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1  aggregation, confirming a role for ABCC4 in platelet function.
2 the platelet-enriched miRNA, miR-223, affect platelet function.
3  host physiology, modulating GI motility and platelet function.
4 tases have emerged as critical regulators of platelet function.
5 ategy for patients with diseases that affect platelet function.
6 ism in SCD as well as a modulator of healthy platelet function.
7 or strategies based on the interference with platelet function.
8 entional and microfluidic assays to evaluate platelet function.
9 elets to a number of well-accepted models of platelet function.
10 ), but little is known how JAK2V617F affects platelet function.
11 ts Cu,Zn-superoxide dismutase (Cu,Zn-SOD) in platelet function.
12 , abnormal platelet morphology, and impaired platelet function.
13 re mice to investigate the role of Cyfip1 in platelet function.
14 th current literature linking the disease to platelet function.
15 ich the cAMP-PKA signaling pathway regulates platelet function.
16 gh heteromeric interactions in regulation of platelet function.
17  roles for hemichannels and gap junctions in platelet function.
18 n, baroreflex sensitivity, inflammation, and platelet function.
19 -leukocyte aggregate formation, and improved platelet function.
20 lets functions as an endogenous inhibitor of platelet function.
21 y used to demonstrate the role of P2Y(12) in platelet function.
22 tter understanding for the impact of mHtt on platelet function.
23 erized by macrothrombocytopenia and impaired platelet function.
24 for </= 15% of total phenotypic variation in platelet function.
25 oskeletal and adhesion machinery critical to platelet function.
26 prevailing concept that No and cGMP inhibits platelet function.
27  ITAM-like-containing receptor signaling and platelet function.
28 denafil, potentiates NO signaling to inhibit platelet function.
29 le-associated membrane protein-3 (VAMP-3) in platelet function.
30 ded for clinically meaningful restoration in platelet function.
31 gic receptors (P2Y1, P2Y12), and thus normal platelet function.
32 platelet production and had a mild effect on platelet function.
33 reduced ceramide levels in skin and impaired platelet function.
34 ional derangements related to fibrinogen and platelet function.
35 e and the role of dense granule secretion in platelet function.
36 r whether plasma miRNA levels correlate with platelet function.
37 et size, is a potential biological marker of platelet function.
38  on VWF, but also affect specific aspects of platelet function.
39 clin (PGI2) and nitric oxide (NO) to inhibit platelet functions.
40 uggesting distinct roles of PDI and ERp57 in platelet functions.
41 atopoietic stem cell (HSC) and megakaryocyte/platelet functions.
42 g the facilitation of alphaIIbbeta3-mediated platelet functions.
43 n important role in controlling archetypical platelet functions.
44 ltitude of physiological activities in which platelets function.
45 ome who had undergone detailed assessment of platelet function 30 days after the acute event.
46 study demonstrates that PGI2 can reverse key platelet functions after their initial activation and id
47                                              Platelet-function analysis (PFA) of closure times (CT) o
48         Closure times in the shear-dependent platelet function analyzer (PFA)-100 were measured on he
49                                              Platelet function analyzer closure times were lower with
50 osine diphosphate, collagen and epinephrine, Platelet Function Analyzer-100 (Siemens Healthcare Diagn
51 endent platelet hyper-reactivity measured by Platelet Function Analyzer-100 CADP CT are novel indepen
52 ood flow, (2) a bedside point-of-care assay (platelet function analyzer-closure time adenine DI-phosp
53  that aimed to find the genetic structure of platelet function and body mass index, respectively.
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         After AKI resolution (n = 23 of 40), platelet function and coagulation improved to levels obs
57 ic substrates provides devices for measuring platelet function and coagulation with low blood volumes
58 -terminal CGHC motif of PDI is important for platelet function and coagulation.
59 ysregulation leads to significant defects in platelet function and disease.
60 orter localization and expression can affect platelet function and drug sensitivity.
61  light onto the mechanistic underpinnings of platelet function and dysfunction.
62 s involved in mediating the effect of TPO on platelet function and elucidate the underlying mechanism
63 bition may be an effective way of preserving platelet function and eventually decelerating atherothro
64 hat contribute significantly to coagulation, platelet function and fibrin formation.
65 or 12-LOX in regulating FcgammaRIIa-mediated platelet function and identifies 12-LOX as a potential t
66  beta3, Leu33Pro is associated with enhanced platelet function and increased risk for coronary thromb
67 r, despite the importance of shear stress in platelet function and life-threatening thrombus formatio
68                                              Platelet function and mechanisms of activation in ischem
69 tic TFs implicated in patients with impaired platelet function and number include runt-related transc
70 nnection between the influence of statins on platelet function and PECAM-1 signaling.
71 inhibition of platelet mitochondria disrupts platelet function and platelet-activated blood coagulati
72 tic variant in PEAR1 associated with altered platelet function and provide a plausible biologic mecha
73 thrombopoietin receptor agonist (TPO-RA), on platelet function and reactivity.
74                     Widespread monitoring of platelet function and the effect of antiplatelet drugs w
75                            The inhibition of platelet function and the prevention of thrombus formati
76 ly developed a genetic mouse model to assess platelet function and thrombosis in the setting of GPx-3
77  including TLR9; however, the role of TLR in platelet function and thrombosis is poorly understood.
78                      The effects of Slit2 on platelet function and thrombus formation have never been
79 sin displayed a 4-fold greater inhibition of platelet function and thrombus formation in vitro than c
80 at Slit2 is a powerful negative regulator of platelet function and thrombus formation.
81 genomic regulatory effects of PXR ligands on platelet function and thrombus formation.
82 amic forces that contribute significantly to platelet function and thrombus formation.
83 ncy have insulin hypersensitivity, defective platelet function, and abnormal mast cell development.
84 hat participates in both of these aspects of platelet function, and it is the only one to signal thro
85 the insulin receptor substrate (IRS)-1 gene, platelet function, and long-term outcomes in patients wi
86 r E2 in regulating the platelet proteome and platelet function, and point to new potential antithromb
87  association between IRS-1 genetic variants, platelet function, and the risk of major adverse cardiac
88 ranule secretion plays a significant role in platelet function, and they also indicate that abnormal
89 en specific dietary nutrients, gut microbes, platelet function, and thrombosis risk.
90 c regimens on cerebral microembolization and platelet function are equivalent.
91                      Important regulators of platelet function are G proteins controlled by seven tra
92 ts and mechanisms that contribute to altered platelet function are poorly defined.
93  plethora of factors released on activation, platelet functions are also connected to tumor growth, n
94 inin, fibronectin, and collagen, while other platelet functions are normal.
95               In this work, a broad range of platelet functions are quantitatively assessed by levera
96 inogenversusfibrin to alphaIIbbeta3-mediated platelet functions are unknown.
97 rtantly, GSK3 phosphorylation contributes to platelet function as knock-in mice where GSK3alpha Ser(2
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                                              Platelet function assays significantly improve the speci
102 chanism that is not detected by conventional platelet function assays.
103 assessed by standardized bleeding score) and platelet function (assessed by whole blood flow cytometr
104 th cancer may be correlated with the altered platelet functions associated with malignancy.
105 h increasingly novel methods of manipulating platelet function at our disposal, we highlight avenues
106       There was no significant difference in platelet function between groups.
107  a useful tool for predicting differences in platelet function between mice and humans.
108 strate that alpha-granule deficiency impairs platelet function beyond their purely hemostatic role an
109 g the role of these phosphatases not only on platelet function but also on megakaryocyte development
110                 Mg(2+) plays a vital role in platelet function, but despite implications for life-thr
111 tly inhibited VWF activity and VWF-dependent platelet function, but higher BT200 concentrations were
112 at GSK3 functions as a negative regulator of platelet function, but how GSK3 is regulated in platelet
113 as Rac, RhoA, and Cdc42 are vital for normal platelet function, but the role of RhoG in platelets has
114                   There was full recovery of platelet function by 24 hours.
115 N85 complex in supporting integrin-dependent platelet function by dampening the phosphatase activity.
116          Ticagrelor and dipyridamole inhibit platelet function by inhibiting P2Y12 receptors and plat
117 orphisms, which exert a cumulative effect on platelet function by modifying basic platelet parameters
118 s demonstrate that PKCalpha and Akt modulate platelet function by phosphorylating and inhibiting GSK3
119 model of thrombus formation, coagulation and platelet function can be accurately measured in vitro in
120           Thus, the basic scientist studying platelet function can think beyond the traditional hemos
121      Loss of VAMP-3 also affected some acute platelet functions, causing enhanced spreading on Fg and
122                                     Impaired platelet function coincided with reduced thrombus growth
123 ith significant changes in blood pressure or platelet function compared with CF-free controls in norm
124                                 Dysregulated platelet functions contribute to the development and pro
125 rolled patients, 2796 (99.98%) had evaluable platelet function data.
126 asma prostacyclin and NO leading to acquired platelet function defects and thrombosis delay.
127 lood from healthy subjects and patients with platelet function deficiencies.
128  this issue of Blood, Stritt et al show that platelet functions dependent on integrin activation are
129 le for Fc gammareceptor IIa (FcgammaRIIa) in platelet functions dependent on integrin alpha(IIb)beta(
130               AnxA1 administration regulated platelet function directly (eg, via reducing thromboxane
131                        We analyzed candidate platelet function disorder genes in 13 index cases with
132                                    Heritable platelet function disorders (PFDs) are genetically heter
133 worldwide for the investigation of heritable platelet function disorders (PFDs), but interpretation o
134 clinically efficacious in patients with mild platelet function disorders but it is not known which me
135 everity and mortality, little is known about platelet function during COVID-19.
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         Decades of research and knowledge of platelet function exist and the same is true for inflamm
141 ion, and studied CD69 expression, as well as platelet function, fibrin(ogen) deposition, and VWF (von
142 ts, 2 new assays were developed to determine platelet function: first, the microaggregation test, mea
143 ot selecting platelet donors on the basis of platelet function for prophylactic platelet transfusion.
144 honey and passionflower on the modulation of platelet function, haemostasis and thrombosis.
145                      A variety of changes in platelet function have been observed in patients with as
146 n is thought to contribute to variability in platelet function; however, the specific variants and me
147 lood, in a departure from studies of classic platelet function, Huang et al turn their attention to e
148 cancer, infection, and neuroscience, and how platelet function impacts the pathophysiology of each cl
149 1000 platelets/nL, are widely used to assess platelet function in (patho-)physiology, but also in thi
150 y used whole blood flow cytometry to examine platelet function in 20 patients receiving eltrombopag t
151  normal healthy conditions is different from platelet function in chronic ischemic and inflammatory c
152 alizing platelet miRNA processing as well as platelet function in diabetes mellitus.
153 g the observed association between PEAR1 and platelet function in genome-wide association studies.
154 pography of platelet mRNA and how it impacts platelet function in health and disease.
155                                  We assessed platelet function in healthy volunteers before and after
156 hisms) that have small individual effects on platelet function in humans, but can cumulatively lead t
157 bopag, a thrombopoietin-receptor agonist, on platelet function in immune thrombocytopenia (ITP) are n
158               To determine if differences in platelet function in ITP patients account for this varia
159 thrombocytopenia, myelofibrosis and aberrant platelet function in mice and humans.
160                   We show in this study that platelet function in mice mediates suppression of CD8(+)
161                       This demonstrates that platelet function in normal healthy conditions is differ
162 unctional tests that allow for evaluation of platelet function in patients with extremely low platele
163 ts of tocotrienol form of vitamin E (TCT) on platelet function in patients with stroke or transient i
164                   The effect of variation in platelet function in platelet donors on patient outcome
165 vent a complete mechanistic understanding of platelet function in these other diseases.
166  establish RhoA as an important regulator of platelet function in thrombosis and hemostasis.
167 ting granule release from platelets and thus platelet function in thrombosis and hemostasis.
168 ate-depleted beetroot juice) on vascular and platelet function in untreated hypercholesterolemics.
169         Notably, these effects of statins on platelet function in vitro and in vivo were diminished i
170 opment of arterial atheroma, their effect on platelet function in vivo remains unclear.
171 eans for evaluating human thrombopoiesis and platelet function in vivo using immunodeficient mice.
172 gnificance of these distinct interactions on platelet function in vivo, we generated knock-in mice ex
173 RP4, or ABCC4), a nucleotide transporter, in platelet functions in vivo and in vitro by investigating
174 NA and platelet reactivity (PR), a marker of platelet function, in two cohorts following a non-ST ele
175 lls, RhoG orchestrates processes integral to platelet function, including actin cytoskeletal rearrang
176 gation and secretion, indicative of impaired platelet function (increased bleeding tendency), without
177 rs1354034) and affects a module enriched for platelet function, independent of platelet counts.
178 although PIP5KIgamma is essential for normal platelet function, individual isoforms of PIP5KIgamma fu
179 ts roles in vasodilation, cell permeability, platelet function, inflammation, and other vascular proc
180 als and investigated whether polyP-dependent platelet function is altered in IP6K1 knockout (Ip6k1(-/
181                                   Testing of platelet function is central to the cardiovascular pheno
182                                       Normal platelet function is critical to blood hemostasis and ma
183                                        While platelet function is dynamic in individual patients beca
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 eins, but the importance of glycosylation to platelet functions is poorly understood.
187 to create an NO deficiency which can augment platelet function leading to a prothrombotic state.
188 ized by defective neutrophil trafficking and platelet function, leading to recurrent bacterial infect
189 included platelet aggregation and secretion (platelet function markers) and von Willebrand factor.
190 e warranted to clarify whether assessment of platelet function may help tailoring antithrombotic ther
191 mount and intake duration on blood pressure, platelet function, metabolic variables, and potential ad
192                         This article reviews platelet function, molecular targets of antiplatelet age
193 ed before coronary stenting to a strategy of platelet function monitoring (VerifyNow P2Y12/aspirin po
194 icant improvements in clinical outcomes with platelet-function monitoring and treatment adjustment fo
195 nary stenting at 38 centers to a strategy of platelet-function monitoring, with drug adjustment in pa
196 th bleeding symptoms, and detects changes in platelet function more readily than LTA.
197  to thrombosis in the carotid artery despite platelet function not being affected.
198 ough physiologically relevant measurement of platelet function now is more important than ever, a cri
199                                      Routine platelet function or genetic testing is currently not re
200                                    Targeting platelet function pharmacologically in tumor-bearing mic
201  for the relation between the PEAR1 gene and platelet function phenotype.
202 tion between variation in the PEAR1 gene and platelet function phenotype.
203 iently reverse the effects of ibrutinib, and platelet functions recovered after treatment interruptio
204  the molecular characterization of the first platelet function-related CpG-SNP, a genetic predisposit
205 Eph kinase or ephrin signaling in regulating platelet function remained unidentified.
206 cessing machinery, but their contribution to platelet function remains incompletely understood.
207 ria, the role of bioenergetics in regulating platelet function remains unclear.
208                   These results suggest that platelet function represents a continuous, supplemental
209 t Module, related to collagen catabolism and platelet function respectively.
210 ficient platelet production and/or defective platelet function results in bleeding disorders resultin
211                     Patients with at least 2 platelet function results on the same maintenance dose o
212                                       Normal platelet function results were particularly predictive (
213     Platelet function was assessed using the platelet function score (PFS) in HV1 and HV2 and the Ver
214 ors contribute to a substantial variation in platelet function seen among normal persons.
215     Primary outcomes were blood pressure and platelet function, select metabolic variables, and the o
216 atment with PXR ligands was found to inhibit platelet functions stimulated by a range of agonists, wi
217 ed, unblinded investigation (Timing Based on Platelet Function Strategy to Reduce Clopidogrel-Associa
218                                              Platelet function studies in patients are difficult to i
219  prasugrel LD in 149 patients with evaluable platelet function studies.
220 zed, single-center, open, 2-period crossover platelet function study conducted in 30 healthy voluntee
221  9326 participants, 27.5% were included in a platelet function substudy: 1286 treated with prasugrel
222 among participants >/=75 years of age in the platelet-function substudy (P=0.06).
223 l platelet reactivity unit measurements in a platelet-function substudy.
224  much is known about extrinsic regulators of platelet function such as nitric oxide and prostaglandin
225 ocetin inhibited a range of collagen-induced platelet functions such as fibrinogen binding, calcium m
226                   If so, should results of a platelet function test be used to guide the dose or type
227                              Because regular platelet function test cannot be performed in patients w
228  of antiplatelet therapies based on a single platelet function test is beneficial.
229                                              Platelet function test results (vasodilator-stimulated p
230 eening tests, coagulation factor assays, and platelet function test results were within normal limits
231 iables identified in univariate analysis and platelet function test results.
232 ction units according to the VerifyNow P2Y12 platelet function test.
233 Three randomized trials examined the role of platelet function testing (PFT) in clopidogrel-treated p
234 sis And Safety) trial screened patients with platelet function testing after PCI and randomly assigne
235      Thus, treatment adjustment according to platelet function testing at a single time point might n
236  in the genetics cohort; of these, 2,236 had platelet function testing data.
237   Individualizing antiplatelet therapy after platelet function testing did not improve outcome after
238                 These results do not support platelet function testing for MACE risk evaluation in st
239                     We evaluated the role of platelet function testing in clopidogrel-treated patient
240    Detection of platelet hyper-reactivity by platelet function testing in patients undergoing coronar
241 el and high-dose clopidogrel on the basis of platelet function testing in patients with acute coronar
242 ove outcomes in cardiovascular patients, but platelet function testing is not routine in clinical pra
243                          The relationship of platelet function testing measurements with outcomes in
244 lowing clopidogrel loading was determined by platelet function testing on a Multiplate analyzer (Veru
245 among intervention arm patients who received platelet function testing than untested usual care arm (
246             A strategy based on preoperative platelet function testing to determine the timing of CAB
247     Little is known about how clinicians use platelet function testing to guide choice and dosing of
248 ry intervention with drug-eluting stents and platelet function testing using the VerifyNow assay.
249 00 hospitals were assigned access to no-cost platelet function testing versus usual care for acute my
250                                              Platelet function testing was performed in 66.9% of pati
251      In patients with high OTR identified by platelet function testing, the CYP2C19 genotype provides
252 PS found that when clinicians routinely used platelet function testing, they were more likely to adju
253 ions in the past decade on the usefulness of platelet function tests (PFTs) in clinical cardiology, i
254                                      Several platelet function tests have been developed for use in t
255                                  Traditional platelet function tests have been developed primarily fo
256 lated plasma miRNAs and YRNAs correlate with platelet function tests in patients with acute coronary
257                                        Thus, platelet function tests related to platelet age (IPF, FS
258 ry, and clopidogrel effects were measured by platelet function tests.
259 elated miRNAs and YRNAs were correlated with platelet function tests.
260 ted with a significantly greater increase in platelet function than placebo, as measured by multiple
261 tivation, indicate a genomic contribution to platelet function that differs by race and emphasize a n
262 ultiple connexins are involved in regulating platelet function, thereby contributing to haemostasis a
263 monstrate that 2MeSAMP and Cangrelor inhibit platelet function through the P2Y(12)-dependent mechanis
264  coronavirus 2 (SARS-CoV-2) infection alters platelet function to contribute to the pathophysiology o
265 cetylsalicylate (L-ASA; 1-300 mumol/L) on 1) platelet function under shear stress; 2) aggregation ind
266                      Baseline fibrinogen and platelet function using the VerifyNow P2Y12 assay (Accum
267 rsial functions of TLR4 in the modulation of platelet function using various chemotypes and preparati
268 ect programmed cell death, female fertility, platelet function, vasculature inflammation, and diet-in
269                               CD36 modulates platelet function via binding to oxidized LDL (oxLDL), c
270                           In this study, the platelet function was assessed in a well-defined cohort
271                                              Platelet function was assessed using the platelet functi
272                                              Platelet function was assessed using VerifyNow P2Y12 Rea
273                                              Platelet function was assessed with a Multiplate analyze
274                                              Platelet function was assessed with the use of light tra
275                                              Platelet function was compared by varying levels of RPs,
276                                              Platelet function was evaluated at baseline, 30 minutes,
277            PXR ligand-mediated inhibition of platelet function was found to be associated with the in
278                                              Platelet function was intact in RIAM-deficient animals.
279                                              Platelet function was measured 12 to 36 h after PCI with
280                                              Platelet function was measured at baseline and then, at
281                                              Platelet function was measured by aggregometry.
282                         Impaired Nbeal2(-/-) platelet function was shown by flow cytometry, platelet
283                  Together with the defect in platelet function we previously observed in SPL(-/-) mic
284 ms by which this sequence variation modifies platelet function, we produced transgenic knockin mice e
285 d group antigens on platelet proteins alters platelet function; we hypothesized that platelet functio
286       Preoperative demographics and baseline platelet function were equivalent in both groups.
287 sised and their effects on the modulation of platelet function were evaluated.
288                    The effects of albumin on platelet function were investigated in vitro.
289 pidogrel active metabolite and inhibition of platelet function were reduced less by the coadministrat
290 ean platelet volume, which indirectly affect platelet function, were the subjects of GWAS.
291 atelet surfaces that play essential roles in platelet functions, were partially proteolyzed in EHC Co
292 f SLAP or SLAP2 had only moderate effects on platelet function, whereas double deficiency of both ada
293 e plasma are reduced following inhibition of platelet function, while others have shown a correlation
294  This review summarizes current knowledge of platelet functions with a special focus on inflammation
295 ding clotting cascade factors and markers of platelet function) with risk of developing ischaemic (AI
296 ansfer was explored as a strategy to improve platelet function within a canine model for GT.
297 rate that EphB2 signaling not only modulates platelet function within a thrombus but is also involved
298 sight into the role of LOX in thrombosis and platelet function without compounding the influences of
299 ters platelet function; we hypothesized that platelet function would be different between donors with
300                   To examine whether altered platelet function would compensate for the lack of TFPI

 
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