ライフサイエンスコーパス: hemostasis

1 rmation at sites of vascular injury (primary hemostasis).

2 nges probably result in a rebalanced primary hemostasis.

3 recovery of infused FIX and plays a role in hemostasis.

4 as a marker of patients requiring emergency hemostasis.

5 ective properties, which have less impact on hemostasis.

6 at NHEJ-mediated insertion of BDDF8 restores hemostasis.

7 s excessive coagulation without compromising hemostasis.

8 otic disease while playing a limited role in hemostasis.

9 and platelet participation in thrombosis and hemostasis.

10 at regulates platelet integrin activation in hemostasis.

11 ote during adverse therapeutic modulation of hemostasis.

12 fects without significantly impairing normal hemostasis.

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

14 ing the vasculature with factors controlling hemostasis.

15 ssess whether steroid-naive asthma modulates hemostasis.

16 al link between partial agonism and impaired hemostasis.

17 ated in thrombus stability in thrombosis and hemostasis.

18 c thrombus formation while preserving normal hemostasis.

19 gical thrombosis but have a lesser impact on hemostasis.

20 plays a pivotal adhesive role during primary hemostasis.

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

22 ding compared with standard, visually guided hemostasis.

23 used for risk stratification and endoscopic hemostasis.

24 factors provides only partial mechanisms for hemostasis.

25 Platelets are the chief effector cells in hemostasis.

26 lt techniques were submucosal dissection and hemostasis.

27 Platelets are essential components of hemostasis.

28 on of contributing coagulopathies to achieve hemostasis.

29 ect effects of an activated immune system on hemostasis.

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

31 aling and influences platelet activation and hemostasis.

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

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

34 nctions beyond their roles in thrombosis and hemostasis.

35 hrombosis and its minor relevance for normal hemostasis.

36 rential incision, submucosal dissection, and hemostasis.

37 as a critical function in the maintenance of hemostasis.

38 bbit efficacy model at doses which preserved hemostasis.

39 oxygen-carrying capacity, inflammation, and hemostasis.

40 Thrombin plays a key role in thrombosis and hemostasis.

41 of novel factors involved in thrombosis and hemostasis.

42 be safely targeted with a minimal effect on hemostasis.

43 nators and pumps did not significantly alter hemostasis.

44 nvironment independent of severely defective hemostasis.

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

46 brane serotonin transporter (SERT), modulate hemostasis.

47 tivation during allergic inflammation versus hemostasis.

48 egation and other force-sensing functions in hemostasis.

49 livery of FVIII locally to promote secondary hemostasis.

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

51 ce thrombosis without deleterious effects on hemostasis.

52 sary to seal injured vasculature and achieve hemostasis.

53 ivation, platelet aggregation, and effective hemostasis.

54 al thrombosis models with minimal effects on hemostasis.

55 lly essential for maintaining cell metabolic hemostasis.

56 odeling of a thrombus after its formation in hemostasis.

57 s essential for platelet shape change during hemostasis.

58 ac, and cerebral perfusion before definitive hemostasis.

59 erial thrombosis, with only minor effects on hemostasis.

60 The primary outcome was time to hemostasis.

61 ate the bloodstream and principally maintain hemostasis.

62 atment option due to their essential role in hemostasis.

63 lasminogen activator tPA, without effects on hemostasis.

64 (VWF) that is critically involved in primary hemostasis.

65 elets have long been known for their role in hemostasis.

66 CH provided a high rate of excellent or good hemostasis (81.8%) coupled with a 3.8% thrombosis rate.

67 Disturbed hemostasis, a dysregulated inflammatory state, and a dec

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

69 lammation accompanied by a "cytokine storm," hemostasis alterations and severe vasculitis have all be

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

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

74 ther enzyme or cofactor severely compromises hemostasis and causes hemophilia.

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

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

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

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

79 onal bioactive proteins targeting the host's hemostasis and immune system.

80 important physiological processes, including hemostasis and immunity.

81 gration and, thereby, their significance for hemostasis and immunity.

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

83 ctor and P-selectin, molecules that regulate hemostasis and inflammation, respectively.

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

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

86 can lead to longer time to achieve complete hemostasis and less patent hemostasis rate.

87 cells that store factors regulating vascular hemostasis and local inflammation.

88 concrete molecular and cellular link between hemostasis and lymphangiogenesis during wound healing an

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

90 They also maintain hemostasis and modulate blood flow by reacting to chemok

91 This facilitates hemostasis and modulates the inflammatory response.

92 tion cascade and is required for both normal hemostasis and pathologic thrombogenesis, it also partic

93 Platelets are chief effector cells of hemostasis and pathological thrombosis.

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

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

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

97 cts unique to children include developmental hemostasis and the major role of central venous access d

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

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

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

101 et agents, and highlight differences between hemostasis and thrombosis that may suggest alternative t

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

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

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

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

106 Aside from their roles in hemostasis and thrombosis, thrombocytes or platelets als

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

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

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

110 tivation, aggregation and contraction during hemostasis and thrombosis.

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

112 Platelets play an essential role in hemostasis and thrombosis.

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

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

115 eterotrimeric G protein signaling regulating hemostasis and thrombosis.

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

117 which are circulating cells involved in both hemostasis and thrombosis.

118 form of regulated exocytosis, is crucial for hemostasis and thrombosis.

119 the adhesion dynamics, which is essential to hemostasis and thrombosis.

120 ical pathways involved in blood coagulation, hemostasis and tissue repair.

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

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

123 d plasmin, serine proteases generated during hemostasis and wound healing.

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

125 vailable tools and techniques for endoscopic hemostasis, and be comfortable applying conventional the

126 ith well-documented roles in erythropoiesis, hemostasis, and inflammation.

127 o, postprocedure compression time, occlusive hemostasis, and insufficient anticoagulation are all pre

128 over sutures and staples for wound closure, hemostasis, and integration of implantable devices onto

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

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

131 n forming a selective barrier, inflammation, hemostasis, and vascular tone, and endothelial dysfuncti

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

133 Therefore hemostasis, anticoagulation, hemolysis, and inflammatory

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

135 ment system, immunoglobulin superfamily, and hemostasis are increased in early plaques.

136 Animal models of hemostasis are often extrapolated to humans; however, on

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

138 ransfusion techniques and agents to optimize hemostasis are used during surgery and in the immediate

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

140 uma service (ETS) on case volume and time to hemostasis, as a complement to an existing interventiona

141 ct platelet responses to thrombin and normal hemostasis, as assayed in tail bleeding experiments.

142 5 patients in group A who could be assessed, hemostasis, as determined by local investigators, was re

143 Tertiary hemostasis assessment included fibrinolytic factors and

144 Primary hemostasis assessment included platelet aggregation and

145 Secondary hemostasis assessment included pro-coagulant (factor VII

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

147 Hemostasis associated with tissue injury is followed by

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

149 learning/cognition, endothelial dysfunction, hemostasis, bone mineralization, and body composition.

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

151 Platelets are fundamental to primary hemostasis, but become profoundly dysfunctional in criti

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

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

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

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

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

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

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

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

160 r (VWF) is a key player in the regulation of hemostasis by promoting recruitment of platelets to site

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

162 mouse model of prophylactic therapy (testing hemostasis by saphenous vein bleeding 7 days after infus

163 evelopment to exploit the natural balance of hemostasis by targeting the natural anticoagulants prote

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

165 mostatic changes occur, which affect primary hemostasis, coagulation, and fibrinolysis.

166 r amounts of blood loss and shorter times to hemostasis compared with commercially available absorbab

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

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

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

170 time to bleeding cessation and the extent of hemostasis during procedures are similar.

171 n levels, ultimately improving perioperative hemostasis during SBI.

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

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

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

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

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

177 used as a rescue therapy and not for primary hemostasis, except in cases of malignant bleeding or mas

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

179 and although links between inflammation and hemostasis exist in mammals, they are indirect and slowe

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

181 increases case volume and decreases time to hemostasis for trauma patients requiring time sensitive

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

183 ter understand mechanisms that differentiate hemostasis from thrombosis.

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

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

186 ical mechanisms through which ABO influences hemostasis have remained poorly understood.

187 We observed excellent or good hemostasis in 354 patients (81.8% [95% CI, 77.9-85.2]).

188 f EPCR reduces the level of FVIIa needed for hemostasis in a saphenous vein bleeding assay.

189 and iliac arteries, and it can achieve rapid hemostasis in acutely injured vessels.

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

191 ngest effect on these variables and retained hemostasis in contrast to nontarg-CD39 and potato apyras

192 apy model, none of the FIX products improves hemostasis in CRM(+) mice expressing a dysfunctional FIX

193 0.33%, gel has been reported for the use of hemostasis in dermatologic surgery.

194 We demonstrate that these proteins inhibit hemostasis in ex vivo and in vivo experiments.

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

196 sponse can lead to disruption of immunologic hemostasis in healthy tissues, causing adverse events.

197 minutes in almost all patients, with normal hemostasis in more than 91% of patients.

198 For assessing hemostasis in Non-ACLF and ACLF patients the underlying

199 The goal of this study was to examine hemostasis in patients with stable liver cirrhosis (Non-

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

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

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

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

204 ADVICE 1: Endoscopic therapy should achieve hemostasis in the majority of patients with NVUGIB.

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

206 Hemostasis in vertebrates involves both a cellular and a

207 vessel wall platelet deposition and initial hemostasis in vivo.

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

209 t mice displayed constitutively dysregulated hemostasis, including a consumptive coagulopathy, charac

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

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

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

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

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

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

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

217 nsus is that in patients with cirrhosis, the hemostasis is shifted toward a procoagulant state.

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

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

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

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

222 approved anticoagulant agents interfere with hemostasis, leading to an increased risk of bleeding.

223 01), International Society on Thrombosis and Hemostasis major bleeding (206 of 9,152 [2.3%] vs. 116 o

224 fied International Society on Thrombosis and Hemostasis major bleeding (288 of 9,152 [3.1%] vs. 170 o

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

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

227 Excellent or good hemostasis occurred in 204 of 249 patients (82%) who cou

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

229 s was 65+/-157 seconds with a median time to hemostasis of 24 seconds.

230 ercentage of patients with excellent or good hemostasis on the basis of the modified Sarode criteria.

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

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

233 low is impaired due to loss of lympho-venous hemostasis or using inducible lung-specific ablation of

234 as its own independent function in immunity, hemostasis, or oxygen transport, but in this issue of Bl

235 Inspection of canonical hemostasis pathways identified 29 patients with evidence

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

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

238 g, Metabolism, Regulation, Immune System and Hemostasis pathways, which are consistent with the 256 a

239 pective study comparing all three aspects of hemostasis (platelets, coagulation, and fibrinolysis) in

240 achieve complete hemostasis and less patent hemostasis rate.

241 that transfusion of human PEVs would promote hemostasis, reduce blood loss and attenuate the progress

242 n achieve instant and durable intra-arterial hemostasis regardless of coagulopathy, is developed.

243 ay represent novel mechanisms for mechanical hemostasis regulation in extracellular matrix that are p

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

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

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

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

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

249 is were less frequently obtained and time to hemostasis significantly longer for increasing ACT value

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

251 biting platelet necrosis does not compromise hemostasis, targeting platelet CypD may be a potential t

252 d bleeding disorders characterized by normal hemostasis test results.

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

254 latelets are specialized cells essential for hemostasis that also function as crucial effectors capab

255 ral and systemic vasculature, the heart, and hemostasis that occur in Alzheimer's disease and their r

256 nd life forms and have been shown to control hemostasis, the immune response, and viral infection in

257 ceptor is considered to be of importance for hemostasis, the rate-limiting steps of CLEC-2-induced pl

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

259 h platelets are best known for their role in hemostasis, they are also crucial in development, host d

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

261 t ABO expresser phenotype influences primary hemostasis though several different pathways.

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

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

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

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

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

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

268 arinum model to show mycobacteria drive host hemostasis through the formation of granulomas.

269 eta3 cannot be achieved without compromising hemostasis, thus causing serious bleeding and increased

270 STH (International Society on Thrombosis and Hemostasis), TIMI (Thrombolysis in Myocardial Infarction

271 he injury, thus limiting its contribution to hemostasis to specific physiologic contexts.

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

273 omplex glycoprotein with regulatory roles in hemostasis, tumor development, wound healing, and athero

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

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

276 BEST PRACTICE ADVICE 5: Hemostasis using an over-the-scope clip should be consid

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 The mean time to hemostasis was 65+/-157 seconds with a median time to he

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

281 and 2-octyl cyanoacrylate was applied until hemostasis was achieved.

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

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

286 formation, and carotid occlusion, while tail hemostasis was unaffected.

287 To investigate its potential effect on hemostasis, we genotyped 865 patients with coronary arte

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

289 Patent hemostasis were less frequently obtained and time to hem

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

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

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

293 supportive care and nonspecific support for hemostasis with antifibrinolytic agents or prothrombin c

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

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

296 n of bleeding and the proportion with normal hemostasis with procedures were similar regardless of re

297 T between 150 and 249 s, ACT >250 s), patent hemostasis with reverse Barbeau test was attempted in al

298 ompartment, efficiently prolong prophylactic hemostasis without thrombotic risk.

299 A (FXIII-A), a transglutaminase involved in hemostasis, wound healing, tumor growth, and apoptosis.

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