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

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

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

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

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

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

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

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

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

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

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

13 Hyperacute and delayed rejection are immunologic hurdles

14 Hyperacute and delayed vascular rejection due to natural

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

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

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

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

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

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

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

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

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

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

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

26 The hyperacute edematous wave was ameliorated only in pigs s

27 ately before renal transplantation prevented hyperacute graft rejection.

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

29 identical recipients of PBSC developed fatal hyperacute GVHD.

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

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

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

33 The hyperacute immune response in humans is a potent mechani

34 This hyperacute immune response leads ultimately to graft rej

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

36 the rarity of individuals presenting during hyperacute infection.

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

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

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

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

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

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

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

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

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

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

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

48 Seasonal hyperacute panuveitis (SHAPU) is a potentially blinding

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

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

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

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

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

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

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

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

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

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

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

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

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

62 Hyperacute pulmonary xenograft dysfunction, which occurr

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

64 Hyperacute rejection (HAR) and acute humoral rejection (

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

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

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

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

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

70 Hyperacute rejection (HAR) is the first critical immunol

71 Hyperacute rejection (HAR) mediated by xenoreactive natu

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

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

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

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

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

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

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

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

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

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

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

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

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

85 0(8) nonparenchymal cells (NPC), resulted in hyperacute rejection and death in < or = 1.9 days.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Hyperacute rejection does not occur in guinea pig cornea

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

108 No hyperacute rejection episodes occurred.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 Hyperacute rejection in xenotransplantation is caused by

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

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

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

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

130 When hyperacute rejection is averted, transplanted pig organs

131 When hyperacute rejection is avoided by deletion of Gal expre

132 Classic hyperacute rejection is dependent on the activation of t

133 To avoid hyperacute rejection it is essential that recipient anti

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

135 The hyperacute rejection mediated by preexisting antibodies

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

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

138 Hyperacute rejection occurred only in transplanted kidne

139 No hyperacute rejection occurred.

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

141 Hyperacute rejection of a porcine organ by higher primat

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

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

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

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

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

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

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

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

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

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

152 Hyperacute rejection of mouse lung by human blood occurs

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

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

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

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

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

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

159 Hyperacute rejection of porcine organs by old world prim

160 Hyperacute rejection of porcine organs transplanted into

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

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

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

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

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

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

167 Hyperacute rejection of solid organ pig xenografts in no

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

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

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

171 Hyperacute rejection of vascularized discordant xenograf

172 The hyperacute rejection of vascularized grafts exchanged be

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

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

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

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

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

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

179 Hyperacute rejection results from the deposition of pref

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

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

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

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

184 The clinical diagnosis of hyperacute rejection was made.

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

186 No hyperacute rejection was observed.

187 No hyperacute rejection was seen and histologic findings we

188 Hyperacute rejection was uncommon.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Hyperacute rejection, the initial and immediate barrier

212 Hyperacute rejection, the initial immune barrier to succ

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

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

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

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

217 All renal xenografts avoided hyperacute rejection.

218 some protection against complement-mediated hyperacute rejection.

219 renal transplantation because of the risk of hyperacute rejection.

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

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

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

223 on pig endothelium in the protection against hyperacute rejection.

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

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

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

227 No graft succumbed to hyperacute rejection.

228 acute xenograft rejection was able to induce hyperacute rejection.

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

230 esponse against xenografts in the absence of hyperacute rejection.

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

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

233 component deposition and consumption during hyperacute rejection.

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

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

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

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

238 topes on the graft endothelium could prevent hyperacute rejection.

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

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

241 omerular thrombosis but no other evidence of hyperacute rejection.

242 he very early pathophysiologic events during hyperacute rejection.

243 from Lewis rats by antibody therapy prevents hyperacute rejection.

244 successful discordant xenotransplantation is hyperacute rejection.

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

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

247 ible organ transplantation typically induces hyperacute rejection.

248 ng xenotransplantation antigens resulting in hyperacute rejection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 (16%) genes differentially expressed in the hyperacute window were still expressed in the same direc

276 ere differentially expressed compared to the hyperacute window.

277 differential expression was seen within the hyperacute window.

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

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

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

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

282 Hyperacute xenograft rejection impairs receptor-dependen

283 Hyperacute xenograft rejection may be modified by the ac

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

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

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

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