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1 of fibrinogen was shown to accelerate fibrin clot formation.
2 ss-links the gamma-chains of fibrin early in clot formation.
3  20 fM results in pronounced acceleration of clot formation.
4 pair of enzymes is sufficient to yield rapid clot formation.
5 inogen to non-nitrating oxidants decelerates clot formation.
6 a high propensity for cell adhesion and bulk clot formation.
7 prostaglandin E(2), that are released during clot formation.
8  the inhibition of thrombin-catalyzed fibrin clot formation.
9 nitiating a process that ultimately leads to clot formation.
10 and were found to be efficacious in reducing clot formation.
11 fibrin polymerization that lead to insoluble clot formation.
12 B, a process that does not occur until after clot formation.
13  can actively contribute to the processes of clot formation.
14 oagulant effect, after the initial stages of clot formation.
15   Addition of glucose to the medium prevents clot formation.
16 y recruit adjacent erythrocytes to assist in clot formation.
17 ic sites, which may serve as a nidus for new clot formation.
18 dels, and exhibit long-lasting prevention of clot formation.
19  without leading to histological evidence of clot formation.
20 is not separate but integrated into adaptive clot formation.
21 eading to fast recruitment, aggregation, and clot formation.
22 g of fibrin polymers was designed to enhance clot formation.
23 ce of activated endothelial cells, promoting clot formation.
24 processes are critical for wound healing and clot formation.
25 gnaling pathway and common pathway of fibrin clot formation.
26 ccessory pathways to platelet activation and clot formation.
27 t PLPs selectively bound fibrin and enhanced clot formation.
28 tructure, properties, and dynamics of sickle clot formation.
29 nd neonatal porcine islets prolonged time to clot formation.
30  a multicausal disease involving intravenous clot formation.
31 nge in 70.3% of patients indicative of rapid clot formation.
32 gen is a critical protein for hemostasis and clot formation.
33 nce have been reported and are attributed to clot formation.
34 riances in the ability to tolerate excessive clot formation.
35 del by mapping mutations leading to impaired clot formation.
36 Ia (also known as thrombin) to prevent blood clot formation.
37 lex, plays a procoagulant role during fibrin clot formation.
38 ture, which may then lead to abnormal fibrin clot formation.
39 elet membranes provide a platform to amplify clot formation.
40 ed blood, an agent that could affect in vivo clot formation.
41  caused a dose-dependent increase in time to clot formation (3.6-fold increase at the 300 micrograms/
42                              At the point of clot formation, 80% of the fibrinogen is depleted from t
43 nous inhibitor of fibrinolysis, and enhances clot formation after injury.
44                  XO inactivation resulted in clot formation after reperfusion in all animals, whereas
45               We found significantly greater clot formation after uremic serum exposure, which was su
46 odel that is not associated with significant clot formation, also revealed an essential role for VEGF
47 uences: increased initial velocity of fibrin clot formation, altered fibrin clot architecture, increa
48 ovide an effective strategy to enhance blood clot formation and act as a rapid pan-hemostatic agent f
49   Sheets could be an unanticipated factor in clot formation and adhesion in vivo, and are a unique ma
50 tion that periodontitis promotes accelerated clot formation and an increased risk of thrombosis.
51  complexes are not observed until well after clot formation and are never equivalent to ELISA-TAT val
52 itional studies to investigate the effect of clot formation and blood fractionation on DNA availabili
53                           The rate of fibrin clot formation and clot architecture was restored upon d
54 e for fibrin crosslinking during whole blood clot formation and consolidation and establish FXIIIa ac
55 RU-505 restored Abeta-induced altered fibrin clot formation and degradation in vitro and inhibited ve
56  AD samples, and intravital brain imaging of clot formation and dissolution revealed abnormal thrombo
57  interventions aimed at reducing peritumoral clot formation and enhancing NK cell function in the per
58 de-nitrite system, significantly accelerates clot formation and factor XIII cross-linking, whereas ex
59 strate of mMCP-7, this tryptase can regulate clot formation and fibrinogen/integrin-dependent cellula
60 ma levels of D-dimers, reflective of in vivo clot formation and fibrinolysis.
61 nt role in the balance between intravascular clot formation and fibrinolytic potential.
62 ore detailed view of thrombin generation and clot formation and have been studied in hemophilia for a
63 bin, a crucial enzyme involved in both blood clot formation and immune response.
64  than 150,000/microl) can lead to inadequate clot formation and increased risk of bleeding, while thr
65 oduced cell-derived microparticles on fibrin clot formation and its properties.
66 on or genetic depletion of PAI-1 attenuating clot formation and lesion expansion after brain trauma.
67 nding assay to test the relationship between clot formation and lymphangiogenesis in mice, we find th
68 ssful blood flow through the devices without clot formation and maintenance of cell viability.
69 imental system that can simultaneously model clot formation and measure clot mechanics under shear fl
70 atelets or microorganisms initially promotes clot formation and stability; subsequent degradation of
71 eliberately low blood pressure to facilitate clot formation and stabilization.
72  hemodynamics is essential for understanding clot formation and stroke risk.
73 times faster than native Met-alpha2AP during clot formation and that clot lysis rates are slowed in d
74 s, the implications for our understanding of clot formation and therapeutic intervention may be of ma
75 m that stems from the known vicious cycle of clot formation and tumor growth.
76 ics in patients with CaW are associated with clot formation and vascular dysfunction and suggest that
77 llowed unprecedented insights into how blood clot formation and von Willebrand factor (VWF) depositio
78 d cellular coordination to the enzymology of clot formation and was conceptualized during the growth
79 e von Willebrand factor, a key step in blood clot formation and wound healing.
80 ted against arterial thrombosis (obstructive clot formation) and stroke.
81 functions for thrombin in addition to fibrin clot formation, and identify a previously unrecognized r
82                         Thrombosis, or blood clot formation, and its sequelae remain a leading cause
83 re involved in cell signaling, inflammation, clot formation, and other crucial biological processes.
84 sed on the role of platelets in coagulation, clot formation, and systemic inflammation, we speculate
85        However, the underlying mechanisms of clot formation are not yet fully understood.
86            While spatio-temporal dynamics of clot formation are well characterized, the cell-biologic
87 rform this cleavage function to impede blood clot formation around the worms in vivo.
88  of lateral aggregation, leading to abnormal clot formation, as shown by an impaired increase in turb
89  loss after tail-clip assay, and reinstalled clot formation, as tested by in vivo imaging of laser-in
90 ns/enzymes in the interstitial spaces during clot formation, as well as the design of fibrinolytic dr
91 meter in 5758 simultaneously recorded TG and clot formation assays using frozen plasma samples from c
92 P2Y(1)(2) inhibitors to limit human platelet clot formation at doses recommended by the American Coll
93 tion cascade plays a critical role in fibrin clot formation at extravascular sites, the expression an
94 ets and for vascular collagens to facilitate clot formation at sites of injury.
95 sion improved hemostasis by enhancing fibrin clot formation at the site of vascular injury in mice wi
96 penia, leading to a prothrombotic state with clot formation at unusual anatomic sites.
97       LigBCen2R binding to FgalphaCC reduced clot formation but did not affect plasminogen and tissue
98 nated heparin not only prolongs the onset of clot formation but has a significant effect on its fract
99                           Here, we show that clot formation by TF indirectly enhances tumor cell surv
100 ides reversed inhibition of thrombin-induced clot formation by UFH.
101       We assessed the effects of APIX on (1) clot formation, by ROTEM thromboelastometry; (2) thrombi
102 neutrophil aggregate formation, aggregation, clot formation, Ca2+ increase, and B3 integrin phosphory
103 abigatran and an anti-VWF antibody prevented clot formation, cancer cell arrest, extravasation, and t
104 duction of VCAM-1 is dependent on tumor cell-clot formation, decreasing upon induction of tissue fact
105 creased tumor cell survival without altering clot formation, demonstrating that the recruitment of fu
106 r repair may explain why control of clinical clot formation does not lead to full control of intimal
107 s target antigen beta2GP1, leading to fibrin clot formation due to exposure of anionic phospholipids
108  for advanced numerical simulations of blood clot formation during flow in blood vessels.
109                                           As clot formation ensues, platelets interact with polymeriz
110 od on a sample set of simulations comprising clot formation following laser injury in two mouse crema
111                         Intravascular fibrin clot formation follows a well-ordered series of reaction
112 rmal range (73% and 62% had abnormalities in clot formation from extrinsic and intrinsic clotting cas
113 es present during the early stages of fibrin-clot formation from the beginning of polymerization to t
114 semble multi-protein complexes that regulate clot formation; however, PS is of limited abundance phys
115 onfirmed alterations of proteins involved in clot formation, immune reaction and free heme binding.
116 Ib compared with that of uPA-T, and prevents clot formation in a microfluidic system.
117 ease, we examined its relationship to fibrin clot formation in AD.
118 leeding or high-risk procedures may optimize clot formation in advanced liver disease: hematocrit >=2
119 ance remained consistent without significant clot formation in all experiments with an average resist
120 tor VIIa to initiate thrombin generation and clot formation in blood from healthy donors, blood from
121                                              Clot formation in brain microvessels occurred frequently
122 atelets in peripheral blood critically drive clot formation in health and disease.
123 nted inhibition of FVIIa/TF/FXa and improved clot formation in hemophilia blood and plasma.
124 cipated role of leukocytes for microvascular clot formation in inflamed tissue.
125 ding can be directly assessed by visualizing clot formation in microvessels, and correlations can be
126  concentrations < or = 5.5 nmol/L, prevented clot formation in normal plasma, whereas under similar c
127                                    Following clot formation in PPP, the presence of SAA increased amy
128 et activation, thrombus structure and fibrin clot formation in real time using flowing whole blood.
129 ted to inhibit platelet activation and blood clot formation in samples of plasma and whole blood loca
130 oagulation cascade, leading to intravascular clot formation in small and larger vessels.
131 athway, promoting a procoagulatory state and clot formation in the cerebral microvasculature.
132 utes in 10 of 11 rats tested) with defective clot formation in the WF strain.
133 eleased from activated human neutrophils, on clot formation in vitro and in vivo.
134 60-18[29] inhibits thrombin-catalyzed fibrin clot formation in vitro.
135 f FIXa inhibition on thrombin generation and clot formation in vivo remains unclear.
136 olonged bleeding times in vivo and defective clot formation in WF rats.
137 l thromboelastometry (ROTEM), which assesses clot formation in whole blood, was used to determine the
138 ers associated with vascular dysfunction and clot formation, including shear rate, oscillatory shear
139 h platelets or PCPS vesicles added to induce clot formation indicated that, even in the presence of h
140                                   With blood clot formation inside an artery resulting from influenza
141                                              Clot formation is a crucial process that prevents bleedi
142                                Intravascular clot formation is an important factor in a number of car
143                                        Blood clot formation is crucial to maintain normal physiologic
144 e of margination and shear rate on occlusive clot formation is not fully understood yet.
145                                              Clot formation is promoted via cAMP-mediated secretion o
146 telet, once thought to be solely involved in clot formation, is now known to be a key mediator in var
147  FVIII, which is not biologically active for clot formation, is sufficient for accelerating proteolyt
148  show that the ARFOE-OCE is sensitive to the clot formation kinetics and can differentiate the elasti
149 oagulation metrics, including reaction time, clot formation kinetics and maximum shear modulus.
150 illation is discussed, including left atrial clot formation, maintenance of sinus rhythm after cardio
151                    In addition, local fibrin clot formation may be implicated in host defense against
152 nding of events leading to platelet-mediated clot formation may provide insight into new therapeutic
153  measured effects of hematocrit in 2 in vivo clot formation models.
154 able clot formation without inhibiting early clot formation, offering a new potential target for anti
155  deficiency results in significantly delayed clot formation only at sufficiently low TF concentration
156 uggesting an influence either on intraatrial clot formation or embolization.
157 n of arterial occlusion by the inhibition of clot formation or even atherosclerotic disease process i
158 assembly, suggesting that, in events such as clot formation or injury, reversible Abeta assembly coul
159 rinogen, affect fibrin polymerization during clot formation, or abrogate plasma clotting.
160 vity, leading to differential enhancement in clot formation over protection from blood loss in hemoph
161 n factors to perform its key roles in fibrin clot formation, platelet aggregation, and wound healing.
162                      Bacteria present during clot formation produce a visibly disorganized microstruc
163 on in several ways, that is, by facilitating clot formation, production of antimicrobial proteins, an
164 omboelastography was used to measure time to clot formation (r-time) in both rhesus and human blood,
165 mboelastography (TEG) demonstrated increased clot formation rate, associated with portal vein platele
166          Thrombin generation (TG) and fibrin clot formation represent the central process of blood co
167 o-drugs activated selectively at the site of clot formation represents a new approach to prevent thro
168  ambulatory respiratory support with minimal clot formation, stable gas exchange, blood flow resistan
169      BEST PRACTICE ADVICE 1: Global tests of clot formation, such as rotational thromboelastometry, t
170 ient in CD40L showed markedly delayed fibrin clot formation, suggesting a role for the ligand in bloo
171                                        Blood-clot formation that results in the complete occlusion of
172 n was assessed using assays including fibrin clot formation, thrombin generation, fibrinolysis, and e
173 ent thrombin generation (thrombinoscopy), or clot formation (thromboelastography) but counteracted ac
174  the different phases of wound healing, from clot formation through re-epithelialization, angiogenesi
175 l ranges indicated: clotting time (38-79 s), clot formation time (34-159 s), amplitude at 10 min afte
176 0) versus 33.9 mm (SD 8.6; p<0.0001); median clot formation time 147 s (range 72-255; IQR 101-171) ve
177 tting time, and thromboelastography (maximum clot formation time [R+K], clotting rapidity [alpha], an
178 In a model of arterial photochemical injury, clot formation time was shortened in CRPtg mice; mean ti
179 gnificantly increased coagulation, decreased clot formation time, and increased maximum clot firmness
180  relationship is found between the incipient clot formation time, T(GP), and the activated partial th
181 ponse is characterized by a progression from clot formation, to an inflammatory phase, to a repair ph
182 ly 78% of its normal level and hence improve clot formation under dilution.
183 ipid metabolites play in regulation of blood clot formation under pathologic conditions.
184 uencies using 4 set-points and the effect of clot formation using a chemical trigger.
185 elastometry was used to quantify the rate of clot formation via the intrinsic coagulation pathway.
186                          Thrombin-stimulated clot formation was completely inhibited by heparin.
187                                              Clot formation was delayed from 11.1 to 15.7 minutes, wh
188                                              Clot formation was initiated in whole blood with 5 pM Tf
189 levated APC concentrations (>5.5 nmol/L), no clot formation was observed in either plasma from normal
190  increase in peritumoral fibrin and platelet clot formation was observed in surgically stressed mice,
191 s captured by thrombin-AR-modified cells and clot formation was visualized.
192                  To assess the importance of clot formation, we inhibited coagulation with hirudin, a
193                      Thrombin generation and clot formation were normal in blood from high-dose DAPT-
194         Fibrinopeptide release and insoluble clot formation were only marginally influenced by additi
195 tion in platelet-rich plasma and whole-blood clot formation were studied ex vivo.
196 erexpression is associated with pathological clot formation whereas its absence does not cause severe
197 lar tumor cells in the brain with subsequent clot formation, which led us to discover a novel and spe
198 or to LPS challenge leads to decreased blood clot formation, which protects Gaplinc knockout mice fro
199 >=80 degrees C showed more extensive gastric clot formation with a higher protein digestion rate, but
200  show heightened responses in the setting of clot formation, with corresponding, increased responses
201 metabolic processing, and increase in fibrin clot formation, with significant upregulation of fibrino
202 aggregation, thrombin activation, and fibrin clot formation within (and downstream of) NETs in vivo.
203 Ir-CPI was as efficient as UFH in preventing clot formation within the extracorporeal circuit and mai
204 sure to artificial surfaces that can trigger clot formation within the hemodialysis circuit.
205  lipid signaling pathways involved in stable clot formation without inhibiting early clot formation,
206  as increased platelet activation and fibrin clot formation, Wnt signalling, and hypoxia pathways in

 
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