activity, and urinary prostacyclin metabo

135 pectrometry analysis demonstrated blood from platelet-COX-1-ko and global-COX-1-ko mice produced simi

136 Aspirin prevents thrombosis by inhibiting platelet cyclooxygenase (COX)-1 activity and the product

137 The platelet deformation index for GORE-TEX is 2-fold higher

138 mappings over large areas of single crystal platelets demonstrate the co-existence of both free and

139 nction was also observed in mice that lacked platelet-dense granules, dense granule secretion machine

140 mechanisms involving platelet activation and platelet-dependent monocyte TF expression, which were as

141 ation of diverse alpha-granule proteins; and platelet-dependent, accelerated fibrinolysis.

142 ading frame, under the influence of a 1.5 kb platelet derived growth factor B (PDGFB) promoter.

143 Platelet Derived Growth Factor Receptor (PDGFR) signalin

144 The platelet-derived CD61-positive EVs and CD9-positive EVs,

145 Moreover, platelet factor 4 levels and platelet-derived extracellular vesicles were increased i

146 ted knockdown of TRIM28 and TRIM27 inhibited platelet-derived growth factor (PDGF)-induced migration

147 1 overexpression increases the expression of platelet-derived growth factor (PDGFB) in human pulmonar

148 Platelet-derived growth factor B (PDGFB) plays a crucial

149 in, tissue inhibitor of metalloproteinase 1, platelet-derived growth factor c, transforming growth fa

150 Platelet-derived growth factor receptor (PDGFR)-alpha pl

151 luded expected PI3K interactors, such as the platelet-derived growth factor receptor A (PDGFRA), as w

152 l cells of Cajal (ICC), and cells expressing platelet-derived growth factor receptor alpha (PDGFRalph

153 ation and that it is selectively mediated by platelet-derived growth factor receptor signaling.

154 Adipocyte progenitors (APs) express platelet-derived growth factor receptors (PDGFRs), PDGFR

155 cedures, including enamel matrix derivative, platelet-derived growth factor, platelet concentrates, a

156 A massive release of platelet-derived MVs occurs during HIV infection.

157 Here, we show that platelet-derived PD-L1 regulates the growth of PD-L1 neg

158 ings establish a previously unknown role for platelet-derived PDGFB, whereby it promotes and maintain

159 The PD-L1-overexpressing platelets (designated PD-L1 platelets) accumulate in the

160 disorder characterized by antibody-mediated platelet destruction.

161 Platelets did not modulate the Th-1-polarizing cytokines

162 budding results in the sustained release of platelets directly into the peripheral circulation durin

163 manufacturing and for managing quantitative platelet disorders.

164 sing hemangioblast markers (Flk1, Tal1/Scl1, platelet endothelial cell adhesion molecule 1, vascular

165 a significant increase in the expression of platelet endothelial cell adhesion molecule-1 (PECAM-1)

166 Median times to neutrophil and platelet engraftment were comparable.

167 tor caspase-1 or IL-1beta pathway attenuated platelet EV generation, prevented platelet-neutrophil ag

168 shedding of IL-1beta and caspase-1-carrying platelet EVs promote lung vasoocclusion in SCD.

169 ation and platelet aggregation in mice whose platelets express only talin-1(R35E, R118E) are even mor

170 Moreover, platelet factor 4 levels and platelet-derived extracellu

171 myeloperoxidase (MPO)-DNA complexes (NETs), platelet factor 4, RANTES, and selected cytokines.

172 The presence of platelet factor-4 in the rinse samples was analyzed by W

173 l coagulation tests, whole blood counts, and platelet flow cytometry were performed.

174 Upon examination of isolated platelets from patients with sepsis, we identified that

175 hat contribute significantly to coagulation, platelet function and fibrin formation.

176 ding clotting cascade factors and markers of platelet function) with risk of developing ischaemic (AI

177 aggregation, confirming a role for ABCC4 in platelet function.

178 Here, we investigate the role of Chk in platelets, functional redundancy with Csk, and the physi

179 revents hematogenic dissemination, rendering platelets gate-keepers of the inflamed microvasculature.

180 dies demonstrated that the interplay between platelet GPVI and tumor cell-expressed galectin-3 uses I

181 In this study, the genetic deficiency of platelet GPVI in mice decreased experimental and spontan

182 RGS10-/- platelets have an enhanced response to agonists in vitro

183 multiple mechanisms including hyperreactive platelets, hypercoagulable status, and endothelial dysfu

184 In contrast, significantly fewer platelets in PNAs were PS+ in CypDplt-/- counterparts.

185 However, the participation of platelets in the pathogenesis of COVID-19 remains elusiv

186 del systems to show that CFTR dysfunction in platelets increased calcium entry though the transient r

187 These results are the first to identify that platelet-inflammasome-dependent shedding of IL-1beta and

188 nt clinical events through mechanisms beyond platelet inhibition and with an acceptable associated ri

189 Whether stronger platelet inhibition by an intensified oral loading strat

190 Current guidelines recommend intensified platelet inhibition by prasugrel or ticagrelor in patien

191 eceptor antagonists exhibit delayed onset of platelet inhibition in patients with acute myocardial in

192 TRILOGY ACS (Targeted Platelet Inhibition to Clarify the Optimal Strategy to M

193 vement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis In Myoca

194 rect effector of Rap1 GTPases that regulates platelet integrin activation in hemostasis.

195 e Ca(2+) waves and fibrinogen binding to the platelet integrin alpha(IIb)beta(3) (GPIIb/IIIa) through

196 ition of vascular thrombosis by antagonizing platelet integrin alphaIIbbeta3 cannot be achieved witho

197 19 lung autopsies were examined for NETs and platelet involvement.

198 We sequenced the transcriptome of platelets isolated repeatedly up to 4 years from healthy

199 more impaired, resembling the defect seen in platelets lacking both Rap1a and Rap1b.

200 A lack of PDGFB in platelets led to enhanced hypoxia and epithelial-to-mese

201 Post-surgery, SPM and platelet levels decreased in morbidly obese nondiabetic

202 ling leads to reversal of age-associated HSC platelet lineage bias, increased generation of lymphoid

203 be relevant targets for increasing in vitro platelet manufacturing and for managing quantitative pla

204 fened RBCs in flow, suggesting a decrease of platelet margination due to an increased fraction of sti

205 arked reduction in the surface expression of platelet markers (CD41, CD42a, and CD61), a decreased po

206 types of microparticles (iMP) that expressed platelet markers, tumor markers, or both.

207 lly elevated levels of 36 blood cell traits (platelets, mature/immature red cells, and myeloid/lympho

208 n a variety of other diseases and syndromes, platelets may also contribute to nonpulmonary manifestat

209 hese results suggest that megakaryocytes and platelets may be a source of circulating histones during

210 observations in animal models, indicate that platelets may drive lung injury and contribute to dysreg

211 osis inhibition or C5aR1 blockade attenuated platelet-mediated NET-driven thrombogenicity.

212 egakaryocytes (MKs), the precursor cells for platelets, migrate from the endosteal niche of the bone

213 rates that increased platelet activation and platelet-monocyte aggregate formation are observed in se

214 th laboratory-confirmed dengue with <=20 000 platelets/muL and without persistent mild bleeding or an

215 ils and platelets, and functional assays for platelet, neutrophil functions, and coagulation tests, a

216 after stroke, significantly more circulating platelet-neutrophil aggregates (PNAs) were found in CypD

217 attenuated platelet EV generation, prevented platelet-neutrophil aggregation, and restored microvascu

218 Platelet-neutrophil interactions are important for innat

219 Circulating platelet-neutrophil, -monocyte, and -T-cell aggregates w

220 vestigated how complement interacts with the platelet/neutrophil extracellular traps (NETs)/thrombin

221 CC involved platelets, neutrophils, fibrin, and extracellular DNA.

222 s by applying them to receptor clustering in platelets, nuclear pore components, endocytic proteins a

223 e presence of SARS-CoV-2 RNA associated with platelets of COVID-19 patients.

224 anism at level of several cell lines such as platelets or endothelial cells.

225 hether it remains intact or sheds individual platelets or larger fragments (emboli).

226 hocyte activation molecule) family-on either platelets or T cells displayed reduced cerebral CD4(+) T

227 : use of aspirin/NSAIDs/anti-coagulants/anti-platelets, pathologic diagnoses (including different typ

228 se through the activation of coagulation and platelet pathways with the production of fibrin degradat

229 throcytes in vitro and these were added to a platelet phagocytosis assay.

230 We suggest that inhibition of in vitro platelet phagocytosis may prove to be a valuable tool fo

231 riteria, based on white blood cell (WBC) and platelet (PLT) counts, were developed and prospectively

232 hted that ABO group significantly influences platelet plug formation at sites of vascular injury (pri

233 -/-) mice have prolonged bleeding, defective platelet plug formation, and delayed thrombotic occlusio

234 clearance is critical, as mice with an aged platelet population displayed a bleeding phenotype.

235 ebrand factor/glycoprotein Ibalpha-dependent platelet 'priming' induces integrin alpha(IIb)beta(3) ac

236 bout the role of miRs in normal human MK and platelet production is limited.

237 icial for ex vivo gene editing, for enhanced platelet production, and for the improved usage of cord

238 volved in megakaryocyte (MK) development and platelet production.

239 lear histones and transfer histones to their platelet progeny.

240 Platelets promote metastasis, however, their role in tum

241 Our study revealed a new mechanism by which platelets promote the metastasis of colon and breast can

242 e of FIB-4 and aspartate aminotransferase to platelet ratio index (APRI) on HCC risk.

243 o unknown rivaroxaban effect that impacts on platelet reactivity and arterial thrombosis.

244 ive to cyclo-oxygenase-1 blockade, including platelet reactivity in response to arachidonic acid (mea

245 f this approach on blood thrombogenicity and platelet reactivity remain unknown.

246 atients receiving placebo, whereas levels of platelet reactivity were similar with adenosine diphosph

247 The activation of platelet receptor C-type lectin-like receptor II-type (C

248 We found a significant interaction between platelet recovery and transfusion; patients with poor pl

249 ploidy are normal in all 3 mouse lines, but platelet recovery from severe acute thrombocytopenia is

250 The mechanisms of poor platelet recovery need to be determined.

251 Poor platelet recovery was defined as a platelet count of <=2

252 recovery and transfusion; patients with poor platelet recovery were more likely to bleed if given a p

253 acterized, the cell-biological mechanisms of platelet recruitment to inflammatory micro-environments

254 imulations attribute the previously-observed platelet-recruitment reduction and heparin-size modulati

255 DIC), with patients generally not displaying platelet reductions typical of consumptive coagulopathie

256 registry (Patterns of Non-Adherence to Anti-Platelet Regimens in Stented Patients) were categorized

257 In the context of platelet-related organ injury seen in a variety of other

258 d SFK activity, but paradoxically hypoactive platelets resulting from negative feedback mechanisms, i

259 sheet and improves the alignment of graphene platelets, resulting in much higher compactness and high

260 ascertain if a combination of leukocyte and platelet-rich fibrin (L-PRF) + autogenous bone graft (AB

261 implant surface disinfectant, leukocyte- and platelet-rich fibrin (L-PRF), on a mature oral multispec

262 Platelet-rich fibrin (PRF) membranes can preserve alveol

263 Platelet-rich fibrin (PRF) serves as a reservoir of bioa

264 Whole blood (WB) and platelet-rich plasma (PRP) were perfused at high shear r

265 eatment of control neutrophils with COVID-19 platelet-rich plasma generated TF-bearing NETs that indu

266 Platelet-rich plasma mitochondrial activity, protein exp

267 en individual variation and repeatability of platelet RNA expression and exon skipping, a readily mea

268 y confined to a six faceted hexahedron (cube/platelet) shape.

269 Furthermore, gel nanocomposites containing platelets showed an enhanced resistance to breaking unde

270 A decrease is observed in the fluorescent platelet signal at the wall due to the increase of stiff

271 al origin of fragmentation and regulation of platelet size in flow-accelerated platelet biogenesis.

272 Platelet-specific abrogation of Arp2/3 interferes with h

273 rs6128 is a platelet splice QTL that alters SELP exon 14 skipping an

274 The interaction induced platelet spreading, release of their granule content, an

275 rexpression leads to a >100-fold increase in platelet stores of urokinase plasminogen activator (PLAU

276 We analyzed patients from the Adult Dengue Platelet Study with laboratory-confirmed dengue with <=2

277 ants are also expressed on several different platelet surface glycoprotein receptors.

278 vels of A or B blood group antigens on their platelet surfaces (high expresser phenotype, HXP or low

279 are expressed on different glycoproteins on platelet surfaces.

280 l responses to platelet agonists, and normal platelet survival.

281 Gray platelet syndrome (GPS) is a rare recessive disorder cau

282 of each antibody to inhibit phagocytosis of platelets, the antibodies were used to sensitize erythro

283 curs when the slip length is larger than the platelet thickness; a slip length of a few nanometers ma

284 nd decreased the adhesion of Abeta-activated platelets to injured carotid arteries in mice.

285 interferes with haptotactic repositioning of platelets to microlesions, thus impairing vascular seali

286 ng chimera (PROTAC) technology to reduce the platelet toxicity of navitoclax (also known as ABT263),

287 limited by their on-target and dose-limiting platelet toxicity.

288 Lupus onset initiated major changes to the platelet transcriptome, both in FcgammaRIIA-expressing a

289 Analyses of MK and platelet transcriptomes identified LCP1 as a miR-125a-5p

290 more likely to bleed if given a prophylactic platelet transfusion (odds ratio 2.34, 95% confidence in

291 evere thrombocytopenia requiring one or more platelet transfusions.

292 The incidence of Anti-Platelet Trialists' Collaboration-defined arterial throm

293 dem MS, here we first demonstrate that human platelet-type 12-lipoxygenase (12-LOX) can directly cata

294 The mean number of platelet units requested per day was 16.2 (range 0-30);

295 (AMR) deficiency alone had little effect on platelet uptake.

296 Functionally, platelets were hyperactivated in COVID-19 subjects prese

297 h surface components or releasable products, platelets were pretreated with an inhibitor of actin pol

298 Platelets were transfused on 68% of extracorporeal membr

299 owed partial restoration of CFTR function in platelets, which may be a convenient approach to monitor

300 SFKs was almost completely abolished in DKO platelets, which was partially rescued in Src and Fyn in

301 Incubation of platelets with a blocking antibody directed against CD36