ライフサイエンスコーパス: hyperacute

1 cerebral artery occlusion (MCAO) during the hyperacute, acute and chronic phases.

2 Acute liver failure is divided into hyperacute, acute and subacute liver failure.

3 n detecting intracranial hemorrhage (ICH) at hyperacute, acute and subacute stages by comparing with

4 ults showed that APT MRI could detect ICH at hyperacute, acute and subacute stages.

5 (APTw) and SWI signal intensities of ICH at hyperacute, acute and subacute stages.

6 asive imaging biomarker for detecting ICH at hyperacute, acute and subacute stages.

7 primates is now not substantially limited by hyperacute, acute antibody-mediated, or cellular rejecti

8 Rejection may occur in the hyperacute, acute, or chronic settings and requires judi

9 rials (RCT) assessing G-CSF in patients with hyperacute, acute, subacute or chronic stroke, and asked

10 h polycystic kidney disease and a history of hyperacute allograft rejections.

11 Donor-specific alloantibodies (DSA) mediate hyperacute and acute antibody-mediated rejection (AMR),

12 ticular, mean kurtosis (MK) was sensitive to hyperacute and acute stroke changes, and exhibited diffe

13 beta 1-4GlcNAc-R) on pig cells, resulting in hyperacute and acute vascular rejection of pig xenograft

14 Hyperacute and delayed rejection are immunologic hurdles

15 Hyperacute and delayed vascular rejection due to natural

16 Anti-Gal antibodies cause hyperacute and delayed xenograft rejection in pig-to-pri

17 ey role in rejection of xenografts surviving hyperacute and delayed xenograft rejection, but the mech

18 which limits xenotransplantation by causing hyperacute and delayed xenograft rejection.

19 cipient's immune responses that mediate both hyperacute and delayed xenograft rejection.

20 re (n = 3), hemiplegic migraine (n = 1), and hyperacute arterial infarction (n = 1).

21 levels demonstrated the clinical profile and hyperacute biochemical injury pattern associated with ac

22 combined and implemented these as the "ABC" hyperacute care bundle and sought to determine whether t

23 Different aspects of hyperacute cerebral ischemia are depicted at DW and HW i

24 d ears of Ormia ochracea are specialized for hyperacute directional hearing, but the possible role of

25 The hyperacute down-regulation, seen as early as 2 h through

26 y indicates that the DIC associated with the hyperacute dysfunction of pulmonary xenografts is a comp

27 macrophages may play a critical role in the hyperacute dysfunction of pulmonary xenografts.

28 The hyperacute edematous wave was ameliorated only in pigs s

29 ately before renal transplantation prevented hyperacute graft rejection.

30 immune suppression and compared this to the hyperacute GVHD, which develops in unprophylaxed or subo

31 identical recipients of PBSC developed fatal hyperacute GVHD.

32 kthrough acute GVHD that are not observed in hyperacute GVHD: (1) T-cell persistence rather than prol

33 In two patients, hyperacute hemorrhage was noted and removed.

34 od flow, blood volume, and water mobility in hyperacute human stroke.

35 The hyperacute immune response in humans is a potent mechani

36 This hyperacute immune response leads ultimately to graft rej

37 ART during hyperacute infection blunted peak viremia (p<0.0001), bu

38 infected cells in individuals treated during hyperacute infection may be associated with prolonged AR

39 the rarity of individuals presenting during hyperacute infection.

40 a week for plasma HIV RNA and identified 12 hyperacute infections.

41 y of MRI relative to CT for the detection of hyperacute intracerebral hemorrhage has not been demonst

42 iffusion on DWI, typically indicate acute or hyperacute ischemic infarcts; however, they can also be

43 Because of the hyperacute lethality, it is possible that the role of Gz

44 cific humoral immunity and in abrogating the hyperacute liver rejection that is produced by presensit

45 creasing, patients with rapidly progressive (hyperacute) liver failure, such as after acetaminophen o

46 The pathophysiology of hyperacute lung rejection (HALR) is not fully understood

47 ut (KO) but not wild-type (WT) grafts showed hyperacute or acute humoral rejection in nonsensitized G

48 6, 24, 48, and 54 hours revealed no signs of hyperacute or antibody-mediated rejection.

49 munologically privileged and may not undergo hyperacute or chronic rejection.

50 ld-type pig cells and is the main reason for hyperacute organ rejection in pig to primate xenotranspl

51 Surprisingly, hyperacute PAF shock depended entirely on NO, produced n

52 Seasonal hyperacute panuveitis (SHAPU) is a potentially blinding

53 o review advances in stroke treatment in the hyperacute period.

54 iation with the primary outcome for both the hyperacute phase (highest quintile adjusted OR 1.41, 95%

55 We studied 2645 (93.2%) participants in the hyperacute phase and 2347 (82.7%) in the acute phase.

56 were maximum systolic blood pressure in the hyperacute phase and SD of systolic blood pressure in th

57 was released from the ischemic brain in the hyperacute phase of stroke in mice and patients.

58 ystemic blood pressure, CBF and PbrO2 at the hyperacute phase of TBI.

59 during TGA, which is more pronounced in the hyperacute phase than in the postacute phase.

60 e measurements were taken in the first 24 h (hyperacute phase) and 12 over days 2-7 (acute phase).

61 e similar for the secondary outcome (for the hyperacute phase, highest quintile adjusted OR 1.43, 95%

62 r-weight thrombin inhibitor, SDZ MTH 958, in hyperacute porcine heart rejection by human blood ex viv

63 In this study, we showed how the hyperacute postinjury time window contained a focused, s

64 enrolled in the TICH-2 (Tranexamic Acid for Hyperacute Primary Intracerebral Haemorrhage) trial, we

65 ed in the periphery are rejected by a rapid "hyperacute" process that involves preformed antibody bin

66 s over a period of days, DIC associated with hyperacute pulmonary xenograft dysfunction develops with

67 Hyperacute pulmonary xenograft dysfunction, which occurr

68 cy of cobra venom factor (CVF) in preventing hyperacute rejection (HAR) after pig-to-baboon heart tra

69 Hyperacute rejection (HAR) and acute humoral rejection (

70 Xenografts that have been protected from hyperacute rejection (HAR) are termed accommodated if th

71 T) in the donor cell or tissue protects from hyperacute rejection (HAR) by reducing expression of Gal

72 regulatory proteins reduces the frequency of hyperacute rejection (HAR) in Gal-positive cardiac xenot

73 In the pig-to-primate model, xenograft hyperacute rejection (HAR) is mediated by antibody and c

74 layed xenograft rejection (DXR), occurs when hyperacute rejection (HAR) is prevented by strategies di

75 Hyperacute rejection (HAR) is the first critical immunol

76 Hyperacute rejection (HAR) mediated by xenoreactive natu

77 role of anti-Gal Abs and non-anti-Gal Abs in hyperacute rejection (HAR) of concordant pancreas xenogr

78 tibodies) are the primary effectors of human hyperacute rejection (HAR) of nonhuman tissue.

79 Hyperacute rejection (HAR) of pig-to-primate discordant

80 type 1 (sCR1, TP-10) has been shown to delay hyperacute rejection (HAR) of porcine cardiac xenografts

81 e to graft dysfunction during development of hyperacute rejection (HAR), as well as during what we ha

82 owed minimal evidence of complement-mediated hyperacute rejection (HAR), but prominent mononuclear ce

83 ans are rapidly rejected by a process called hyperacute rejection (HAR), there is hope that several n

84 Abs mediate a classical complement-dependent hyperacute rejection (HAR), while anti-Gal IgG1 mAbs med

85 (PVR), which is a characteristic feature of hyperacute rejection (HAR).

86 /kg) as a single dose to evaluate effects on hyperacute rejection (HAR).

87 e diabetes but whether islets are subject to hyperacute rejection after xenotransplantation is conten

88 ation are surmounted, such as suppression of hyperacute rejection allowing improved graft survival, i

89 There were no episodes of hyperacute rejection and 1 episode of early antibody-med

90 0(8) nonparenchymal cells (NPC), resulted in hyperacute rejection and death in < or = 1.9 days.

91 sfunction, with the potential to progress to hyperacute rejection and death.

92 lactose-alpha1,3-galactose epitope prevented hyperacute rejection and extended survival of pig hearts

93 an factor Xa inhibition by porcine EC during hyperacute rejection and loss of porcine EC TFPI during

94 pecific antibodies have been associated with hyperacute rejection and primary graft failure in lung t

95 gh the use of GalT-KO swine donors prevented hyperacute rejection and prolonged graft survival, slowl

96 Immediate pretransplant IA can prevent hyperacute rejection and provide an opportunity for succ

97 pients (median titer, 1:512), with 2 showing hyperacute rejection and rapid cessation of graft pulsat

98 studies in this patient are consistent with hyperacute rejection and support a pathogenic role of th

99 y, infants may have relative protection from hyperacute rejection and thus could undergo transplantat

100 The clinical and pathologic findings seen in hyperacute rejection are well documented in renal and ca

101 None had hyperacute rejection but 11 (39%) had acute antibody med

102 arts transplanted into rats do not encounter hyperacute rejection but are rejected within 3-4 days wh

103 f complement receptor type 1 (sCR1) prevents hyperacute rejection but not subsequent irreversible acc

104 This conditioning regimen prevented hyperacute rejection but was ineffective in preventing t

105 The recent advances in avoiding hyperacute rejection by producing transgenic pigs with c

106 Current data suggest that hyperacute rejection can be overcome in a clinically acc

107 In pig-to-primate organ transplantation, hyperacute rejection can be prevented, but the organ is

108 The ability of serum to induce hyperacute rejection correlated with its ability to indu

109 Hyperacute rejection did not occur in alpha1,3-galactosy

110 We have previously demonstrated that hyperacute rejection does not occur in a pig-to-newborn

111 Hyperacute rejection does not occur in guinea pig cornea

112 Our study demonstrates that hyperacute rejection does not occur, allowing limited pr

113 drate antigens, posing significant risks for hyperacute rejection during ABO-incompatible transplanta

114 No hyperacute rejection episodes occurred.

115 membrane attack complex (C5b-9) in mediating hyperacute rejection has been demonstrated previously in

116 Significant advances in controlling hyperacute rejection have been achieved recently through

117 tion of the immediate pathologic features of hyperacute rejection in a lung allograft which are simil

118 We describe the second case of hyperacute rejection in a pulmonary allograft and detail

119 third case and first successful treatment of hyperacute rejection in a pulmonary allograft recipient

120 ement regulatory proteins (CRPs) can prevent hyperacute rejection in discordant xenogenic recipients,

121 The expression of DAF prevents hyperacute rejection in mice with low titers of anti-alp

122 R), which are the major xenoantigens causing hyperacute rejection in pig-to-human xenotransplantation

123 lpha1,3Gal) is the major xenoantigen causing hyperacute rejection in pig-to-human xenotransplantation

124 suitable potential donor species, results in hyperacute rejection in primate recipients, due to the p

125 ccommodation of IEC may confer resistance to hyperacute rejection in sensitized recipients.

126 There was no evidence of hyperacute rejection in six of the nine patients; the ot

127 To address the pathogenesis of hyperacute rejection in the pig-to-human combination, F1

128 ositive, CXM negative, but no grafts lost to hyperacute rejection in this group.

129 on by a process that has features similar to hyperacute rejection in vascularized organs and we propo

130 etermine whether sensitization would lead to hyperacute rejection in VCTA as in other organs, such as

131 Hyperacute rejection in xenotransplantation is caused by

132 veloped to help overcome complement-mediated hyperacute rejection in xenotransplantation.

133 dence for complement activation in xenograft hyperacute rejection includes prolongation of graft surv

134 ions are designed to reduce or eliminate the hyperacute rejection inherent in pig-to-primate xenotran

135 However, when hyperacute rejection is averted, the xenografts are reje

136 When hyperacute rejection is averted, transplanted pig organs

137 When hyperacute rejection is avoided by deletion of Gal expre

138 Classic hyperacute rejection is dependent on the activation of t

139 To avoid hyperacute rejection it is essential that recipient anti

140 le to cross-species transplantation has been hyperacute rejection mediated by complement fixing antib

141 The hyperacute rejection mediated by preexisting antibodies

142 on; however, none has been shown to manifest hyperacute rejection mediated by the classical pathway o

143 olyreactive, a new prophylactic strategy for hyperacute rejection might be based on down-regulation o

144 Hyperacute rejection occurred only in transplanted kidne

145 No hyperacute rejection occurred.

146 t's anti-alphaGal profile, (2) prevention of hyperacute rejection of a pig organ, and (3) specific im

147 Hyperacute rejection of a porcine organ by higher primat

148 strate that C5b-9 plays an important role in hyperacute rejection of a porcine organ perfused with hu

149 recipient HLA-specific antibodies can cause hyperacute rejection of a transplanted kidney if they ar

150 almost certainly be sufficient to delay the hyperacute rejection of a transplanted pig organ, but fu

151 lusion resulting in infarction occurs during hyperacute rejection of allografts transplanted into sen

152 ciation of preformed anti-donor Abs with the hyperacute rejection of bone marrow and solid organ allo

153 ral antibodies (XNAs) and complement mediate hyperacute rejection of discordant xenografts.

154 dergo delayed rejection as compared with the hyperacute rejection of discordant xenografts.

155 n anti-GAL antibodies and are able to induce hyperacute rejection of GAL+ heart allografts.

156 donor-specific sensitization would result in hyperacute rejection of IECs and prevent islet engraftme

157 whether accommodation of IECs would prevent hyperacute rejection of islets in sensitized recipients.

158 Hyperacute rejection of mouse lung by human blood occurs

159 sitization against donor antigens results in hyperacute rejection of murine islets.

160 ajor role of anti-alphaGal antibodies in the hyperacute rejection of pig organs by humans and baboons

161 lphaGal) antibodies can prevent or delay the hyperacute rejection of pig organs transplanted into pri

162 l (alphaGal) natural antibodies leads to the hyperacute rejection of pig organs transplanted into pri

163 n by human blood ex vivo, a working model of hyperacute rejection of porcine by fresh, heparinized (6

164 motif is the primary contributing factor in hyperacute rejection of porcine organ xenograft, due to

165 Hyperacute rejection of porcine organs by old world prim

166 Hyperacute rejection of porcine organs transplanted into

167 Although preformed natural antibodies cause hyperacute rejection of primarily vascularized xenograft

168 embrane-bound complement regulation to blunt hyperacute rejection of pulmonary xenografts, but even t

169 e therapy, whereas delayed vascular and even hyperacute rejection of rat hearts occurred in condition

170 The same process results in hyperacute rejection of renal allografts transplanted in

171 antibodies to HLA class I antigens can cause hyperacute rejection of renal allografts.

172 ew model enabling serial biopsies of ongoing hyperacute rejection of small intestinal discordant xeno

173 Hyperacute rejection of solid organ pig xenografts in no

174 , but not third-party, sensitization induced hyperacute rejection of subsequent islet allografts (med

175 a series of violent reactions that result in hyperacute rejection of the xenograft.

176 ing factor (hCRF) in porcine organs prevents hyperacute rejection of these organs after xenotransplan

177 Hyperacute rejection of vascularized discordant xenograf

178 The hyperacute rejection of vascularized grafts exchanged be

179 ion may be beneficial to patients undergoing hyperacute rejection of xenografts or allografts.

180 The results may have relevance to hyperacute rejection of xenografts, as from pigs to prim

181 ress human CD59 (hCD59) in order to suppress hyperacute rejection of xenotransplants in human recipie

182 mplement-fixing IgG3 mAbs resulted in either hyperacute rejection or acute vascular rejection of the

183 ssion regimen was immediately modified and a hyperacute rejection protocol applied including plasmaph

184 tissues usually results in antibody-mediated hyperacute rejection response.

185 Hyperacute rejection results from the deposition of pref

186 est that sublytic deposition of C5b-9 during hyperacute rejection results in the expression of porcin

187 nd may therefore be of use in preventing the hyperacute rejection that follows discordant organ xenot

188 trast, an anti-Gal IgG3 mAb induced classic, hyperacute rejection that was solely dependent on comple

189 regulate complement activation and overcome hyperacute rejection upon transplantation of a vasculari

190 The clinical diagnosis of hyperacute rejection was made.

191 Hyperacute rejection was observed in 8/8 A-Tg grafts aft

192 No hyperacute rejection was observed.

193 No hyperacute rejection was seen and histologic findings we

194 Hyperacute rejection was uncommon.

195 No instances of hyperacute rejection were observed, and no grafts were l

196 e accommodated islets were resistant against hyperacute rejection when transplanted into donor-(splen

197 e conditions, nontransgenic grafts underwent hyperacute rejection within 90 min.

198 ition by human natural antibodies results in hyperacute rejection would allow for the development of

199 nograft model to examine our hypothesis that hyperacute rejection would be absent in newborn recipien

200 cular injury due to immune damage (acute and hyperacute rejection).

201 be divided temporally into three categories: hyperacute rejection, acute humoral rejection and chroni

202 antigen antibodies were then found to cause hyperacute rejection, acute rejection, and chronic rejec

203 stological examination showed no evidence of hyperacute rejection, although deposits of IgG2a and C3

204 he role of antibodies is incontrovertible in hyperacute rejection, although what fraction of acute re

205 into baboons, the grafts did not succumb to hyperacute rejection, and survival extended for up to 23

206 No patient experienced hyperacute rejection, and the persistence of low levels

207 most striking immunologic obstacle, that of hyperacute rejection, appears to be the closest to being

208 transgenic organs expressing hCD69 resisted hyperacute rejection, as measured by increased organ fun

209 Liver allografts rarely undergo hyperacute rejection, but transplants performed across a

210 was detected in pig control organs and after hyperacute rejection, but was lost from the vasculature

211 Unlike acute and hyperacute rejection, chronic rejection (CR) still const

212 a pig organ is transplanted into a primate, hyperacute rejection, induced by anti-pig antibody and m

213 nkeys after column perfusion did not undergo hyperacute rejection, remaining functional for 2-10 days

214 transgenic pigs may overcome the barrier of hyperacute rejection, special strategies will need to be

215 mulated T cells were relatively resistant to hyperacute rejection, suggesting an explanation for the

216 In the absence of complement-mediated hyperacute rejection, the ADCC induced by anti-Gal IgG m

217 Hyperacute rejection, the initial and immediate barrier

218 Hyperacute rejection, the initial immune barrier to succ

219 as being a major xenoantigen responsible for hyperacute rejection, the removal of anti-alphaGal antib

220 Using a rat model of hyperacute rejection, we investigated the potential of o

221 ajor obstacle to this xenotransplantation is hyperacute rejection, which is believed to be initiated

222 unological barrier to xenotransplantation is hyperacute rejection, which is mediated by xenoreactive

223 e solid organ transplantation and preventing hyperacute rejection.

224 a high likelihood of success with respect to hyperacute rejection.

225 All renal xenografts avoided hyperacute rejection.

226 some protection against complement-mediated hyperacute rejection.

227 renal transplantation because of the risk of hyperacute rejection.

228 and continuing cyclosporin A (CyA) prevented hyperacute rejection.

229 s treated by cobra venom factor to avoid the hyperacute rejection.

230 elicited anti-donor IgM and IgG that caused hyperacute rejection.

231 on pig endothelium in the protection against hyperacute rejection.

232 ot receive PP, lost her allograft because of hyperacute rejection.

233 i-A2 antibodies and for reducing the risk of hyperacute rejection.

234 ar endothelium of the graft, consistent with hyperacute rejection.

235 No graft succumbed to hyperacute rejection.

236 acute xenograft rejection was able to induce hyperacute rejection.

237 y of IgM to induce complement activation and hyperacute rejection.

238 esponse against xenografts in the absence of hyperacute rejection.

239 onse to xenografts that are not subjected to hyperacute rejection.

240 rn goats: none of these xenografts underwent hyperacute rejection.

241 component deposition and consumption during hyperacute rejection.

242 anges in anti-Gal activity in the absence of hyperacute rejection.

243 No graft was lost as a result of classic hyperacute rejection.

244 to evaluate the ability of hCD59 to inhibit hyperacute rejection.

245 d are liable to immediate graft loss through hyperacute rejection.

246 topes on the graft endothelium could prevent hyperacute rejection.

247 be of therapeutic value in the prevention of hyperacute rejection.

248 omerular thrombosis but no other evidence of hyperacute rejection.

249 he very early pathophysiologic events during hyperacute rejection.

250 from Lewis rats by antibody therapy prevents hyperacute rejection.

251 successful discordant xenotransplantation is hyperacute rejection.

252 course, such as primary graft dysfunction or hyperacute rejection.

253 r-specific antibodies (DSAs) are culprits of hyperacute rejection.

254 ft and one patient lost her graft because of hyperacute rejection.

255 ipients and is essential in the treatment of hyperacute rejection.

256 ible organ transplantation typically induces hyperacute rejection.

257 ng xenotransplantation antigens resulting in hyperacute rejection.

258 onal immunosuppression is unable to overcome hyperacute rejection; however, recent efforts in molecul

259 There were no hyperacute rejections and very infrequent acute rejectio

260 ic abnormalities, peripheral neuropathy, and hyperacute relapse of symptoms during treatment disconti

261 hese results show how mice locate objects at hyperacute resolution using a learned motor strategy and

262 care units, but then developed highly lethal hyperacute respiratory, renal, and cardiac failure due t

263 ing more detailed analyses of drivers of the hyperacute response and different MODS phenotypes, and r

264 ment not only abrogated the development of a hyperacute response but also allowed the primary graft t

265 r the sensitization of B cells mediating the hyperacute response but also validate therapeutic strate

266 from pigs genetically altered to reduce the hyperacute response in humans are able to induce elongat

267 nally, we could tolerize the potential for a hyperacute response, by pretreating recipients with a si

268 nd graft of donor cells was used to assess a hyperacute response.

269 ts with acute ischemic stroke are in need of hyperacute secondary prevention because the risk of recu

270 sensitive as CT to detect haemorrhage in the hyperacute setting, and superior to CT in the subacute a

271 atients by ischemic blood probing during the hyperacute stage of vascular occlusion is crucial to ass

272 decision making about treatment with rtPA in hyperacute stroke and hence to inform development of app

273 ccumulate in the ischemic vasculature during hyperacute stroke and may affect outcome.

274 diate triage of 35 patients with symptoms of hyperacute stroke and thus helped avoid the risks from a

275 Decision making about rtPA in hyperacute stroke presented three conundrums for patient

276 ce of functional stroke mimics admitted to a hyperacute stroke unit (HASU); to compare their clinical

277 ce of functional stroke mimics admitted to a hyperacute stroke unit (HASU); to compare their clinical

278 challenges of decision making about rtPA in hyperacute stroke were relational decision support and s

279 tant part of the assessment of patients with hyperacute stroke.

280 >/= 25) at The Royal London Hospital in the hyperacute time period within 2 hours of injury.

281 ons (n = 8) showed varied morphology, but at hyperacute time points (<8 hours) showed a tendency to g

282 of cisplatin-induced acute kidney injury and hyperacute TNF-shock models in mice suggested the distin

283 The evolution of hyperacute treatment has led to the current standard of

284 iting toxicity using this novel schedule was hyperacute tumor lysis syndrome.

285 ow developed a role in the very early phase (hyperacute units) plus outreach for patients who return

286 We postulated that the hyperacute window after trauma may hold the key to under

287 transcripts differentially expressed in the hyperacute window showed enrichment among diseases and b

288 (16%) genes differentially expressed in the hyperacute window were still expressed in the same direc

289 ere differentially expressed compared to the hyperacute window.

290 differential expression was seen within the hyperacute window.

291 ater development of MODS was present in this hyperacute window; it showed a strong signal for cell de

292 v6-targeted T cells and complete rescue from hyperacute xenogeneic graft-versus-host disease modeling

293 r of these XAb into naive nude rats provoked hyperacute xenograft rejection (38 +/- 13 min).

294 ans and is the basis for complement-mediated hyperacute xenograft rejection and antibody-dependent ce

295 Hyperacute xenograft rejection impairs receptor-dependen

296 Hyperacute xenograft rejection may be modified by the ac

297 cells have been suggested to participate in hyperacute xenograft rejection.

298 agents for application in the prevention of hyperacute xenograft rejection.

299 to donor organ vasculature is a hallmark of hyperacute xenograft rejection.

300 ouse-to-rabbit species combination manifests hyperacute xenograft rejection.