ライフサイエンスコーパス: hemostasis

1 ote during adverse therapeutic modulation of hemostasis.

2 nctions beyond their roles in thrombosis and hemostasis.

3 hrombosis and its minor relevance for normal hemostasis.

4 rential incision, submucosal dissection, and hemostasis.

5 as a critical function in the maintenance of hemostasis.

6 oxygen-carrying capacity, inflammation, and hemostasis.

7 Thrombin plays a key role in thrombosis and hemostasis.

8 of novel factors involved in thrombosis and hemostasis.

9 be safely targeted with a minimal effect on hemostasis.

10 nators and pumps did not significantly alter hemostasis.

11 nvironment independent of severely defective hemostasis.

12 fects without significantly impairing normal hemostasis.

13 hts the pivotal role of TM as a regulator of hemostasis.

14 dine, 0.33%, gel applied under occlusion for hemostasis.

15 brane serotonin transporter (SERT), modulate hemostasis.

16 tivation during allergic inflammation versus hemostasis.

17 egation and other force-sensing functions in hemostasis.

18 livery of FVIII locally to promote secondary hemostasis.

19 g activity and a follow-up CT scan confirmed hemostasis.

20 and thus platelet function in thrombosis and hemostasis.

21 chanism through which VWF variants may alter hemostasis.

22 ease of BK but appears to be dispensable for hemostasis.

23 tracellular signals contributing to vascular hemostasis.

24 on Willebrand factor (vWF) play key roles in hemostasis.

25 ll migration, host-pathogen interaction, and hemostasis.

26 y secondary end point was the restoration of hemostasis.

27 re not able to support normal thrombosis and hemostasis.

28 lebrand factor (VWF) plays a central role in hemostasis.

29 e acidic calcium stores essential for normal hemostasis.

30 agulation factor XI (FXI) may play a role in hemostasis.

31 he primary physiological role of maintaining hemostasis.

32 ing the vasculature with factors controlling hemostasis.

33 tributes in a major way to the regulation of hemostasis.

34 ory anticoagulation mechanisms essential for hemostasis.

35 Significantly, this effect is independent of hemostasis.

36 e used prophylactically to provide effective hemostasis.

37 xamination in mouse models of thrombosis and hemostasis.

38 ets are abundant in blood where they promote hemostasis.

39 herapeutic modalities available in achieving hemostasis.

40 ssess whether steroid-naive asthma modulates hemostasis.

41 and drives thrombin formation essential for hemostasis.

42 ccess-site complications and reduced time to hemostasis.

43 cognized that platelets are key mediators of hemostasis.

44 specific lineages involved in thrombosis and hemostasis.

45 carotid artery thrombosis without affecting hemostasis.

46 ld exclude interference of VWF blockade with hemostasis.

47 ation, which is considered the first wave of hemostasis.

48 se bioactive lipids plays essential roles in hemostasis.

49 lebrand factor (VWF) is critical for primary hemostasis.

50 s a novel device that can be used to achieve hemostasis.

51 ated in thrombus stability in thrombosis and hemostasis.

52 c thrombus formation while preserving normal hemostasis.

53 gical thrombosis but have a lesser impact on hemostasis.

54 plays a pivotal adhesive role during primary hemostasis.

55 opical brimonidine, 0.33%, gel when used for hemostasis.

56 ding compared with standard, visually guided hemostasis.

57 used for risk stratification and endoscopic hemostasis.

58 factors provides only partial mechanisms for hemostasis.

59 Platelets are the chief effector cells in hemostasis.

60 lt techniques were submucosal dissection and hemostasis.

61 Platelets are essential components of hemostasis.

62 ect effects of an activated immune system on hemostasis.

63 ebrand factor (VWF) is essential for primary hemostasis.

64 aling and influences platelet activation and hemostasis.

65 multiple sclerosis (MS) beyond their role in hemostasis.

66 VII levels (>10% normal) results in improved hemostasis.

67 ary hypothesis to be tested was that femoral hemostasis achieved through VCD is noninferior to manual

68 Platelets maintain hemostasis after injury, but also during inflammation.

69 or IIa [FIIa]) is both a central protease in hemostasis and a key modifier of inflammatory processes.

70 received a high dose, with stabilization of hemostasis and a profound reduction in factor VIII use i

71 -derived VWF does not play a crucial role in hemostasis and arterial thrombosis, it aggravates thromb

72 mbrane receptors that play a central role in hemostasis and arterial thrombosis.

73 yte (MK)-derived cells, play a major role in hemostasis and arterial thrombosis.

74 Similarly, hemostasis and arterial thrombus formation were indistin

75 The tissue factor (TF) pathway serves both hemostasis and cell signaling, but how cells control the

76 Fibrinogen is a critical protein for hemostasis and clot formation.

77 d, the TAM receptors have effects on primary hemostasis and coagulation and display an anti-inflammat

78 ts frequently care for patients with altered hemostasis and coagulation.

79 Our understanding of hemostasis and coagulopathy has improved, leading to a c

80 ivation of coagulation proteases coordinates hemostasis and contributes to host defense and tissue re

81 with only platelet-derived VWF had defective hemostasis and defective carotid artery thrombosis, but

82 fII activation may differentially influence hemostasis and disease depending on the pathway of activ

83 ll analyze the interplay between complement, hemostasis and endothelial cells in physiological condit

84 r, more patients in the 1:1:1 group achieved hemostasis and fewer experienced death due to exsanguina

85 important physiological processes, including hemostasis and immunity.

86 on, which is critical for the maintenance of hemostasis and in which a role for platelet purinergic r

87 The intricate relationship between hemostasis and inflammation has major consequences in in

88 h platelets have been extensively studied in hemostasis and inflammation, their role is not well unde

89 the TAM receptors and their ligands have on hemostasis and inflammation, we compare studies that rep

90 role in pathological states like thrombosis, hemostasis and inflammation.

91 osine kinases that have important effects on hemostasis and inflammation.

92 oteins that have been shown to modulate host hemostasis and innate immune responses.

93 es the current understanding of lymphovenous hemostasis and its effect on lymphatic vessel maturation

94 PolyP is a novel player in normal hemostasis and likely plays roles in thrombotic diseases

95 ormal platelet function is critical to blood hemostasis and maintenance of a closed circulatory syste

96 htly regulated in order to promote effective hemostasis and prevent occlusive thrombus formation.

97 cytoplasmic fragments with critical roles in hemostasis and related biology.

98 ndary end points included the restoration of hemostasis and safety measures.

99 ect interaction between starter molecules of hemostasis and the classical pathway of complement.

100 nostic strategies for inherited disorders of hemostasis and the development of recombinant clotting f

101 rgical intervention was required for durable hemostasis and the patient was able to resume anticoagul

102 Platelets play crucial functions in hemostasis and the prevention of bleeding.

103 e essential platelet activating receptors in hemostasis and thrombo-inflammatory disease, which signa

104 Fibrin(ogen) is central to hemostasis and thrombosis and also contributes to multip

105 Platelets are crucial for hemostasis and thrombosis and exacerbate tissue injury f

106 Blood platelets are critical for hemostasis and thrombosis and play diverse roles during

107 of platelets fulfills a procoagulant role in hemostasis and thrombosis by enabling the thrombin burst

108 ression of tissue factor can directly affect hemostasis and thrombosis by modulating the size and den

109 d activation motif signaling in platelets in hemostasis and thrombosis by stabilizing the LAT signalo

110 shortened bond lifetime, yielding defects in hemostasis and thrombosis comparable to VWF-deficient an

111 as regulatory elements that facilitate both hemostasis and thrombosis in response to vascular injury

112 demonstrated that platelet activation during hemostasis and thrombosis is heterogeneous.

113 et function can think beyond the traditional hemostasis and thrombosis paradigms, while the practicin

114 coagulation, portending future insights into hemostasis and thrombosis through the use of this model.

115 For example, during hemostasis and thrombosis, ATP-gated P2X1 channels and A

116 important implications for the regulation of hemostasis and thrombosis, local vascular tone and redox

117 secreted by endothelial cells is central to hemostasis and thrombosis, providing a multifunctional a

118 established role for platelets in regulating hemostasis and thrombosis, recent research has revealed

119 h once primarily recognized for its roles in hemostasis and thrombosis, the platelet has been increas

120 Beyond its traditional role in hemostasis and thrombosis, the platelet's involvement in

121 olvement, and the known importance of G13 in hemostasis and thrombosis, the present study examined wh

122 is study, we investigated the role of APP in hemostasis and thrombosis, using APP knockout (KO) mice.

123 the specific contribution of platelet VWF in hemostasis and thrombosis, we performed crossed bone mar

124 Platelets play an essential role in hemostasis and thrombosis.

125 von Willebrand factor (VWF) are critical for hemostasis and thrombosis.

126 ereby significantly affect VWF's function in hemostasis and thrombosis.

127 eterotrimeric G protein signaling regulating hemostasis and thrombosis.

128 indicative of platelets' important roles in hemostasis and thrombosis.

129 ction) has been implicated to play a role in hemostasis and thrombosis.

130 minent role in EC vWF secretion required for hemostasis and thrombosis.

131 from shear to elongational flow at sites of hemostasis and thrombosis.

132 n of this receptor in the regulation of both hemostasis and thrombosis.

133 ce continue to increase our understanding of hemostasis and thrombosis.

134 plication of this technology to the study of hemostasis and thrombosis.

135 lasma membrane, and plays a critical role in hemostasis and thrombosis.

136 tivation, aggregation and contraction during hemostasis and thrombosis.

137 TAM signaling-independent role for CLEC-2 in hemostasis and thrombosis.

138 system plays a key role in the regulation of hemostasis and thrombosis; however, it also has multiple

139 by endothelial cells (ECs) is essential for hemostasis and thrombosis; however, the molecular mechan

140 g in human platelets is directly involved in hemostasis and thrombus formation, the sequence of event

141 erived microparticles (PMPs) are involved in hemostasis and vascular health and have recently been sh

142 n cascade in the developmental regulation of hemostasis and vasculogenesis.

143 ts form an impermeable barrier important for hemostasis and wound healing and help explain how fibrin

144 and an over-expression of genes involved in hemostasis and wound responsiveness suggesting that chro

145 ontal therapy due to ablation, vaporization, hemostasis, and field sterilization.

146 ial membrane potential, mitochondrial Ca(2+) hemostasis, and mitochondrial respiration.

147 Platelets are essential for hemostasis, and thrombocytopenia is a major clinical pro

148 of eosinophils during plasmatic coagulation, hemostasis, and thrombosis.

149 did not show any differences with regard to hemostasis, anticoagulation, hemolysis, and inflammatory

150 Therefore hemostasis, anticoagulation, hemolysis, and inflammatory

151 ially a drug target, as its contributions to hemostasis appear to be to accelerate blood clotting but

152 Disturbances of coagulation and hemostasis are common in patients with liver cirrhosis.

153 mmalian vertebrates, the functional units of hemostasis are thrombocytes.

154 Routine laboratory tests of hemostasis are unable to reflect these changes and shoul

155 that we refer to as "inflammation-associated hemostasis" are engaged in different contexts in which t

156 activation in vitro, but its in vivo role in hemostasis, arterial thrombosis, and postischemic infarc

157 5 patients in group A who could be assessed, hemostasis, as determined by local investigators, was re

158 hemostasis (control, n = 76), or endoscopic hemostasis assisted by Doppler monitoring of blood flow

159 ependent manner, ensuring that VWF initiates hemostasis before inactivation by proteolytic cleavage.

160 pecified ancillary outcomes included time to hemostasis, blood product volumes transfused, complicati

161 at sites of vascular injury is essential for hemostasis but also thrombosis.

162 d coagulation is essential for physiological hemostasis but simultaneously contributes to thrombotic

163 let secretion not only drives thrombosis and hemostasis, but also mediates a variety of other physiol

164 a clotting cascade is dispensable for normal hemostasis, but contributes to thrombosis and serves as

165 at sites of vascular injury is essential for hemostasis, but it is also a major pathomechanism underl

166 of vascular injury is not only essential for hemostasis, but may also cause acute ischemic disease st

167 latelet GPIbalpha during bleeding to mediate hemostasis, but not in the normal circulation to avoid t

168 ses are largely responsible for the improved hemostasis by Cv-PC.

169 function is to regulate intracellular fluid hemostasis by enabling the transport of water and glycer

170 othelial cells (ECs) are major modulators of hemostasis by expressing and releasing pro- and anticoag

171 Platelets play a central role in primary hemostasis by forming aggregates that plug holes in inju

172 ic plasma glycoprotein that is activated for hemostasis by increased hydrodynamic forces at sites of

173 circulate within blood vessels to establish hemostasis by repairing vascular injury.

174 PCA is safe even in small infants, and hemostasis can be achieved without surgical repair, with

175 ng endothelial dysfunction and disruption of hemostasis caused by exposure to particulate matter (PM)

176 derwent standard, visually guided endoscopic hemostasis (control, n = 76), or endoscopic hemostasis a

177 ebrand factor or point-of-care assessment of hemostasis could be used to monitor aortic regurgitation

178 However, Stxbp5 KO mice also displayed hemostasis defects, including prolonged tail bleeding ti

179 that STXBP5 is required for normal arterial hemostasis, due to its contributions to platelet granule

180 latelet transfusion is often used to restore hemostasis during operations, but its effectiveness and

181 n levels, ultimately improving perioperative hemostasis during SBI.

182 Maintaining cerebral hemostasis during stroke treatment is of high clinical r

183 onstituents are essential for maintenance of hemostasis during thrombo-inflammatory brain infarction

184 thic disorders, resulting from complement or hemostasis dysregulation-mediated endothelial damage: at

185 the adaptive immune response, inflammation, hemostasis, embryogenesis, and organ repair and developm

186 eosinophils and neutrophils) and markers of hemostasis (endogenous thrombin potential [ETP], thrombi

187 ates coagulation of blood platelets (primary hemostasis) especially when it is stretched under shear

188 ury, pFn was rapidly deposited and initiated hemostasis, even before platelet accumulation, which is

189 mph flow, and mice deficient in lymphovenous hemostasis exhibit lymphedema and sometimes chylothorax

190 In addition to a central role in hemostasis, fibrin is thought to enhance bone repair by

191 Platelets are essential in maintaining hemostasis following inflammation or injury to the vascu

192 that antibiotic prophylaxis after endoscopic hemostasis for acute PUB prevented infections and reduce

193 ogastroduodenal pneumatosis after endoscopic hemostasis for duodenal ulcer bleeding.

194 B1 identified new candidate genes related to hemostasis for follow-up replication and functional geno

195 It may be a useful tool for achieving hemostasis for patients who failed endoscopic therapy wi

196 rrhosis, who underwent successful endoscopic hemostasis for variceal bleeding, covered TIPS was super

197 a variety of animal models of thrombosis and hemostasis has played in the development of new antiplat

198 a multimeric protein with a central role in hemostasis, has been shown to interact with complement c

199 n) has long been suspected to be involved in hemostasis; however, direct evidence has been lacking.

200 endothelial VWF stores, demonstrated normal hemostasis in a tail bleeding model and normal carotid a

201 poreal membrane oxygenation systems on blood hemostasis in adults during veno-venous extracorporeal m

202 0.33%, gel has been reported for the use of hemostasis in dermatologic surgery.

203 e endothelium, the complement system and the hemostasis in health and in disease.

204 hat human platelet-derived FVIII can improve hemostasis in hemophilia A.

205 e, we study whether EPCR facilitates rhFVIIa hemostasis in hemophilia using a mouse model system.

206 ting antithrombin (AT) as a means to promote hemostasis in hemophilia.

207 10(9)/L were sufficient to largely maintain hemostasis in infected lungs.

208 Treatment with ALN-AT3 promoted hemostasis in mouse models of hemophilia and led to impr

209 closure devices (VCD) for the achievement of hemostasis in patients undergoing transfemoral coronary

210 animals displayed significantly compromised hemostasis in tail bleeding assays, but did not demonstr

211 sion rebleeding within 30 days of endoscopic hemostasis in the control group (26.3%) vs the Doppler g

212 in the tail transection model and defective hemostasis in the FeCl3-induced carotid injury model.

213 latelet granule release resulted in impaired hemostasis in the ischemic brain after transient middle

214 gh it was shown that platelets help maintain hemostasis in the ischemic brain, their exact contributi

215 the introduction of the cell-based model of hemostasis in the mid-1990s, our understanding of the he

216 gulation factor, FXa(I16L), rapidly restores hemostasis in the presence of the anticoagulant effects

217 Hemostasis in vertebrates involves both a cellular and a

218 ion of such agents is effective at restoring hemostasis in vivo.

219 vessel wall platelet deposition and initial hemostasis in vivo.

220 understanding of the molecular mechanisms of hemostasis, including a platform for screening variants

221 siological processes that govern blood flow, hemostasis, inflammation, and angiogenesis.

222 ystems and organs enables processes, such as hemostasis, inflammation, angiogenesis, matrix remodelin

223 erlapping phases of wound healing, including hemostasis, inflammation, proliferation, and resolution/

224 von Willebrand factor (VWF) is essential for hemostasis initiation at sites of vascular injury.

225 system, the future of genetic therapies for hemostasis is bright.

226 Our data suggest that fetal hemostasis is distinct and that impairment of angiogenes

227 antiplatelet therapy by Src inhibition where hemostasis is maintained while reducing risk for cardiov

228 Lymphovenous hemostasis is required for normal lymph flow, and mice d

229 fects when brimonidine is used topically for hemostasis is unknown.

230 Therefore, stoppage of bleeding (hemostasis) is of paramount clinical significance in pro

231 irst responder to vascular injury in primary hemostasis, is designed to capture platelets under the h

232 This process, known as "lymphovenous hemostasis," is mediated by activation of platelet CLEC-

233 tions open unsuspected new roles for EPCR in hemostasis, malaria pathogenesis, innate immunity, and c

234 linical implications and provide a basis for hemostasis management during ibrutinib treatment.

235 Xa(I16L) is more potent (by >50-fold) in the hemostasis models tested than a noncatalytic antidote th

236 clotting cascade" and "primary and secondary hemostasis." Moreover, this article shows how a bleeding

237 Dynamic changes to hemostasis occur in patients with hepatic insufficiency.

238 ed with factor Xa inhibitors, with effective hemostasis occurring in 79%.

239 atelets play a key role in the physiological hemostasis or pathological process of thrombosis.

240 able to predict platelets' phenotypes during hemostasis or thrombosis.

241 eneration could contribute either to promote hemostasis or to augment thrombosis risk with consequent

242 t that gastrointestinal mucus production and hemostasis pathways may also play a role.

243 e etiology appears to entail perturbation of hemostasis pathways, the key molecular determinants duri

244 on for understanding individual variation in hemostasis pathways.

245 In addition to their role in hemostasis, platelets have the capacity to influence the

246 Platelets are central to the process of hemostasis, rapidly aggregating at sites of blood vessel

247 this study, we found upregulation of several hemostasis-related genes, including the thrombin-activat

248 rlying mechanisms of inflammation-associated hemostasis remain to be fully elucidated, they can diffe

249 ous thromboembolism (VTE), caused by altered hemostasis, remains the third most common cause of morta

250 Secondary end points: time to hemostasis, repeat manual compression, and VCD failure.

251 e expression profiling while controlling for hemostasis, resulting in few complications.

252 the International Society of Thrombosis and Hemostasis Scientific and Standardization Subcommittee c

253 her lesions, Doppler probe guided endoscopic hemostasis significantly reduced 30-day rates of rebleed

254 These proteins serve a limited role in hemostasis, suggesting that antithrombotic therapies tar

255 More patients in the 1:1:1 group achieved hemostasis than in the 1:1:2 group (86% vs 78%, respecti

256 ild-type FIX to collagen IV, provides better hemostasis than wild-type FIX, long after both are undet

257 for platelet G protein-coupled receptors in hemostasis, the contribution of immunoreceptor tyrosine-

258 To fulfill its role in hemostasis, the platelet is equipped with various G prot

259 Despite successful endoscopic hemostasis, there is a significant risk of rebleeding of

260 While platelets are primary mediators of hemostasis, there is emerging evidence to show that they

261 use MCs do not directly contribute to normal hemostasis, they can be considered potential targets for

262 d multiple blood biomarkers of inflammation, hemostasis, thrombin generation, cardiac dysfunction, an

263 ed role in skin diseases, diabetes, platelet hemostasis, thrombosis, and cancer.

264 Vascular endothelial cells (ECs) link hemostasis, thrombosis, and complement.

265 the blood clotting and complement systems in hemostasis, thrombosis, and inflammation.

266 s plays significant roles in vasoregulation, hemostasis, thrombosis, and vascular remodeling.

267 telet's involvement in the interplay between hemostasis, thrombosis, inflammation, and cancer is like

268 rculate in the blood and have major roles in hemostasis, thrombosis, inflammation, and vascular biolo

269 In fact, traditional plasma-based hemostasis-thrombosis laboratory testing, by assessing f

270 These findings link hemostasis-thrombosis with the AP of complement and open

271 vascular development, vascular integrity, or hemostasis/thrombosis.

272 polymer in antimicrobial host defense and in hemostasis/thrombosis.

273 re, pFn may gradually switch from supporting hemostasis to inhibiting thrombosis and vessel occlusion

274 CH (Comparison of Acute Treatments in Cancer Hemostasis) trial.

275 responsible for platelet adhesion to VWF in hemostasis, unfolds through a molten globule intermediat

276 odel of hemophilia A, the complex normalized hemostasis upon vascular injury at a dose of 0.3 nmol/kg

277 e and summarize currently available tests of hemostasis, utilization of prohemostatic agents, transfu

278 t required for normal platelet exocytosis or hemostasis, VAMP-3(-/-) mice had less platelet-associate

279 he vascular wall, and thus how they regulate hemostasis, vascular integrity, and inflammation, as wel

280 te, systolic and diastolic blood pressures), hemostasis (von Willebrand factor, soluble CD40 ligand,

281 After sheath withdrawal, hemostasis was achieved with manual compression, with no

282 hours after the andexanet infusion, clinical hemostasis was adjudicated as excellent or good in 37 of

283 nded procedure was 1.6 hours; periprocedural hemostasis was assessed as normal in 93.4% of the patien

284 blood clotting time analysis confirmed that hemostasis was improved in NSGF8KO mice that received 2b

285 Surgical hemostasis was rated as excellent/good in 100% of major

286 ted in 33, and mildly or moderately abnormal hemostasis was reported in 2 patients and 1 patient, res

287 underwent a procedure, normal intraoperative hemostasis was reported in 33, and mildly or moderately

288 Time to hemostasis was significantly shorter among patients with

289 Time to hemostasis was significantly shorter in patients with VC

290 However, they still felt that hemostasis was the most difficult techniques to master.

291 Here, using experimental mouse models of hemostasis, we show that a variant coagulation factor, F

292 the cells responsible for the dysfunctional hemostasis, we used transgenic mice expressing JAK2V617F

293 osphate (CT-ADP), a point-of-care measure of hemostasis, were assessed at baseline and 5 minutes afte

294 thought to promote wound closure and secure hemostasis while preventing vascular occlusion.

295 Here, we show that apelin is a key player in hemostasis with an ability to inhibit thrombin- and coll

296 Platelet activity plays a major role in hemostasis with increased platelet activity likely contr

297 Most patients with ineffective hemostasis with PCCs had ICH (n = 16; 61.5%).

298 n is often unsuccessful in achieving durable hemostasis with surgery being required for definitive ma

299 ompartment, efficiently prolong prophylactic hemostasis without thrombotic risk.

300 ide signaling is inconsequential for in vivo hemostasis, yet is critical for in vivo dissemination.