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1 re bleeding phenotype and complex defects in platelet aggregation.
2 le antithrombotic activity via inhibition of platelet aggregation.
3 S13-mediated proteolysis of VWF and promoted platelet aggregation.
4 inity to the GPIIb/IIIa receptor involved in platelet aggregation.
5 ne proteases, contributes to coagulation and platelet aggregation.
6 R4 gene (F2RL3) associated with PAR4-induced platelet aggregation.
7 receptor for, e.g., fibrinogen and mediates platelet aggregation.
8 nule secretion, which is required to augment platelet aggregation.
9 osphate and thromboxane A2 are mandatory for platelet aggregation.
10 IIbbeta3 (GPIIb-IIIa) with fibrinogen during platelet aggregation.
11 uction to complete inhibition of ADP-induced platelet aggregation.
12 nent clinical drug targets for inhibition of platelet aggregation.
13 P), collagen, and rhodocytin (Rhod)-mediated platelet aggregation.
14 rotease-activated receptor 1 (PAR1)-mediated platelet aggregation.
15 lant platelet formation in the regulation of platelet aggregation.
16 ts into the cellular and molecular basis for platelet aggregation.
17 c outlet region, contributing to exacerbated platelet aggregation.
18 usly unrecognized abnormality that may favor platelet aggregation.
19 and has no activity in coagulation tests or platelet aggregation.
20 lial cell damage, permeability increase, and platelet aggregation.
21 imary brain tumors via its ability to induce platelet aggregation.
22 ceptors (GPCRs), and its activation triggers platelet aggregation.
23 and production of adenosine, an inhibitor of platelet aggregation.
24 face and this abnormality is associated with platelet aggregation.
25 blood and the ability of aspirin to inhibit platelet aggregation.
26 , and plasma factors, such as antibodies, on platelet aggregation.
27 but in contrast inhibited ristocetin-induced platelet aggregation.
28 mit vascular smooth muscle proliferation and platelet aggregation.
29 rs of von Willebrand factor, thus regulating platelet aggregation.
30 biological events, including endocytosis and platelet aggregation.
31 strated increased MBL/MASP complex-dependent platelet aggregation.
32 ide-binding motifs, modulating the extent of platelet aggregation.
33 mechanism to prevent excessive VWF-mediated platelet aggregation.
34 ion of thrombi rather than the prevention of platelet aggregation.
35 nflammation, cell adhesion, vessel tone, and platelet aggregation.
36 ibited thrombin-, ADP-, and collagen-induced platelet aggregation.
37 leads to potent and reversible inhibition of platelet aggregation.
38 Inhibition of miR-126 in mice reduced platelet aggregation.
39 elet inhibition was monitored by ADP-induced platelet aggregation.
40 ing its prothrombotic activity and promoting platelet aggregation.
41 vel alphaIIbbeta3 antagonists, which inhibit platelet aggregation.
42 moderately decreased thrombin-induced human platelet aggregation.
43 s an important signaling molecule regulating platelet aggregation.
44 ts of histones and decreases histone-induced platelet aggregation.
45 resulted in defective ITAM receptor-mediated platelet aggregation.
46 sphodiesterase inhibition, strongly impaired platelet aggregation.
47 ation is distinct from purine involvement in platelet aggregation.
48 reduced nitric oxide-mediated inhibition of platelet aggregation.
49 h platelet TLR4 and promotes agonist-induced platelet aggregation.
50 ecretion, and impaired fibrin generation and platelet aggregation.
51 ng, delta-granule content and secretion, and platelet-aggregation; (2) significant decreases of secre
52 on achieved with 80% proportion PT (residual platelet aggregation 80% PT mix/residual platelet aggreg
54 actin polymerization after GPIb-IX-mediated platelet aggregation, actin polymerization inhibitors di
55 tide exhibiting both FXa inhibition and anti-platelet aggregation activities, with a low bleeding ris
57 rimary end point of the study, inhibition of platelet aggregation after arachidonic acid 1.5 mmol/L a
58 s of CPT and NPT showed potent inhibition of platelet aggregation after pretreatment with 1 mM GSH, c
59 far the most potent inhibitor of ADP-induced platelet aggregation among the P2Y12 antagonists describ
60 s at all other time points and inhibition of platelet aggregation; an exploratory analysis evaluated
62 acks and abolished the enhanced PAR4-induced platelet aggregation and 1,4,5-triphosphate generation a
64 on assays and viscometer-based shear-induced platelet aggregation and activation studies reduced plat
67 tures of platelets but significantly impairs platelet aggregation and adenosine triphosphate secretio
72 as associated with higher PAR4-induced human platelet aggregation and Ca2+ flux, and generated greate
74 hich has pro-inflammatory effects, increases platelet aggregation and clot strength, and reduces fibr
76 iological functions, including inflammation, platelet aggregation and endothelial cell apoptosis, and
79 ood cell (RBC) transfusion increases in vivo platelet aggregation and inflammation in coronary and no
80 (GPIIb/IIIa) is the key receptor involved in platelet aggregation and is a validated target for thera
81 levels in Ip6k1(-/-) mice, along with slower platelet aggregation and lengthened plasma clotting time
82 hear rates (3000-10 000 seconds(-1)) induced platelet aggregation and metalloproteinase-dependent app
84 al insight into the underlying mechanisms of platelet aggregation and platelet activation heterogenei
86 fold increase in inhibitory activity against platelet aggregation and release reactions in response t
89 In contrast, 2-MeSADP- and AYPGKF-induced platelet aggregation and secretion were minimally affect
92 nding to the integrin alphaIIbbeta3 mediates platelet aggregation and spreading on fibrinogen-coated
94 We conclude that ATL regulates neutrophil-platelet aggregation and that platelet-neutrophil intera
96 in fluid mechanical conditions that promote platelet aggregation and thrombus formation by increased
97 versibly block substrate binding and inhibit platelet aggregation and thrombus formation in vivo.
100 hemostatic potential is important to mediate platelet aggregation and to recruit platelets to the sub
101 gger CD36-dependent JNK2 activation, enhance platelet aggregation, and accelerate thrombus formation.
102 adhesion to surface-coated PEAR1, diminished platelet aggregation, and eliminated PEAR1 phosphorylati
103 thrombocytosis, exaggerated agonist-induced platelet aggregation, and enhanced extra-intestinal thro
104 ted with production of procoagulant factors, platelet aggregation, and facilitation of thrombotic eve
105 of intravascular thrombin activity, reduced platelet aggregation, and improved microvascular perfusi
106 mage, inflammation, vascular reactivity, and platelet aggregation, and improvement in immune function
109 rotein coupled, 12) plays a critical role in platelet aggregation, and P2RY12 inhibitors are used cli
110 , A23187-induced thromboxane A(2) synthesis, platelet aggregation, and secretion were inhibited by pr
112 all shown to inhibit alphaIIbbeta3 dependent platelet aggregation, and these inhibitors became the fo
113 phate, the P2Y1 receptor (P2Y1R) facilitates platelet aggregation, and thus serves as an important an
114 te thrombocytopenia; absent collagen-induced platelet aggregation; and large, fused alpha-granules in
115 ses such as cell adhesion, vasoconstriction, platelet aggregation, angiogenesis, inflammatory gene ex
117 nd convulxin (CVX) (IC50 = 5.7 muM) mediated platelet aggregation as compared to losartan (LOS) (coll
122 rmore, we show that NPP1 is unable to induce platelet aggregation at physiologic concentrations repor
126 emostasis in vivo by augmenting ADP-mediated platelet aggregation at the site of vascular injury.
128 ) were expressed and discovered to attenuate platelet aggregation, ATP secretion, and thromboxane A2
129 otype associated with increased clotting and platelet aggregation attributable to a promoter variant
130 otent P2Y(1)(2) antagonists as inhibitors of platelet aggregation based on a phenylpyrazole glutamic
131 ual platelet aggregation 80% PT mix/residual platelet aggregation baselinex100) significantly decreas
132 METHODS AND RESULTS- We measured ex vivo platelet aggregation before and after dual antiplatelet
133 racellular signaling inhibited shear-induced platelet aggregation but minimally affected shear-induce
134 Gi signaling; this is insufficient to cause platelet aggregation, but it is enough to predispose pla
135 phil oxidative burst and negatively modulate platelet aggregation by a unique salivary mechanism.
136 osphotyrosine-binding (PTB) domain, inhibits platelet aggregation by competing with fibrinogen for al
139 ayed generation of fIIa(MZ) enzyme activity, platelet aggregation by fII(MZ) is similar to fII(WT) Co
142 displayed enhanced inhibition of ADP-induced platelet aggregation by the nitric oxide donor sodium ni
145 ochemical endpoints were measured, including platelet aggregation, calcium mobilization, and integrin
146 t S. aureus lipoteichoic acid (LTA) inhibits platelet aggregation caused by physiological agonists an
148 n expression in primary brain tumors induces platelet aggregation, correlates with hypercoagulability
149 s reports have shown that rhodocytin-induced platelet aggregation depends on secondary mediators such
150 ver, flavocetin-A inhibited collagen-induced platelet aggregation even after GPIb was blocked with ot
153 wed a significant reduction in PAR4-mediated platelet aggregation, fibrinogen binding, and P-selectin
154 an platelets or its deletion in mice reduces platelet aggregation, fibrinogen binding, granule secret
155 Cx37 gene (Gja4) in transgenic mice reduced platelet aggregation, fibrinogen binding, granule secret
156 ine (0.1-100 microM) significantly increased platelet aggregation harvested from healthy volunteers i
158 multimers (ULVWF), which are prone to induce platelet aggregation; however, the actual trigger of TTP
159 did not suffer from bleeding and have normal platelet aggregation; however, their platelets mimicked
160 tiple mosquito salivary components mediating platelet aggregation (i.e., Aegyptin, apyrase, D7) repre
161 aIIbbeta3 and ability to inhibit ADP-induced platelet aggregation (IC50) showed that two designed lig
162 orted in human blood, but it could stimulate platelet aggregation if localized at low nanomolar conce
163 r, a genome-wide association study (GWAS) of platelet aggregation in African Americans has not been r
166 ylurea chemotype that inhibited ADP-mediated platelet aggregation in human blood samples is described
170 occurrence of bleeding events and decreased platelet aggregation in response to collagen in platelet
171 y effect on resting platelets, cLDL enhanced platelet aggregation in response to different agonists.
173 ular integrity; this function is mediated by platelet aggregation in response to recognition of the e
174 as an important function preventing maternal platelet aggregation in response to the early developing
175 nhibition of 12-LOX significantly attenuates platelet aggregation in response to various agonists.
176 iminished neutrophil adhesion and neutrophil-platelet aggregation in SCD mice, thereby improving bloo
179 eptor but also a low nanomolar inhibition of platelet aggregation in the human platelet rich plasma a
180 ulting in spatially confined and exacerbated platelet aggregation in the stenosis outlet region.
181 itions in a stenotic artery, showed enhanced platelet aggregation in the stenotic outlet region at 60
182 e target organ with rapid onset of extensive platelet aggregation in the ventricles and myocardial ne
183 vel promising tool, which allows analysis of platelet aggregation in thrombocytopenic patients or inf
185 is enhanced, with a concomitant increase in platelet aggregation in vitro and a reduced duration of
186 were able to inhibit both thrombin-triggered platelet aggregation in vitro and clot consolidation in
188 nzymatic basis for NPP4 and Ap3A activity in platelet aggregation in vitro and suggest that NPP4 prom
189 and selective COX-1 inhibitors that affected platelet aggregation in vitro through the inhibition of
190 uman HIT IgG-induced platelet activation and platelet aggregation in vitro, and thrombus progression
191 h plasma from Fib(AEK) mice supported normal platelet aggregation in vitro, highlighting that fibrino
196 ave developed a novel flow cytometry test of platelet aggregation, in which 10- to 25-fold lower plat
197 xamination of mice lacking integrin-mediated platelet aggregation indicated that platelet aggregation
198 al cells (ECs) showed enhanced inhibition of platelet aggregation induced by adenosine 5'-diphosphate
199 el with a Ki value of 9.02 muM and inhibited platelet aggregation induced by ADP and U46619 in a dose
200 in a number of physiologic responses such as platelet aggregation, inflammation, and cell proliferati
201 times as well as reduced thrombus formation, platelet aggregation, inflammation, and organ damage dur
202 ing dose is feasible, and it does not hinder platelet aggregation inhibition in patients with acute c
203 ding further support for the hypothesis that platelet aggregation inhibition is a vital salivary func
204 Aegyptin did not affect salivary ADP-induced platelet aggregation inhibition or disturb anticlotting
205 ) and 3 antithrombotic/anticoagulant agents (platelet aggregation inhibitors excluding heparin, direc
208 ogrel therapy, device-reported inhibition of platelet aggregation (IPA) trended lower in nonsmokers t
210 s whereas Glanzmann thrombasthenia, in which platelet aggregation is reduced, is a bleeding syndrome.
214 atelets and released upon tumor cell-induced platelet aggregation, leading to the production of LPA.
215 tion on hematopoietic cells is essential for platelet aggregation, leukocyte adhesion, and transmigra
217 ary comparison was noninferiority of maximum platelet aggregation (MPA) comparing the median for pras
218 12) platelet reactivity index (PRI), maximal platelet aggregation (MPA) to adenosine phosphate, and V
221 Morphine delayed the maximal inhibition of platelet aggregation on average by 2 h (n = 24; p < 0.00
222 ailable antithrombotic agents inhibit either platelet aggregation or fibrin generation, inhibition of
224 Six SNPs were significantly associated with platelet aggregation (P<5x10(-8)) in the discovery sampl
225 egometry (11.6% relative increase in maximal platelet aggregation, p = 0.004; 10.8% increase in resid
226 ation, p = 0.004; 10.8% increase in residual platelet aggregation, p = 0.005) and vasodilator-stimula
227 ggregation, p = 0.04, and 12.7% for residual platelet aggregation, p = 0.02) but not with collagen or
228 ide (relative increases of 11.7% for maximal platelet aggregation, p = 0.04, and 12.7% for residual p
234 telets, platelet life span, thrombin-induced platelet aggregation response, and light/dye-induced thr
239 at elevated levels of plasma 5-HT accelerate platelet aggregation resulting in a hypercoagulable stat
241 e inside-out pathway as an approach to block platelet aggregation should be paralog-specific, as it m
242 ing array of biological functions, including platelet aggregation, smooth muscle cell proliferation,
243 58), was associated with reduced ADP-induced platelet aggregation (Spearman's rank correlation coeffi
244 mediated platelet aggregation indicated that platelet aggregation stabilizes thrombi that form in the
245 virulent infection, including signatures for platelet aggregation, stronger and prolonged anemia and
246 ssments, transthoracic echocardiography, and platelet aggregation studies at baseline and after 3 men
248 platelet integrin mechanics and its role in platelet aggregation, suggesting that platelets are phys
249 duce TXA2 generation, but rather accelerated platelet aggregation, suggesting that the role of LIMK1
250 ition, 23 potently inhibits collagen-induced platelet aggregation, suggesting that this class of inhi
251 latelet adhesion and clot retraction but not platelet aggregation, supporting the role of these regio
252 tients does not exhibit a full inhibition of platelet aggregation, termed 'aspirin resistance' (AR).
254 iovascular system from drugs used to inhibit platelet aggregation, the focus of this article will be
255 letion in mice resulted in modestly enhanced platelet aggregation, the formation of large thrombi and
256 C-type lectin-like receptor 2-induced human platelet aggregation, thereby phenocopying the effect of
257 for pathological conditions associated with platelet aggregation/thrombi (e.g., stroke), where vWF l
258 mouse models of sepsis, we observed profound platelet aggregation, thrombin activation, and fibrin cl
260 sis, denudation of the underlying matrix and platelet aggregation, thrombotic microangiopathy, and ne
262 raise intra-platelet cAMP levels and inhibit platelet aggregation through a P2Y(12)-independent mecha
263 agonist that induces integrin activation and platelet aggregation through its receptors P2Y(1) (Galph
264 n P2Y(12) platelet reactivity index, maximal platelet aggregation to 5 and 20 mumol/l adenosine dipho
265 platelet RNA and expression-1 study measured platelet aggregation to arachidonic acid, ADP, protease-
267 L5 enhanced adenosine diphosphate-stimulated platelet aggregation twofold more than did L1 and induce
269 odies inhibit atherosclerotic plaque-induced platelet aggregation under static and flow conditions mo
270 ns bear the GPVI-binding sites that initiate platelet aggregation upon blood exposure during injuries
271 protein expression by Western blot analysis, platelet aggregation using an aggregometer, and shear st
274 onize their hosts' hemostasis, which include platelet aggregation, vasoconstriction and blood clottin
275 eptor blockade we confirm that NPP4 mediates platelet aggregation via release of ADP from Ap3A and ac
276 gregation receptor-1 (PEAR1) participates in platelet aggregation via sustaining alphaIIbbeta3 activa
277 otein on brain vascular endothelium inducing platelet aggregation via the hydrolysis of Ap3A, whereas
279 genotyped for ABCB1 C3435T, and ADP-induced platelet aggregation was assessed in whole blood on a Mu
289 s creatine kinase level of 4664, ADP-induced platelet aggregation was undetectable, normalizing after
290 sfusion measurements of maximal and residual platelet aggregation were considered with different agon
291 brinogen binding, P-selectin expression, and platelet aggregation were lower on treatment with clopid
293 adenosine diphosphate-, or thrombin-induced platelet aggregation were significantly attenuated in Ty
295 rterio-venous shunt model was used to assess platelet aggregation, whereas a healthy rabbit model of
296 tococci in biofilms were also able to induce platelet aggregation, which facilitates multilayer biofi
298 , BLO8-1 and 5C4 almost completely inhibited platelet aggregation while preserving platelet adhesion
299 in blood flow and inhibition of ADP-induced platelet aggregation with antithrombotic ED50 values of
300 ability and faster and greater inhibition of platelet aggregation with arachidonic acid compared with
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