ライフサイエンスコーパス: hemostatic

1 ) protein activity mirrored native hFVIII in hemostatic ability.

2 Patients with severe COVID-19 present with hemostatic abnormalities that mimic disseminated intrava

3 e administered mFVIIa-FMR exhibited superior hemostatic activity compared with mFVIIa.

4 jury) may represent a means to enhance VWF's hemostatic activity where needed.

5 tivities while supporting the activation and hemostatic adhesion of single platelets to neutrophil-in

6 possible impact on the biology, therapy, and hemostatic adverse effects of both disease progression a

7 Recombinant factor VIIa (rFVIIa), a hemostatic agent approved for hemophilia, is increasingl

8 blood clot formation and act as a rapid pan-hemostatic agent for the treatment of bleeding condition

9 human factor VII (rhFVIIa) is an established hemostatic agent in hemophilia, but its mechanism of act

10 8 (79.6%) patients treated with a first-line hemostatic agent or ancillary therapy alone.

11 portant unmet clinical need for a rapid, pro-hemostatic agent to reverse the effects of several new a

12 against the use of topical brimonidine as a hemostatic agent until its safety is further investigate

13 Among 307 patients treated with a first-line hemostatic agent, 174 (56.7%) received rFVIIa, 63 (20.5%

14 Polyphosphate may have utility as a hemostatic agent, whereas antagonists of polyphosphate m

15 nervous system toxic effects when used as a hemostatic agent.

16 ort the effectiveness of various hematinics, hemostatic agents and devices, as well as intermittent d

17 or larger vessels may play a minor role, and hemostatic agents could be of higher importance.

18 Nonspecific hemostatic agents such as prothrombin complex concentrat

19 rily based on ex-vivo or animal models using hemostatic agents with uncertain implications in bleedin

20 Bioadhesives such as tissue adhesives, hemostatic agents, and tissue sealants have potential ad

21 trials evaluating the safety and efficacy of hemostatic agents.

22 ceived platelets, clotting factors, or other hemostatic agents.

23 erative disorder with important vascular and hemostatic alterations that should be taken into account

24 polyphylla), a monocot medicinal plant with hemostatic and antibacterial properties, and fenugreek (

25 The canonical role of the hemostatic and fibrinolytic systems is to maintain vascu

26 s, and structural differences between mature hemostatic and growing pathological clots.

27 A clot contraction assay, along with other hemostatic and hematologic tests, was performed 1-3 days

28 A survey of hemostatic and hemodynamic parameters revealed no detect

29 gakaryocyte subfragments that participate in hemostatic and host defense reactions and deliver pro- a

30 from a lower vertebrate cell type with both hemostatic and immunologic roles.

31 NP) were more likely to be hospitalized with hemostatic and infection-related disorders, suggesting t

32 Although platelets bolster hemostatic and inflammatory defense of the healthy lung,

33 ids, blood pressure, insulin resistance, and hemostatic and inflammatory factors.

34 ) is a multifunctional plasma protein of the hemostatic and inflammatory pathways, although mechanism

35 ive study describes the rate and severity of hemostatic and thrombotic complications of 400 hospital-

36 expression of target mRNAs important for the hemostatic and thrombotic function of platelets.

37 ss using genetically engineered mice affects hemostatic and thrombotic functions of platelets.

38 ations normalized both bond kinetics and the hemostatic and thrombotic properties of VWF.

39 e that platelet Galpha(i2) not only controls hemostatic and thrombotic responses but also is critical

40 t demonstrates conservation of the mammalian hemostatic and vascular systems.

41 The coagulation system links immediate (hemostatic) and late (inflammatory, angiogenic) tissue r

42 ed with anti-CD14 on the early inflammatory, hemostatic, and hemodynamic responses in porcine Escheri

43 The recent development of novel hemostatic approaches for hemophilia, such as the use of

44 C) during trauma hemorrhage for viscoelastic hemostatic assays (VHAs).

45 In trauma care, viscoelastic hemostatic assays allows for rapid and timely identifica

46 Concurrently, whole blood viscoelastic hemostatic assays have gained acceptance by allowing a r

47 t of the resuscitation concept, viscoelastic hemostatic assays seem to improve outcome also in trauma

48 Viscoelastic hemostatic assays such as thrombelastography and rotatio

49 cted transfusion therapy, using viscoelastic hemostatic assays to guide ongoing resuscitation of acti

50 evidence supporting the use of viscoelastic hemostatic assays to guide trauma resuscitation.

51 Daily chest tube bleeding, results from hemostatic assays, transfusion volumes, 90-day PICU-free

52 Daily hemostatic assessments were performed.

53 ent knowledge of the impact of the disturbed hemostatic balance in the lungs on asthma severity and m

54 iologic responses and for fine tuning of the hemostatic balance in the vascular system.

55 ve greatly advanced our understanding of the hemostatic balance.

56 s method provides an insight into the global hemostatic capabilities and has been suggested to provid

57 storage organelles, thereby influencing the hemostatic capacity of the endothelium.

58 n counterparts, FXII(-/-) mice have a normal hemostatic capacity.

59 ompared with FVIII-BDD following a series of hemostatic challenges.

60 ent studies have focused on markers of these hemostatic changes as being most prevalent in cerebral m

61 We aimed to determine whether hemostatic changes in HIV-tuberculosis were associated w

62 he setting of liver cirrhosis (LC), profound hemostatic changes occur, which affect primary hemostasi

63 Mycobacteremia modestly influenced hemostatic changes without affecting mortality.

64 conventional electrosurgical coagulation and hemostatic clips are unsuccessful or predicted to be ine

65 n of thrombin generation within a developing hemostatic clot, thereby explaining the phenotype of pos

66 n increased risk of bleeding due to lysis of hemostatic clots that prevent hemorrhage in damaged bloo

67 causing systemic fibrinolysis or disrupting hemostatic clots.

68 l role of platelet-derived FV/Va in ensuring hemostatic competence.

69 However, device-related hemostatic complications remain common and have negative

70 multiple causes of AVWS and LVAD-associated hemostatic complications.

71 nds on transfusion of whole blood or blood's hemostatic components (platelets, fibrinogen, and coagul

72 boxyglutamic acid (Gla) domain, with unknown hemostatic consequences in vivo.

73 We also highlight the thrombotic and hemostatic consequences of targeting platelet SFKs.

74 An understanding of the coagulopathy, hemostatic considerations, and therapeutic approaches is

75 eatment of acute bleeding, and perioperative hemostatic control in 165 previously treated males aged

76 pies provide an opportunity for steady-state hemostatic control without exposure to immunogenic clott

77 ing to desmopressin or requiring a sustained hemostatic correction because of major surgery or bleedi

78 c18-2 conditional knockout mice had a severe hemostatic defect and prolonged arterial and venous blee

79 vely, these data showed for the first time a hemostatic defect associated with the loss of a specific

80 ector nucleases results in a major embryonic hemostatic defect.

81 cal regulation of platelet adhesion to cause hemostatic defects as found in patients with von Willebr

82 Hemostatic defects were not concomitant with the inducti

83 notypes could not be explained by concurrent hemostatic defects.

84 Zebrafish are able to tolerate severe hemostatic deficiencies that are lethal in mammals.

85 rgeted therapy of unexpected bleeding when a hemostatic derangement was not anticipated preoperativel

86 ften can present for surgery with underlying hemostatic disorders due to these acquired disorders or

87 ugh the direct link between the mutation and hemostatic disorders is not strictly established.

88 aches to reveal and to manage thrombosis and hemostatic disorders.

89 d functional properties for the treatment of hemostatic disorders.

90 pared with commercially available absorbable hemostatic dressings, and are highly biocompatible.

91 ing bleeding through the use of tourniquets, hemostatic dressings, direct pressure, or pressure devic

92 he important, but poorly understood, role of hemostatic dysfunction in malaria progression and, impor

93 at have identified novel roles through which hemostatic dysfunction may directly influence malaria pa

94 n blood plasma, which is relevant to predict hemostatic dysfunction.

95 been restricted to preventing blood loss in hemostatic dysregulation because of poor efficacy and ad

96 This report indicates that the beneficial hemostatic effect of DDAVP is not limited to an increase

97 al showed that binding to EPCR enhances the hemostatic effect of FVIIa in a mouse hemophilia model,

98 IIa interaction with EPCR contributes to the hemostatic effect of FVIIa in hemophilia.

99 Our results suggest that the hemostatic effect of pharmacologic doses of FVIIa is TF

100 s, this study puts forth a means to identify hemostatic effectors, biomarkers, and therapeutic target

101 in lieu of vasoconstrictors achieved similar hemostatic effects with fewer side-effects.

102 oinflammatory functions independent of their hemostatic effects.

103 12 hours after the end of the infusion, with hemostatic efficacy adjudicated on the basis of prespeci

104 surrogate end point to conservatively assess hemostatic efficacy and enable comparison with recombina

105 al evaluation and has demonstrated excellent hemostatic efficacy and safety.

106 ercentage of patients with excellent or good hemostatic efficacy at 12 hours after the end of the inf

107 y, and 82% of patients had excellent or good hemostatic efficacy at 12 hours, as adjudicated accordin

108 r Xa activity and were assessed for clinical hemostatic efficacy during a 12-hour period.

109 Of these, 433 patients met criteria for hemostatic efficacy evaluation.

110 asma for the coprimary end points of 24-hour hemostatic efficacy from start of infusion and internati

111 is a novel rFVIII molecule showing excellent hemostatic efficacy in surgery and in the control of ble

112 duce septic transfusion risk, and to enhance hemostatic efficacy in the bleeding patient.

113 This phase 3 trial evaluated the safety and hemostatic efficacy of a recombinant von Willebrand fact

114 e results are the first demonstration of the hemostatic efficacy of continuous expression, in the pre

115 atelet Therapy trial, our results suggest no hemostatic efficacy of early platelet transfusion in int

116 nti-factor Xa activity was not predictive of hemostatic efficacy overall but was modestly predictive

117 Hemostatic efficacy was rated by the investigator as exc

118 ours of PCC administration were assessed for hemostatic efficacy.

119 dy had 2 primary analysis groups: safety and hemostatic efficacy.

120 The designed hydrogels demonstrate promising hemostatic efficiency, as a physiologically-benign appro

121 e in the surface area of chitosan to improve hemostatic efficiency.

122 ion factor XIII (FXIII-A2B2), FXIII-A*, is a hemostatic enzyme essential for inhibiting fibrinolysis

123 tes with levels of hepatic mRNA encoding the hemostatic enzyme factor XI (FXI).

124 During thrombotic or hemostatic episodes, platelets bind collagen and release

125 ns that associate with and activate the host hemostatic factor prothrombin, and the bacterial surface

126 (rFVIII) and subsequently alone, as long as hemostatic factor VIII activity (FVIII : C) levels were

127 will give way to the identification of novel hemostatic factor-targeted therapies for a range of tiss

128 tment decisions, including administration of hemostatic factors (eg, prothrombin complex concentrate)

129 t influence plasma concentrations of these 4 hemostatic factors by meta-analyzing exome chip data fro

130 More generally, it is unknown whether hemostatic factors expressed on tumor cells influence ti

131 raction of DNA and histones with a number of hemostatic factors has been shown to promote clotting an

132 Ticks secrete several anti-hemostatic factors in their saliva to suppress the host

133 at therapeutic interventions at the level of hemostatic factors may be an effective means to prevent

134 Several hemostatic factors showed a procoagulant shift with decr

135 Several complement proteins interact with hemostatic factors.

136 elopment and translation of ADDSs that spare hemostatic fibrin clots hold promise for extending the u

137 ay layer-by-layer assembly is used to create hemostatic films containing thrombin and tannic acid.

138 BEST PRACTICE ADVICE 4: Monopolar hemostatic forceps with low-voltage coagulation can be a

139 Similarly, the hemostatic function and maintenance of vascular integrit

140 Thrombin-mediated proteolysis is central to hemostatic function but also plays a prominent role in m

141 educing the WPB size abates endothelial cell hemostatic function by drastically diminishing platelet

142 In parallel, however, they exercise their hemostatic function by securing the integrity of inflame

143 This primary hemostatic function is perturbed in type 2 dysfunctional

144 Variants of this recently appreciated hemostatic function of platelets that we refer to as "in

145 The hemostatic function of VWF depends upon the formation of

146 ng interface of the VWF A1 domain impair the hemostatic function of VWF.

147 al transmembrane glycoprotein that modulates hemostatic function through a domain that controls throm

148 Remarkably, improved hemostatic function was evident, with </=135-fold reduce

149 hagic agents without interfering with normal hemostatic function.

150 is essential for long multimers required for hemostatic function.

151 pharmacokinetic properties while maintaining hemostatic function.

152 mount of circulating VWF are known to impact hemostatic function.

153 The bidirectional signaling and hemostatic functions of platelet alphaIIbbeta3 are regul

154 tion and pathways that are important for non-hemostatic functions.

155 e effects of using gelatin- and fibrin-based hemostatic hydrogels as a scaffold on pulp regeneration

156 In severe infections, hemostatic impairment is frequently observed, and pathop

157 othelial cell activation coupled to possible hemostatic incompatibilities may be the primary stimulus

158 hospital-based intervention (transfusion or hemostatic intervention) or death within 30 days.

159 ve (AUCs) for a composite outcome, including hemostatic intervention, transfusion, and in-hospital mo

160 tihemophilic cofactor, FVIII, triggering the hemostatic intrinsic coagulation pathway independently o

161 els increased rapidly after rVWF alone, with hemostatic levels achieved within 6 hours and sustained

162 The Rao group showed that hemostatic levels of FVIIa displace PC from EPCR, and bl

163 stable conditions and to investigate whether hemostatic markers correlate with airway inflammation.

164 rom the oral cavity, elevated thrombotic and hemostatic markers that promote a prothrombotic state an

165 ipoprotein composition, and inflammatory and hemostatic markers.

166 od clot (PC), gelatin-based and fibrin-based hemostatic matrices (GM and FM), or without the insertio

167 in-I activity as a potentially self-limiting hemostatic mechanism.

168 barachnoid hemorrhage, potentially through a hemostatic mechanism.

169 eleases von Willebrand factor as its primary hemostatic mechanism.

170 animals, suggesting that alternative primary hemostatic mechanisms can partially rescue the bleeding

171 o mimic, leverage, and amplify physiological hemostatic mechanisms.

172 The recent advances in hemostatic monitoring, and discussion of the clinical im

173 ed, leading to a change in the protocols for hemostatic monitoring.

174 gan hemorrhaging, i.v. administration of the hemostatic nanoparticles led to a significant improvemen

175 To address this need, we have developed hemostatic nanoparticles that are administered intraveno

176 cleation of the prostate to provide superior hemostatic outcomes compared to classic monopolar transu

177 phenolic fraction and non-polar fraction on hemostatic parameters of plasma was also compared to act

178 lgorithms based on readily available routine hemostatic parameters.

179 Hemostatic patches were applied 286 (69.1%) times.

180 Septic infections dysregulate hemostatic pathways, prompting coagulopathy.

181 matory damage by activating inflammatory and hemostatic pathways, such as complement, the TLRs, coagu

182 complications of HIT, while sparing systemic hemostatic pathways.

183 se two variants did not associate with known hemostatic plasma markers.

184 Eltrombopag increases and maintains hemostatic platelet counts; however, to date, outcome ha

185 oenvironmental cues in a growing thrombus or hemostatic plug and then mechanotransduce those cues int

186 important in platelet aggregation to form a hemostatic plug as evidenced by the increased bleeding t

187 y serve in concert as building blocks of the hemostatic plug but also act individually as gatekeepers

188 Platelet spreading is critical for hemostatic plug formation and thrombosis.

189 tegrate classic studies on the physiology of hemostatic plug formation into modern molecular understa

190 erate within the biological milieu to affect hemostatic plug formation remains unaddressed.

191 Injury-induced bleeding is stopped by a hemostatic plug formation that is controlled by a comple

192 2Y(12) signaling in establishing a competent hemostatic plug is related to the size of the injury, th

193 to the blood vessel triggers formation of a hemostatic plug, which is meant to prevent bleeding, yet

194 skeletal forces to compact and reinforce the hemostatic plug.

195 atelets, harnesses the same forces to form a hemostatic plug.

196 sts and changes in solute transport within a hemostatic plug.

197 allow them to aggregate, thus forming either hemostatic plugs or pathologic thrombi.

198 dies offer insights into the organization of hemostatic plugs, provide a detailed understanding of th

199 gation were normal in PAD4(-/-) mice, as was hemostatic potential determined by bleeding time and pla

200 However, no studies of efficacy or hemostatic potential in trauma patients were performed b

201 ted at sites of vascular injury, where VWF's hemostatic potential is important to mediate platelet ag

202 ADAMTS13, thereby potentially increasing the hemostatic potential of platelet VWF during the formatio

203 s in the circulation, which can regulate the hemostatic potential of VWF by reducing VWF binding to p

204 icient enzyme that needs FVIIIa to drive its hemostatic potential, by a mechanism that has remained l

205 Permeability is the measurement of a clot's hemostatic potential.

206 BEST PRACTICE ADVICE 7: Hemostatic powder should be preferentially used as a res

207 Use of TC-325 (hemostatic powder) was suggested as temporizing therapy,

208 BEST PRACTICE ADVICE 6: Hemostatic powders are a noncontact endoscopic option th

209 s in the mid-1990s, our understanding of the hemostatic process and of coagulopathy has improved.

210 ar structure that enables VWF to orchestrate hemostatic processes, in particular factor VIII (FVIII)

211 dies investigating the use of whole blood or hemostatic products.

212 f activated factor VII (FVIIa) with enhanced hemostatic properties are highly attractive for the trea

213 Taking advantage of the similar hemostatic properties of pigs and humans, the authors pe

214 On the basis of evidence that hemostatic proteases are powerful modifiers of both infl

215 le therapeutic approach to achieve prolonged hemostatic protection and less frequent dosing in patien

216 le therapeutic approach to achieve prolonged hemostatic protection and less frequent dosing in patien

217 g factors, which is associated with variable hemostatic protection, a high treatment burden, and a ri

218 Von Willebrand factor (VWF) is a key hemostatic protein synthesized in both endothelial cells

219 von Willebrand factor (VWF) is an essential hemostatic protein that is synthesized in endothelial ce

220 ibel-Palade bodies (WPBs), which contain the hemostatic protein von Willebrand factor (VWF) and a coc

221 The hemostatic protein von Willebrand factor (VWF) released

222 It's major component, the hemostatic protein von Willebrand factor (VWF), is known

223 A growing number of cardiovascular and hemostatic proteins are recognized to undergo reversible

224 de continuing access to missing or defective hemostatic proteins.

225 protein transport rates emerge early in the hemostatic response and are preserved as the thrombus de

226 Thus, the hemostatic response is shown to produce a hierarchical s

227 range of symptoms, including lack or loss of hemostatic response to infused VWF concentrates up to an

228 s platelet reactivity in vivo, modulates the hemostatic response to injury, promotes platelet product

229 sfunctional FIX can deleteriously affect the hemostatic response to prophylactic therapy.

230 A normal hemostatic response to vascular injury requires both fac

231 d into balloonlike structures as part of the hemostatic response.

232 of penetrating injury were used to evoke the hemostatic response.

233 well as limiting the magnitude of the normal hemostatic response.

234 ) platelets are fully capable of physiologic hemostatic responses and functional regulation of adhesi

235 The concept that hemostatic responses might be linked to wound healing re

236 s, and have also been implicated in platelet hemostatic responses.

237 s for understanding NETs-mediated immune and hemostatic responses.

238 ) and Idelvion (FIX(Alb)) produce comparable hemostatic results in CRM(-) mice.

239 This prospective evidence suggests hemostatic resuscitation as an interim standard of care

240 Hemostatic resuscitation has been shown to be beneficial

241 ced massive transfusion protocols leading to hemostatic resuscitation is lifesaving.

242 Prompt balanced hemostatic resuscitation of major hemorrhage from trauma

243 early, accurate, and efficient activation of hemostatic resuscitation protocols.

244 All with HF (fc31.2%) corrected after hemostatic resuscitation without tranexamic acid.

245 d, uncrossmatched whole blood during initial hemostatic resuscitation.

246 system modulates autonomic, hemodynamic, and hemostatic risk markers at rest, and that behavioral str

247 mpairs platelet function beyond their purely hemostatic role and that Nbeal2 deficiency has a protect

248 However, recent studies suggest the hemostatic role of FXI may not be restricted to the acti

249 Together, these results suggest that the hemostatic role of FXIa may be attributed not only to ac

250 e model may also be useful for assessing the hemostatic safety of other therapeutic Abs.

251 vidence supports the concept of a rebalanced hemostatic state in liver disease as a result of a comme

252 dicting precrisis changes in an individual's hemostatic state one step closer.

253 results indicate that human PEVs provide pro-hemostatic support following uncontrolled bleeding.

254 bolization; one patient underwent additional hemostatic surgery.

255 indicates multiple interactions between the hemostatic system and innate immunity, and the coagulati

256 In this context, the hemostatic system and its associated signaling pathways

257 ttlefield while highlighting the role of the hemostatic system as a clinical indicator of chronic-bas

258 In recent years, the traditional view of the hemostatic system as being regulated by a coagulation fa

259 Many pathogens usurp the host hemostatic system during infection to promote pathogenes

260 d procoagulant materials and the traditional hemostatic system is an attractive target for the develo

261 crosstalk between the immune system and the hemostatic system might be instrumental for the preventi

262 r regulation of individual components of the hemostatic system, including platelets, coagulation fact

263 Thrombin, the major enzyme of the hemostatic system, is involved in biological processes a

264 ver disease acquire complex changes in their hemostatic system, which results in a fragile rebalanced

265 utations on enzyme-cofactor complexes in the hemostatic system.

266 ens exploit the initiation phase of the host hemostatic system.

267 -volume therapeutic to rebalance a disturbed hemostatic system.

268 ntial interaction between the complement and hemostatic systems on the level of initiating molecules.

269 It has long been appreciated that hemostatic systems represent complicated dynamics, invol

270 n the physiologic role of the complement and hemostatic systems.

271 ious topical, intracavitary, and intravenous hemostatic technologies in terms of materials, mechanism

272 s have undergone robust research, leading to hemostatic technologies including glues, bandages, tampo

273 The development of hemostatic technologies that suit a diverse range of eme

274 defects and a high value for a point-of-care hemostatic test, the CT-ADP, were each predictive of the

275 upport the broader adoption of point-of-care hemostatic testing into clinical practice.

276 fusion algorithm incorporating point-of-care hemostatic testing was sequentially implemented at 2 hos

277 We hypothesized that point-of-care hemostatic testing within the context of an integrated t

278 Implementation of point-of-care hemostatic testing within the context of an integrated t

279 difficult to optimally manage using standard hemostatic testing.

280 ndependently associated with the majority of hemostatic testing.

281 an acceptance of the adequacy of whole blood hemostatic tests to monitor these patients.

282 st tube bleeding, whereas platelet count and hemostatic tests were not.

283 d discussion of the clinical implications of hemostatic therapies based on different blood components

284 t role in guiding fibrinogen replacement for hemostatic therapy in clinical settings such as cardiova

285 Optimal hemostatic therapy is controversial, and available data

286 ess the risk of bleeding and the efficacy of hemostatic therapy.

287 Hemostatic thrombi develop a characteristic architecture

288 Hemostatic thrombi formed after a penetrating injury hav

289 Hemostatic thrombi formed after a penetrating injury hav

290 Previous studies have shown that hemostatic thrombi formed in response to penetrating inj

291 lethality of CLEC-2 KO models, but not their hemostatic/thrombotic defect.

292 nduced vascular injury showed that defective hemostatic thrombus formation in HPS mice largely reflec

293 Hemostatic transfusion ratios of RBC to FFP approaching

294 Although most hemostatic transfusions were independently associated wi

295 poreal membrane oxygenation were free of any hemostatic transfusions.

296 o active bleeding, FVIII restored >50 IU/dL, hemostatic treatment stopped >24 hours) was achieved by

297 Endoscopic hemostatic treatment was administered at initial endosco

298 Hemostatic treatment was reportedly effective in 96% of

299 tients who received blood products and other hemostatic treatments.

300 The primary hemostatic von Willebrand factor (vWF) functions to sequ