ライフサイエンスコーパス: hemostatic

1 Changes in the hemostatic system and chronic hemostatic activation are frequently observed in patient

2 , adhesion molecule expression, platelet and hemostatic activation, and reactive oxygen species gener

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 Hemostatic adaptation by the Ashwell receptor moderates

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

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

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

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

10 dicate that further evaluation of AV513 as a hemostatic agent in hemophilia A patients is warranted.

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

12 8 (79.6%) patients treated with a first-line hemostatic agent or ancillary therapy alone.

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

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

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

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

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

18 rix thrombin has proven to be an efficacious hemostatic agent.

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

20 -based oxygen carriers as well as the use of hemostatic agents and special blood products.

21 Tissue glues and hemostatic agents are effective, safe, and their use is

22 Published experience with biologic hemostatic agents for percutaneous nephrolithotomy is di

23 st decade, the number of different effective hemostatic agents has increased drastically.

24 se urologic applications of tissue glues and hemostatic agents over the past 3 years in the managemen

25 Nonspecific hemostatic agents such as prothrombin complex concentrat

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

27 mprehensive review of the most commonly used hemostatic agents, subcategorized as physical agents, ab

28 trials evaluating the safety and efficacy of hemostatic agents.

29 -four reports (38%) noted concomitant use of hemostatic agents.

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

31 A survey of hemostatic and hemodynamic parameters revealed no detect

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

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

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

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

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

37 and fibrinogen, the principal components of hemostatic and pathological thrombi, may represent biolo

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

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

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

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

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

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

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

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 hemostatic assessments were performed.

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

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

54 ve greatly advanced our understanding of the hemostatic balance.

55 er selective pressure by the requirements of hemostatic balance.

56 luding transfusion of blood products, use of hemostatic bandages/agents, and treatment with hemostati

57 , creatinine, homocysteine, and inflammatory/hemostatic biomarkers (high-sensitivity C-reactive prote

58 of risk factors were examined, inflammatory/hemostatic biomarkers made the largest contribution to l

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

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

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

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

63 Mycobacteremia modestly influenced hemostatic changes without affecting mortality.

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

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

66 causing systemic fibrinolysis or disrupting hemostatic clots.

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

68 Close attention to hemostatic complications during antiangiogenic treatment

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

70 verview, we discuss specific drug-associated hemostatic complications, the already known pathogenetic

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

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

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

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

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

76 tion included occasionally inadequate buccal hemostatic control and short-lived anesthesia of the max

77 t techniques and technologies being used for hemostatic control during laparoscopic partial nephrecto

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

79 AMSA injection included outstanding palatal hemostatic control, avoidance of undesirable collateral

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

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

82 ector nucleases results in a major embryonic hemostatic defect.

83 rombocytopenia, suggesting the presence of a hemostatic defect.

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

85 Hemostatic defects were not concomitant with the inducti

86 notypes could not be explained by concurrent hemostatic defects.

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

88 and can present for surgery with underlying hemostatic disorders because of pre-existing preoperativ

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

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

91 d functional properties for the treatment of hemostatic disorders.

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

93 We also evaluate novel hemostatic dressings and their application in the curren

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

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

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

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

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

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

100 Recombinant factor VIIa seems to have hemostatic effects in posttrauma and perisurgery excessi

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

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

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

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

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

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

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

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

109 Hemostatic efficacy was rated by the investigator as exc

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

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

112 sential for platelet aggregation and related hemostatic events.

113 e generally best controlled with 'bypassing' hemostatic factor concentrates.

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

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

116 emoglobin A1c/diabetes (25.3%), inflammatory/hemostatic factors (5%), and blood pressure factors (4.6

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

118 riuretic peptide [BNP], renin, aldosterone), hemostatic factors (plasminogen activator inhibitor-1 [P

119 thogens and suggest that common variation in hemostatic factors among humans could affect host suscep

120 nown risk factors, particularly inflammatory/hemostatic factors and blood pressure.

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

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

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

124 een tumor cell-associated TF and circulating hemostatic factors in malignancy, we generated a set of

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

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

127 Several hemostatic factors showed a procoagulant shift with decr

128 range of adult (aged approximately 25 years) hemostatic factors were assessed in the Barry Caerphilly

129 year 9 months-5 years) with adult levels of hemostatic factors were assessed.

130 els of hemoglobin A1c, inflammatory markers, hemostatic factors, and lipids were measured.

131 omain, but dependent on each of these distal hemostatic factors.

132 particulate matter may induce alterations in hemostatic factors.

133 Several complement proteins interact with hemostatic factors.

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

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

136 Platelets harbor several MMPs that modulate hemostatic function and platelet survival; however their

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

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

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

140 hrombus formation without undermining normal hemostatic function is the primary goal of this area of

141 This hemostatic function of endothelial cell-derived hFVIII w

142 ta3 in TxA(2) formation and in the defective hemostatic function of mouse or human platelets deficien

143 rkedly improved posttransfusion recovery and hemostatic function of platelets in mice.

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

145 her and how these receptors cooperate in the hemostatic function of platelets.

146 itory effect of anti-FVIII antibodies on the hemostatic function of transgene-derived hFVIII as is se

147 The hemostatic function of VWF depends upon the formation of

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

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

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

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

152 t enables an immune-type receptor to adopt a hemostatic function.

153 o-maternal interface in a mother with normal hemostatic function.

154 orphology yet manifested profoundly impaired hemostatic function.

155 ss development of the vasculature and normal hemostatic function.

156 hagic agents without interfering with normal hemostatic function.

157 is essential for long multimers required for hemostatic function.

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

159 of production to participate in its numerous hemostatic functions.

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

161 o a 3-mm diameter x 2-mm thick bioabsorbable hemostatic gelatin and placed onto the surface of the CA

162 Despite the persisting hemostatic imbalance and incomplete intra-alveolar eradi

163 This may contribute to the hemostatic imbalance in disseminated intravascular coagu

164 ses in vascular permeability coincident with hemostatic imbalances manifested by thrombocytopenia, tr

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

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

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

168 ed a protocol to support decisions regarding hemostatic management and prevention and treatment of in

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

170 Changes were observed in some hemostatic markers during the normobaric exposure, attri

171 tive protein, while childhood SEP influences hemostatic markers more than does adult SEP.

172 ested the hypothesis that elevated levels of hemostatic markers of endothelial dysfunction, plasminog

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

174 ipoprotein composition, and inflammatory and hemostatic markers.

175 fects of life-course SEP on inflammatory and hemostatic markers: fibrinogen, C-reactive protein, von

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

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

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

179 mostatic bandages/agents, and treatment with hemostatic medications.

180 In the hemostatic milieu, platelet-platelet interactions may be

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

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

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

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

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

186 ciated viral (AAV) vector corrected abnormal hemostatic parameters in hemophilia B mice.

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

188 for morbidity, mortality, viral replication, hemostatic parameters, cytokine production, and lung his

189 lgorithms based on readily available routine hemostatic parameters.

190 es sequence analysis of members of the three hemostatic pathways using the Sulfinator prediction algo

191 Septic infections dysregulate hemostatic pathways, prompting coagulopathy.

192 complications of HIT, while sparing systemic hemostatic pathways.

193 herapy with minor impairment of TF-dependent hemostatic pathways.

194 lly activated coagulation system and display hemostatic perturbations, but it is unknown whether they

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

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

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

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

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

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

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

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

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

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

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

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

207 cretion, and aggregation to form the primary hemostatic plug.

208 skeletal forces to compact and reinforce the hemostatic plug.

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

210 scular endothelial damage by forming primary hemostatic plugs.

211 rand factor (VWF) concatamers correlate with hemostatic potency.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 simple methodology for the identification of hemostatic proteins that are subjected to posttranslatio

231 ipitation of targeted [(35)S]sulfate-labeled hemostatic proteins, and tyrosine O-[(35)S]sulfate analy

232 Three new tyrosine-sulfated hemostatic proteins-protein S, prekallikrein, and plasmi

233 de continuing access to missing or defective hemostatic proteins.

234 ntly reported that polyphosphate is a potent hemostatic regulator, serving to activate the contact pa

235 clopidogrel group had a higher likelihood of hemostatic reoperations (odds ratio [OR], 5.1; 95% confi

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

237 regulatory mechanisms designed to limit the hemostatic response can be uncoupled to provide a sustai

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

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

240 A normal hemostatic response to vascular injury requires both fac

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

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

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

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

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

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

247 Hemostatic resuscitation has been shown to be beneficial

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

249 Prompt balanced hemostatic resuscitation of major hemorrhage from trauma

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

251 bjective of the study was to measure fasting hemostatic risk factors and postprandial changes in acti

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

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

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

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

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

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

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

259 bolization; one patient underwent additional hemostatic surgery.

260 Changes in the hemostatic system and chronic hemostatic activation are

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

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

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

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

265 Given substantial evidence that hemostatic system components are powerful modulators of

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

267 of the complement and its crosstalk with the hemostatic system in the pathophysiology and therapeutic

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

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

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

271 on can affect monocytes, lymphocytes and the hemostatic system.

272 ther states of generalized activation of the hemostatic system.

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

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

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

276 attention to patient preparation, sedation, hemostatic techniques, and postprocedure care.

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

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

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

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

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

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

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

284 difficult to optimally manage using standard hemostatic testing.

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

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

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

288 Optimal hemostatic therapy is controversial, and available data

289 Hemostatic therapy with rFVIIa reduced growth of the hem

290 Hemostatic thrombi develop a characteristic architecture

291 Hemostatic thrombi formed after a penetrating injury hav

292 Hemostatic thrombi formed after a penetrating injury hav

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

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

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

296 Hemostatic transfusion ratios of RBC to FFP approaching

297 Hemostatic transfusion strategies, with early and more a

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

299 valve and an adjustable resistance element (hemostatic valve) in series allow replication of various

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