ライフサイエンスコーパス: allograft

1 onsequences of immune-mediated damage to the allograft.

2 d to the CF-lung remained able to invade the allograft.

3 or vasoplegia after revascularization of the allograft.

4 ts who may not have an option to wait for an allograft.

5 the donor microbiota and adapt to the non-CF allograft.

6 ify active JCPyV infection within the kidney allograft.

7 dy or immune cell responses against the DFTD allograft.

8 ative for children with AL in need of urgent allograft.

9 rylation, and macrophage infiltration of the allograft.

10 the priority of the candidate for the kidney allograft.

11 A2(-) individual received an HLA-A2(+) liver allograft.

12 JCPyV infection originating from the kidney allograft.

13 lant tolerance induction to mismatched islet allografts.

14 presence of apatite in both donor aortas and allografts.

15 idney allografts, but not in those of stable allografts.

16 revents macrophage infiltration into cardiac allografts.

17 ath to using more ischemically damaged renal allografts.

18 son's disease who had received foetal neural allografts.

19 nued immunosuppression for functional kidney allografts.

20 tive in modifying T- and B-cell responses to allografts.

21 al cells, including but not limited to human allografts.

22 ntributes to progression of fibrosis in lung allografts.

23 ients of concomitantly recovered solid organ allografts.

24 strongest among recipients of T-cell-replete allografts.

25 lecules, which are ubiquitously expressed in allografts.

26 d the activity of the IRE1alpha-XBP1 axis in allografts.

27 ion and limits the life span of transplanted allografts.

28 ed bone regeneration using titanium mesh and allografts.

29 ) and 2C10R4-treated (124 +/- 37, P < 0.020) allografts.

30 ody response toward xenografts compared with allografts.

31 treatment strategies for the maintenance of allograft acceptance frequently target ubiquitously-expr

32 ies have established its role in maintaining allograft acceptance without significant short- or long-

33 ression of TGFbeta mRNA and abrogated kidney allograft acceptance.

34 ssociated with significantly higher pancreas allograft [adjusted hazard ratio [aHR], 1.37; 95% confid

35 s with functional kidney but failed pancreas allografts after 90 days were included.

36 fidence interval (CI], 1.04-1.79] and kidney allograft (aHR, 1.36; CI, 1.02-1.82) failure over the st

37 e ability of an HDAC11i to promote long-term allograft allografts in fully MHC-disparate strains.

38 10 MSC sheet-wrapped groups when compared to allograft alone.

39 Clinical improvement followed removal of the allograft and cessation of immunosuppression.

40 sults showed more bony callus formed between allograft and host bone ends in both young P3 MSC and ag

41 Allograft and patient survival at 1-year posttransplanta

42 kidney transplant is associated with shorter allograft and patient survival.

43 overview of the impact of aging on both the allograft and the recipient and its effect on the immune

44 nalyzed whether these chemokines rise in the allograft and/or the blood and are associated with HCMV

45 Osteoclasts were absent in the allografts and there was no expression of the macrophage

46 ith increased expression of miR-146a in both allografts and urine of human kidney transplant recipien

47 had CKD stage 1-4, five had received a renal allograft, and three were dialysis-dependent at study en

48 Moreover, Akita mice readily rejected islet allografts, and chronic hyperglycemia had no impact on t

49 he number of donors for patients waiting for allografts, and enable better prediction of graft reject

50 Human limb allografts appeared viable after 24 hours of near-normot

51 Macrophages infiltrating the allografts are heterogeneous, consisting of proinflammat

52 and intensity of CXCR4 upregulation in renal allografts as determined by SUVs on PET and diffusion re

53 (NPI) xenografts compared with rhesus islet allografts at 1 hour, 24 hours, and 7 days.

54 pig liver, even if only as a bridge until an allograft becomes available.

55 DSA characteristics and performed systematic allograft biopsies at the time of post-transplant serum

56 expression and localization of US28 in renal allograft biopsies by immunohistochemistry and determine

57 r clinical data, histologic characteristics (allograft biopsy specimen), and donor-specific anti-HLA

58 chemical stainings for calprotectin in renal allograft biopsy specimens confirmed the serological res

59 hymal cells (MCs) derived from fibrotic lung allografts (BOS MCs) demonstrated constitutive nuclear b

60 nal proximal tubules of injured human kidney allografts, but not in those of stable allografts.

61 is the 'infectious' agent transmitted as an allograft by biting.

62 a promising strategy to reduce damage to an allograft by the recipient's immune system.

63 alf of transplant recipients will lose their allografts by 10 years after transplant.

64 HCMV replication in the allograft causes an intrapulmonary increase of CCL-18 an

65 urally or received RP with freeze-dried bone allograft covered by a non-resorbable dense polytetraflu

66 Allograft CXCR4 signal was paralleled by CXCR4 upregulat

67 mechanisms that differentially contribute to allograft damage among transplant recipients.

68 Chronic allograft damage, defined by interstitial fibrosis and t

69 e ischemia-reperfusion injury (IRI) of renal allografts donated after cardiac death (DCD) in a porcin

70 we report on a nationwide analysis of facial allograft donor surgery experience and long-term outcome

71 re transplant on development of Chronic Lung Allograft Dysfunction (CLAD) or CLAD-related death.

72 cant difference in freedom from chronic lung allograft dysfunction (CLAD) or survival between the two

73 Chronic lung allograft dysfunction (CLAD), presenting as bronchioliti

74 Unlike the categorical early allograft dysfunction (EAD) classification, MEAF is a co

75 plasma of 95 kidney transplant patients with allograft dysfunction and compared with 23 healthy volun

76 a significant difference in EC between early allograft dysfunction and normal functioning grafts (0.0

77 the target therapeutic window may result in allograft dysfunction as subtherapeutic tacrolimus level

78 s nor DSA translated to an increased risk of allograft dysfunction or death if prospective crossmatch

79 242 kidney transplant recipients with acute allograft dysfunction, higher urinary angiogenin concent

80 Moreover, chronic lung allograft dysfunction-free (P = 0.86) and overall surviv

81 within 72 hours) and long-term (chronic lung allograft dysfunction-free and overall survival) follow-

82 -associated nephropathy (BKVAN) causes renal allograft dysfunction.

83 Seven of the 19 grafts developed early allograft dysfunction.

84 thesized that because AMR is associated with allograft endothelial injury and C4d deposition, plasma

85 utively expressed on the cell surface of the allograft endothelium, autoantigens are usually cryptic.

86 Simultaneous allograft enterectomy and retransplantation was performe

87 ial reference to indications and outcomes of allograft enterectomy and the procedure's validity as a

88 l transplantation patient underwent isolated allograft enterectomy due to bowel necrosis.

89 There is no comprehensive assessment of allograft enterectomy regarding indications and outcomes

90 sible intestinal graft dysfunction, isolated allograft enterectomy successfully provides recovery fro

91 dications, surgical factors, and outcomes of allograft enterectomy were investigated.

92 ction is sometimes irreversible and requires allograft enterectomy with or without retransplantation.

93 ith delayed graft function but not all-cause allograft failure (adjusted hazard ratio 1.01, 95% CI 0.

94 eys with WIT>48 minutes had a higher risk of allograft failure (hazard ratio, 1.23; 95% CI, 1.07 to 1

95 [95% CI], 1.03 to 1.26; P<0.01) and death or allograft failure (HR, 1.18; 95% CI, 1.09 to 1.28; P<0.0

96 e similar longitudinal risk of mortality and allograft failure compared with tacrolimus-based regimen

97 for death, all-cause allograft failure, and allograft failure excluding death as a cause (competing

98 y], but ADPKD associated with a lower HR for allograft failure excluding death as a cause [0.85 (0.79

99 .34 to 1.81), respectively, and with HRs for allograft failure excluding death as a cause of 1.20 (1.

100 methodology, can offer insight into chronic allograft failure phenotypes and provide prognostic info

101 ients with IgAN or vasculitis had the lowest allograft failure rates.

102 sociations of D-BMI with pancreas and kidney allograft failure were assessed by multivariate Cox regr

103 Results for death as well as death or allograft failure were generally consistent among elderl

104 jects including 125 cases of intrinsic acute allograft failure, 27 prerenal graft failures, 118 patie

105 ted hazard ratios (HRs) for death, all-cause allograft failure, and allograft failure excluding death

106 We conclude that AMR may cause allograft failure, but that the diagnosis requires a mul

107 ogic lesions, and a risk predictor of kidney allograft failure.

108 y outcomes included death and death-censored allograft failure.

109 bular atrophy (IF/TA), is a leading cause of allograft failure.

110 ft arteriosclerosis (GA), the major cause of allograft failure.

111 ejection (ABMR) is a leading cause of kidney allograft failure.

112 iation of prerenal and intrinsic acute renal allograft failure.

113 for mortality, rehospitalization and kidney allograft failure/rejection for weekend (defined as Frid

114 for 1-year mortality, rehospitalization, or allograft failure/rejection.

115 esponses are responsible for the majority of allograft failures.

116 and cancellous mineralized freeze-dried bone allografts (FDBA) are available for use in alveolar ridg

117 pecifically contribute to the development of allograft fibrosis and chronic graft dysfunction.

118 hological factors known to predict and drive allograft fibrosis include graft quality, inflammation (

119 ed with a higher risk of relapse in patients allografted for myeloid malignancies.

120 Donor allografts from Brown Norway rats treated with Universit

121 ary, HCMV-encoded US28 was detected in renal allografts from HCMV-positive donors independent of vire

122 didates (who have previously lost at least 2 allografts from rapid recurrence of native kidney diseas

123 ions was independently associated with worse allograft function (P = 0.002) although abnormal blood p

124 ection remains an important cause of loss of allograft function after kidney transplantation.

125 latory hypertension is associated with worse allograft function and left ventricular hypertrophy (LVH

126 ow over 14 months posttransplant with stable allograft function.

127 to evaluate outcomes and predictors of renal allograft futility (RAF-patient death or need for renal

128 meters, histopathology, circulating DSA, and allograft gene expression for all patients with ABMR (n=

129 and used histopathology, immunostaining, and allograft gene expression to assess rejection phenotypes

130 ts who received a CYP3A5*1 allele expressing allograft had a lower risk of resistance to methylpredni

131 To determine the value of renal allograft histology in predicting outcomes, we evaluated

132 nsplant recipients maintain generally stable allograft histology in spite of apparently active humora

133 RI and subsequent tissue injury in DCD renal allografts in a large animal transplant model.

134 ng guidelines, SLKT potentially wastes renal allografts in both high-acuity liver recipients at risk

135 poietic cell kinase (Hck), as upregulated in allografts in CAI.

136 and are particularly effective in protecting allografts in experimental transplant models.

137 nce to combined hematopoietic cell and organ allografts in humans.

138 MPs can be liberated by early insults to the allograft, including ischemia/reperfusion injury, infect

139 Combined PET/MRI detected acute allograft infection in 9 patients and lower UTI/nonurolo

140 sion for patients with CKD and chronic renal allograft injury (CAI), but the underlying mechanisms re

141 Chronic allograft injury (transplant chronic glomerulopathy [cg]

142 ing multiple immune pathways responsible for allograft injury and loss.

143 ver, how these processes compare in terms of allograft injury and outcome has not been addressed.

144 a Syk inhibitor significantly reduced renal allograft injury in a model of severe antibody-mediated

145 on and stellate cell activation demonstrates allograft injury in proximity to non-HLA autoantibody bi

146 anding of the mechanisms by which DSA causes allograft injury, and effective strategies targeting hum

147 All causes of renal allograft injury, when severe and/or sustained, can resu

148 inserted after placement of bioglass and/or allograft into the sinus area using an osteotome techniq

149 and L-fucose, in both the recipient and the allograft, is an attractive target for therapies intende

150 iew is to highlight recent evidence that the allograft kidney can be infected by the virus after tran

151 y originating from the sinuses, may seed the allograft leading to infections and reduced allograft su

152 The adjusted 10-year mean kidney allograft lifespan was higher in Ki/SPK compared with SL

153 he utility, defined as posttransplant kidney allograft lifespan, of this practice.

154 team approach and expedited transfer of the allograft, limiting the recovery to a small geographic a

155 oped using Cox models for (a) mortality, (b) allograft loss (death censored), and (c) combined death

156 epresents one of the cardinal causes of late allograft loss after kidney transplantation, and there i

157 g system of PAT to identify risk factors for allograft loss and outline a management algorithm by ret

158 ssified patients at lower or higher risk for allograft loss at transplant (category-free net reclassi

159 recently predicted 50%10-year death-censored allograft loss in patients with donor-specific alloantib

160 The risk of allograft loss increased in patients with a cAMR score g

161 The diagnosis system for allograft loss lacks accurate individual risk stratifica

162 Rejection remains the leading cause of allograft loss, and a major barrier to improving long-te

163 experienced DGF and 2553 (33.9%) experienced allograft loss.

164 ediated rejection (AMR) contributes to heart allograft loss.

165 ve individual risk stratification for kidney allograft loss.

166 002) as the main independent determinants of allograft loss.

167 d rejection (AMR) is a major cause of kidney allograft loss.

168 g them all to have the same level of risk of allograft loss.

169 to the previously reported IDEC-131-treated allografts, median survival time (35 +/- 31 days) was si

170 In a pancreatic cancer allograft model, co-injection of PDAC cancer cells and S

171 Sixteen out of 21 allograft models were sensitive to HDM201 but ultimately

172 ed, 30c, displayed activity in xenograft and allograft models, strengthening the potential of NAMPT i

173 ne can reduce tumour growth in xenograft and allograft models.

174 as tissue engineered periosteum in a femoral allograft mouse model similar to fresh passaged (P3) you

175 Deeper analysis on chronic allograft nephropathy biopsy specimens suggested that SN

176 n markers was then assessed in human chronic allograft nephropathy biopsy specimens.

177 lated (MUD) donor T-cell-replete bone marrow allografting, obviating the need for additional prophyla

178 ion and repeat procedure in case of failure, allograft OSST can provide true long-term ocular surface

179 All patients underwent allograft OSST from March 1998 to June 2009.

180 LSCD, (2) surgical treatment with at least 1 allograft OSST procedure, and (3) minimum follow-up >/=

181 challenge, because the parameters governing allograft outcome are incompletely identified.

182 and treatment of this condition and improve allograft outcome.

183 ion (AR) is a risk factor for inferior renal allograft outcome.

184 sion regimen has greatly improved short-term allograft outcomes but not long-term allograft survival.

185 onse and are pointing to new ways to improve allograft outcomes in the clinic.

186 significant side-effects and poor long-term allograft outcomes.

187 vere obesity (D-BMI, >/=35 kg/m) on pancreas allograft outcomes.

188 risk of technical failure and poor pancreas allograft outcomes.

189 Of these, 50 underwent allograft pancreatectomy (Px) and 196 did not (no-Px).

190 about the incidence and indications for late allograft pancreatectomy while on continued immunosuppre

191 ecipient was associated with higher risk for allograft pancreatectomy.

192 Vascularized composite allografts, particularly hand and forearm, have limited

193 in reliably predicted a positive outcome for allografts, particularly in elderly patients.

194 All bioglass and/or allograft placed in the maxillary sinus after the osteot

195 In lung allografts, progressive terminal airway fibrosis leads t

196 Several characteristics unrelated to allograft quality were independently associated with lat

197 In a retrospective cohort study of renal allograft recipients (n=169), increased baseline levels

198 is is recommended in anti-HBc-positive liver allograft recipients and anti-HBc alone individuals who

199 lower in ES allograft recipients than in SS allograft recipients at 2 weeks, and ES allografts showe

200 tration and albuminuria remained lower in ES allograft recipients than in SS allograft recipients at

201 osuppression withdrawal in highly mismatched allograft recipients using a bioengineered stem cell pro

202 Cynomolgus monkey heterotopic cardiac allograft recipients were treated with either IDEC-131 (

203 orneas can enhance graft survival in corneal allograft recipients with inflamed graft beds.

204 risk for posttransplant malignancy in kidney allograft recipients with negative pretransplant HBc, HC

205 MonoIgG against normal human sera, IVIg, and allograft recipients' sera, it was observed that the num

206 lt diet, BP increased similarly in ES and SS allograft recipients, becoming significantly higher than

207 ogeneic IgG concentrations were augmented in allograft recipients.

208 ediated rejection (ABMR) therapies in kidney allograft recipients.

209 suppressed the growth of prostate carcinoma allografts, reduced tumor growth in both prostate and br

210 Such strategies tend to detect allograft rejection after significant injury has already

211 quences would provide essential insight into allograft rejection and lead to better therapies for tra

212 ecipients is limited because of the risk for allograft rejection and poor tolerability.

213 spects for defining a vascularized composite allograft rejection classification.

214 in type A receptor (ETAR) is associated with allograft rejection in kidney and heart transplantation.

215 ntibodies and autoantibodies are involved in allograft rejection in kidney and heart transplantation.

216 of new LVs has been shown to trigger chronic allograft rejection in kidney transplants.

217 CD4 TFH/GC B cell numbers and hastened islet allograft rejection in naive 12-week old Qa-1 deficient

218 therapy that provides protection from early allograft rejection in the absence of systemic immunosup

219 unosuppressive reagents for preventing islet allograft rejection is associated with severe complicati

220 he effect of complement inhibition on kidney allograft rejection phenotype and the clinical response

221 s of dd-cfDNA and correlated the levels with allograft rejection status ascertained by histology in 1

222 licly and from our Genomics of Chronic Renal Allograft Rejection study.

223 The non-HLAabs group had a higher rate of allograft rejection than controls (80% vs 55%), especial

224 l avenues for the treatment or prevention of allograft rejection that complement contemporary immunos

225 Our algorithm predicts heart and lung allograft rejection with an accuracy that is similar to

226 M2 cells is critical for preventing chronic allograft rejection, and that graft survival under such

227 (CsA), an immunosuppressant used to prevent allograft rejection, can also increase the risk of RCC i

228 ell numbers in naive mice and hastened islet allograft rejection.

229 o the response to steroid treatment of acute allograft rejection.

230 ective cure of HCV infection without risk of allograft rejection.

231 efined roles in the pathophysiology of renal allograft rejection.

232 e for an important role of IL-6 in mediating allograft rejection.

233 stablish the role of RIP3 in chronic cardiac allograft rejection.

234 on and T cell priming, ultimately leading to allograft rejection.

235 s of kidney dysfunction and acute or chronic allograft rejection.

236 sM(C)(re) Mtor(fl/fl) ) did not affect acute allograft rejection.

237 ion necessitated immunotherapy cessation and allograft removal, which led to decreasing serum viral l

238 Immune responses to allografts represent a major barrier in organ transplant

239 ays involved in IRI were not activated after allograft revascularization.

240 Unlike allograft samples showing acute rejection, samples from

241 ive fibrosis suggests that a subset of liver allografts seem resistant to the chronic injury that is

242 The continued kidney allograft shortage has generated interest in the use of

243 n SS allograft recipients at 2 weeks, and ES allografts showed less glomerular injury and interstitia

244 may play an important role in regulation of allograft-specific antibody responses to prevent organ r

245 n, this technology has promise for extending allograft storage times.

246 Px was not associated with kidney allograft survival (P = 0.16).

247 as no significant difference in 3-year renal allograft survival between the DCD and DBD groups (P = 0

248 +) cells, and significantly improved corneal allograft survival compared to saline-injected controls.

249 e association of HLA mismatching with kidney allograft survival has been well established.

250 by increased rejection or worsening patient/allograft survival in the short term.

251 bits T cell proliferation in vitro, supports allograft survival in vivo, prevents corneal transplant

252 ntified three risk strata with 6-year kidney allograft survival rates of 6.0% (high-risk group, n=40)

253 The 1-, 3-, 5- and 7-year death-censored allograft survival rates were 98%, 91%, 86%, and 78%, re

254 pact of transplant center volume on pancreas allograft survival remains unclear.

255 Three-year renal allograft survival was 95.2% in the DCD group, 87.1% in

256 Death-censored allograft survival was similar in all groups except the

257 onths, there was 100% (death-censored) renal allograft survival with estimated glomerular filtration

258 alysis was performed for PTLD-free survival, allograft survival, and patient survival after PTLD.

259 etween CIT and delayed graft function (DGF), allograft survival, and patient survival for 1267 shippe

260 Perioperative complications, allograft survival, and patient survival were similar be

261 site prognostic ABMR score to predict kidney allograft survival, integrating the disease characterist

262 To improve long-term kidney allograft survival, management paradigms should promote

263 combinant EPO administration prolonged heart allograft survival, whereas pharmacologic downregulation

264 effect of PI3Kdelta inhibition on long-term allograft survival.

265 rt-term allograft outcomes but not long-term allograft survival.

266 nts exhibit indefinite prolongation of heart allograft survival.

267 t of CD4(+) T cell dysfunction and long-term allograft survival.

268 tragraft accumulation of Tregs and prolonged allograft survival.

269 nsplants, analyzing 3-year patient and renal allograft survival.

270 allograft leading to infections and reduced allograft survival.

271 led to HSC mobilization and prolonged islet allograft survival.

272 Death-censored AMR-free and allograft survivals were significantly lower in C1q-dnDS

273 tis obliterans syndrome (BOS) or restrictive allograft syndrome (RAS) is the major limiting factor of

274 l immunosuppression for a functioning kidney allograft, the need for Px for symptoms and radiological

275 Pancreatic allograft thrombosis (PAT) remains the leading cause of

276 ystematic gene expression assessments of the allograft tissue, using microarrays.

277 Histological examination of allograft tissues showed a significant decrease of acute

278 rtantly, a monoclonal anti-TIM-4 Ab promoted allograft tolerance, and this was dependent on B cell ex

279 epatitis C virus (HCV) infection after renal allograft transplantation has been an obstacle because o

280 Allograft transplantation into sensitized recipients wit

281 Here the author show, using mouse heart allograft transplantation models, that PI3Kgamma or PI3K

282 impact of HJURP depletion in pre-established allograft tumors in mice and revealed a major block of t

283 Because cardiac allograft vasculopathy (CAV) is the major cause of late

284 Cardiac allograft vasculopathy (CAV) remains a leading cause of

285 initial TTE for recipient mortality, cardiac allograft vasculopathy (CAV), and primary graft failure

286 ated rejection (AMR) resulting in transplant allograft vasculopathy (TAV) is the major obstacle for l

287 rosis and histologic signs of severe chronic allograft vasculopathy eventually led to amputation of t

288 lar, by chronic rejection leading to cardiac allograft vasculopathy, remains a major cause of graft l

289 lular trafficking, alloimmunity, and cardiac allograft vasculopathy.

290 on, antibody-mediated rejection, and chronic allograft vasculopathy.

291 transcripts showed association with chronic allograft vasculopathy.

292 is known about the role of CD16 in promoting allograft vasculopathy.

293 the impact of facial vascularized composite allograft (VCA) procurement on the transplantation outco

294 HCMV replication in the allograft was associated with a significant increase of

295 els and the deposition of IgG and C4d in the allograft were equivalent in the 2 groups.

296 RAG1(-/-) recipients of BALB/c cardiac allografts were passively transferred with donor-specifi

297 Renal allografts were subjected to 30 minutes of warm ischemia

298 r growth, and increased the survival of mice allografted with S100beta-v-erbB/p53(-/-) glioma stem-li

299 Prograde flushing (PF) of living donor renal allografts with preservation solution via the renal arte

300 of MDSC markedly prolonged survival of islet allografts without requirement of immunosuppression.