ライフサイエンスコーパス: allograft

1 ve such treatment before transplantation (11 allografts).

2 ysis revealed accumulation in the LP treated allograft.

3 glucocorticoid responsive gene Fkbp5 in the allograft.

4 , diabetes, malignancy, or a kidney or heart allograft.

5 d raise concerns about amyloid recurrence in allograft.

6 antibody-mediated immune rejection of heart allografts.

7 n and promotes permanent acceptance of islet allografts.

8 r selection for HCV viremic liver and kidney allografts.

9 inflammation and fibrosis in long-term liver allografts.

10 or selection of HCV viremic liver and kidney allografts.

11 ion, correlating with survival of the kidney allografts.

12 truction is the use of tendon autografts and allografts.

13 Liver allograft (93.3% vs 93.1%, P = .29), kidney allograft (9

14 allograft (93.3% vs 93.1%, P = .29), kidney allograft (93.3% vs 93.1%, P = .91), and patient (96.7%

15 g of how donor intrinsic immunity influences allograft acceptance and survival will provide new oppor

16 Enhanced allograft acceptance resulted from depleting Lama5 or bl

17 Group 4 received allograft ADS followed by photobiomodulation.

18 Group 3 received only the allograft ADS.

19 tion socket was grafted with the combination allograft and covered with a nonresorbable membrane.

20 Indigenous recipients experienced poorer allograft and patient outcomes compared with nonindigeno

21 n of socket grafting with a particulate bone allograft and socket sealing with a nonabsorbable membra

22 able membranes with a combination of osseous allograft and xenograft was used in 73 cases, 53 of whic

23 reatment reduced the frequency of B cells in allografts and spleen.

24 biocompatibility associated with autografts, allografts and synthetic grafts.

25 A total of 24 patients received a stem-cell allograft, and 1 death was related to transplantation (4

26 isolated intestine, LI, modified MV, and MV allografts, and 2.7% (3/113) versus 10.8% (36/332) for t

27 n the absence of immunosuppression, homed to allografts, and suppressed proliferation of CD4 T cells

28 DBA/2J kidney allografts, but not heart allografts, are spontaneously accepted indefinitely in C

29 s self-renewal capacity in both organoid and allograft assays.

30 n newly transplanted allografts, compared to allografts at 6 months, whereas proinflammatory type 1 N

31 prevention of ischemia/reperfusion injury to allografts based on animal data should be considered.

32 allograft longevity lessens the need for new allografts before optimal intervention is available.

33 In 18 patients, allograft biopsies after 51 weeks revealed a negative mo

34 First, we assessed our allograft biopsies diagnosed with MIgARD between 2007 an

35 nce, peripheral blood samples and intestinal allograft biopsies from 51 ITx patients with severe reje

36 For comparison, renal allograft biopsies from a matched control group and nati

37 signaling is activated in protocol pancreas allograft biopsies from recipients on tacrolimus.

38 All for-cause renal allograft biopsies performed in 2007-2014 at the Erasmus

39 of specific molecular expression patterns in allograft biopsies related to different types of allogra

40 Allograft biopsies revealed AMR in 63 cases (73%), regar

41 and protein, a putative stem cell marker, in allograft biopsy samples with ACR compared to acute tubu

42 llowed by a multicenter validation cohort of allograft BKVN (n = 60) vs TCMR (n = 10).

43 exhibited dysbiosis after receiving a kidney allograft but not an isograft, despite the avoidance of

44 fication of Skin-Containing Composite Tissue Allograft, but the role of early vascular lesions in gra

45 DBA/2J kidney allografts, but not heart allografts, are spontaneously

46 conditioning, as well as for patients whose allograft came from a matched sibling versus an unrelate

47 s and prolonging the survival of old cardiac allografts comparable to young donor organs.

48 gnificantly diminished in newly transplanted allografts, compared to allografts at 6 months, whereas

49 Here, we showed that tolerant lung allografts could induce and maintain tolerance of hetero

50 ent advances in immunosuppression protocols, allograft damage inflicted by antibody specific for dono

51 between HCV eradication and immune-mediated allograft damage.

52 association with the release of HLA-bearing allograft-derived sEVs.

53 the recipient, and development of anti-organ allograft dnDSAs were significant predictors of anti-VA

54 tosis and 6 weeks after complete loss of his allograft due to severe CAMR.

55 es, whereas offering protection of implanted allografts during early stages of reperfusion while pati

56 Early allograft dysfunction (cDCD: 18% versus DBD: 32%; P = 0.

57 Chronic lung allograft dysfunction (CLAD) is the major barrier to lon

58 one of the independent predictors for early allograft dysfunction (EAD) in human OLT patients.

59 assessed the association of Sdc-1 with early allograft dysfunction (EAD), 1-year graft survival, and

60 with graft factors, 90-day graft loss, early allograft dysfunction (EAD), L-GrAFT score, acute kidney

61 unction (PNF; 7.7% vs 1.0%; P = .003), early allograft dysfunction (EAD; 70.8% vs 45.6% and 8.3%; P =

62 th primary nonfunction (P = 0.013) and early allograft dysfunction (P < 0.001) compared with the othe

63 rol patients and 89% of patients with active allograft dysfunction (P = 0.001).

64 rolonged ischemic injury can result in early allograft dysfunction and consequent rejection.

65 dies are more common in patients with active allograft dysfunction and may be a risk factor for worse

66 s and determine if they were associated with allograft dysfunction in pediatric liver transplant reci

67 ombined with HLA DSA in patients with active allograft dysfunction were associated with rejection and

68 circulation appears to trigger chronic lung allograft dysfunction.

69 n is whether DWF is a consequence of chronic allograft dysfunction.

70 ic conversion; 11 patients experienced renal allograft failure (10 underwent a repeat kidney transpla

71 ents had significantly higher risk of kidney allograft failure (DD-KA: aHR (1.53) 2.20(3.17) ; LD-KA:

72 s been long recognized as a leading cause of allograft failure after kidney transplantation, the cell

73 Associations of transplant type with kidney allograft failure and death (multivariable-adjusted haza

74 r graft survival than patients who had prior allograft failure as a result of acute rejection (P < .0

75 combinatorial immunosuppression regimens and allograft failure cause significant morbidity and mortal

76 antibody-mediated rejection (AMR) and kidney allograft failure is well established.

77 Among SPK recipients, 6% had pancreas allograft failure within 3 months (SPK,P-) and 94% had a

78 available literature on the causes of kidney allograft failure, both early and late, both nonimmune a

79 ignificantly improve prediction of long-term allograft failure.

80 increases delayed graft function and kidney allograft failure.

81 tion with histology of AMR (AMRh) and kidney allograft failure.

82 ent techniques of RP using freeze-dried bone allograft (FDBA) and a nonresorbable dense polytetrafluo

83 ized and 30% demineralized freeze-dried bone allograft (FDBA) evaluated at 8 to 10 weeks versus 18 to

84 oses [Group A] compared to freeze-dried bone allograft (FDBA) particles covered with a rapidly absorb

85 ively followed and had a functional pancreas allograft for >25 years as of October 31, 2018.

86 ble strategy to improve outcomes in patients allografted for AML.

87 l residual pool of donor cells persisting in allografts for over a decade contained CX3CR1hi/CD163hi/

88 uped as having received a living donor liver allograft from either an offspring or a nonoffspring, wi

89 Spleens and allografts from C57BL/6 recipients were harvested for im

90 hour posttransplant to recipients of cardiac allografts from CMV-infected donors significantly increa

91 g approach for extending survival of cardiac allografts from CMV-infected donors.

92 Kidney allografts from donors with persistent AKI are often dis

93 Male BalbC recipients received renal allografts from male C57BL/6J donors.

94 ents enrolled in the Deterioration of Kidney Allograft Function (DeKAF) study were evaluated: The Pro

95 Spirometry is the cornerstone of monitoring allograft function after lung transplantation (LT).

96 nt recipient relative to infectious risk and allograft function are lacking.

97 The procedure was safe and kidney allograft function remained stable after 3 years.

98 Leukopenia was seen in 20% of patients, and allograft function was stable in 50% of patients.

99 ase classes predicted clinical presentation, allograft function, and outcome independent of therapeut

100 All recipients had good allograft function, with a median creatinine of 1.2 mg/d

101 revir and pibrentasvir), adverse events, and allograft function.

102 ld decrease microvascular damage and improve allograft function.

103 This reduced kidney allograft futility (death or continued need for hemodial

104 Transcriptomic analysis of allografts harvested from donor-derived MDSCs treated re

105 S13 treatment and the impact of NETs on skin allografts, however, remain unexplored.

106 ents designed to uncouple antitumor and anti-allograft immunity.

107 r-derived MDSCs can protect heart transplant allografts in an antigen-specific manner.

108 with the use of HCV viremic liver and kidney allografts in HCV-negative recipients is limited to a fe

109 Cardiac allografts in young mice (2-3 months) treated with CTLA4

110 rejection, including their interaction with allograft-infiltrating recipient immune cells and potent

111 The allograft inflammatory factor (AIF) gene family consists

112 lammation after myocardial infarction and of allograft injury after heart transplantation.

113 graft biopsies related to different types of allograft injury could provide valuable information abou

114 MR although their specific role in mediating allograft injury is not yet understood.

115 Early unresolving molecular allograft injury measured via changes in dd-cfDNA may be

116 edictive of IgG3 DSA generation, more severe allograft injury, and higher rate of allograft loss.

117 onses to the transplanted organ resulting in allograft injury.

118 nity and are uncapable of preventing chronic allograft injury.

119 on of patients who are at risk of subsequent allograft injury.

120 In allografts, innate cell type-related regulatory networks

121 MIgARD in the kidney allograft is associated with poor prognosis.

122 plantation; sufficient microperfusion of the allograft is crucial for postoperative organ function.

123 f months after kidney retransplantation, the allograft is functioning well and the patient's CSCC rem

124 Glomerular size in renal allografts is impacted by donor-recipient factors and re

125 Alloimmune injury to allografts is mediated by pathogenic donor-specific allo

126 he use of MP in human vascularized composite allografts is scarce.

127 ve strategy, decreasing operative times, and allograft ischemic times, whereas offering protection of

128 treatment efficacy can only be found in the allograft itself, meaning that blood-based monitoring ma

129 We evaluated biopsy samples of native and allograft kidneys from patients with COVID-19 at a singl

130 erpetuation of inflammatory responses in the allograft, leading to allograft rejection and vasculopat

131 e new therapeutic strategies to promote skin allograft longevity and, hence, the survival of patients

132 Enhancing skin allograft longevity lessens the need for new allografts

133 sess clinical outcomes of retransplant after allograft loss as a result of BK virus-associated nephro

134 widely recognized as the main cause of late allograft loss in most (if not all) types of solid-organ

135 dies have been associated with rejection and allograft loss in solid organ transplantation and may ac

136 The risk of overall allograft loss was higher in group 1 compared with group

137 PITx and significantly delayed the onset of allograft loss.

138 tients were not associated with rejection or allograft loss.

139 rejection (AMR) accounts for >50% of kidney allograft loss.

140 with de novo DSA development, rejection, or allograft loss.

141 severe allograft injury, and higher rate of allograft loss.

142 r contributing to chronic rejection and late allograft loss.

143 glomerulopathy (TG) is a major cause of late allograft loss.

144 d with antibody-mediated rejection (AMR) and allograft loss.

145 sfunction were associated with rejection and allograft loss.

146 About half of late kidney allograft losses are attributed to death with function (

147 tion (cAMR) results in the majority of renal allograft losses.

148 The cases of allograft lymphangiectasia are characterized by severe,

149 mage to noninfected tissues: Rejecting renal allografts, melanomas clinically responding to anti-PD1

150 this multicenter cohort study, we integrated allograft microarray analysis with extensive clinical an

151 Intraoperative assessment of the allograft microperfusion was performed by near-infrared

152 Allograft MIgARD is infrequently encountered and poorly

153 ressive treatment, long-term survival of the allograft might be compromised by chronic antibody-media

154 g and stimulation of apoptosis in an ovarian allograft model compared to monotherapies.

155 Using primary human VS cells and a mouse allograft model of schwannoma, we evaluated the dual mTO

156 Using murine tumor allograft models, we show that systemic or EC specific s

157 antation (ITx) is the standard technique for allograft monitoring.

158 f immune-related problems that culminated in allograft necrosis and the eventual loss of the facial t

159 urgical management, and ultimately requiring allograft nephrectomy.

160 t survival was similar to those with chronic allograft nephropathy (P = .06) and other causes (P = .0

161 reservation sites treated with a combination allograft of 70% mineralized and 30% demineralized freez

162 and diameters [Formula: see text] from tumor allografts of three cancer cell lines and observed a sub

163 microscopy revealed the presence of NETs in allografts of vehicle, but surprisingly, not in rhADAMTS

164 ct of donation after circulatory death (DCD) allografts on outcomes following liver transplantation i

165 Kidney allograft outcomes are good in APRT deficiency patients

166 ion-to-dose ratio (C/D ratio), affect kidney allograft outcomes.

167 oups (15.5% in AKI vs 15.1% ideal comparator allografts, p = 0.2).

168 tral images of distinct components of kidney allografts (parenchyma, ureter) were acquired 15 and 45

169 The XVth Banff Conference on Allograft Pathology meeting was held on September 23-27,

170 The XV. Banff conference for allograft pathology was held in conjunction with the ann

171 aging (fMRI) was performed on day 6 to study allograft perfusion and organs were retrieved on day 7 f

172 ubulitis and fMRI analysis revealed improved allograft perfusion in LP versus NA mice.

173 ovide additional information regarding renal allograft prognosis.

174 lograft with demineralized bone matrix human allograft putty, and then covered with acellular dermal

175 en that can cause severe clinical disease in allograft recipients and infants infected in utero Virus

176 to be beneficial for vascularized composite allograft recipients and victims of traumatic major limb

177 match-positive sera obtained from 12 cardiac allograft recipients at the time of biopsy-proven reject

178 Overall, pretransplant DSA/DSA-Mpos allograft recipients showed a higher incidence of biopsy

179 ablished that T cell recovery in mouse heart allograft recipients treated with anti-thymocyte globuli

180 cell-derived HLA antibodies (DSA-M) in renal allograft recipients with pretransplant donor-specific H

181 d a single-center cohort study in 1000 renal allograft recipients, transplanted between March 2004 an

182 A high-fiber diet prevented dysbiosis in allograft recipients, who demonstrated prolonged surviva

183 s (0.2%), respectively, and 7 eyes developed allograft rejection (0.7%).

184 a (29.3% vs. 11.6%, respectively; P < .001), allograft rejection (16.6% vs. 1.7%, respectively; P < .

185 The incidence of allograft rejection (28% vs 25%; difference, 3% [95% CI,

186 th anti-VA dnDSAs had a higher rate of organ allograft rejection (45.4% vs 13.8%, P = .03) compared t

187 sidered a new option to inhibit the onset of allograft rejection acting on BOS specific features.

188 of blood and lymphatic neovessels and rapid allograft rejection after corneal penetrating keratoplas

189 inhibiting IL-6/IL-6R to ameliorate chronic allograft rejection and coronary allograft vasculopathy.

190 ) mouse model of T-cell-mediated human islet allograft rejection and developed a therapeutic regimen

191 mportant risk factor for accelerated cardiac allograft rejection and graft dysfunction .

192 profiling in the setting of diagnosing renal allograft rejection and how this will improve transplant

193 Allograft rejection and late endothelial failure account

194 Irreversible allograft rejection and late endothelial failure account

195 key role in transplantation by accelerating allograft rejection and preventing tolerance induction.

196 mbers ex vivo and have been shown to prevent allograft rejection and promote tolerance in animal mode

197 To shed light on the dynamics of ITx allograft rejection and treatment resistance, peripheral

198 atory responses in the allograft, leading to allograft rejection and vasculopathy.

199 ivation of genes related to inflammation and allograft rejection but downregulation of oxidative phos

200 cin has the potential to inhibit human islet allograft rejection by expanding CD4(+)FOXP3(+) Tregs in

201 SAs) have all been implicated in accelerated allograft rejection in sensitized recipients.

202 Renal allograft rejection is more frequent under belatacept-ba

203 mental models of ulcerative colitis and lung allograft rejection led us to test the effect of the PHI

204 In this study, a murine acute renal allograft rejection model was used to investigate whethe

205 Primary graft dysfunction and allograft rejection represent major caveats to successfu

206 plete antitumor response and T cell-mediated allograft rejection requiring reinitiation of hemodialys

207 hich is implicated in the process of chronic allograft rejection, also known as transplant vasculopat

208 included 1-year survival, cardiac or hepatic allograft rejection, and infection.

209 ment of autoimmune disease and prevention of allograft rejection, and our findings help inform therap

210 Within 10 years, 4% of eyes developed allograft rejection, no primary graft failures occurred,

211 Secondary outcomes included acute allograft rejection, opportunistic infections, graft and

212 anti-programmed cell death-1 (PD-1)-related allograft rejection.

213 reduced side effects in patients with renal allograft rejection.

214 locks memory and attenuates kidney and heart allograft rejection.

215 n between isolation and transplantation, and allograft rejection.

216 in animal models of autoimmune disorders and allograft rejection.

217 ehavior; values >=2.5 are predictive of late allograft rejection.

218 transplanted graft and potentiate subsequent allograft rejection.

219 suggest therapeutic approaches to ameliorate allograft rejection.

220 splant and was independently associated with allograft rejection.

221 ation to identify antibodies associated with allograft rejection.

222 Portal blood immediately following allograft reperfusion (liver flush; LF) had increased to

223 sition of donor ILC subsets is altered after allograft reperfusion and is associated with PGD develop

224 companied by elevated ILC2 frequencies after allograft reperfusion.Conclusions: The composition of do

225 Our data indicate VUE represents an allograft response, not an undetected infection.

226 ansplantation of a fully MHC mismatched skin allograft resulted in prolonged allograft survival.

227 cruitment into lymphoid follicles within the allograft, resulting in a significant increase in their

228 ejection and associated tissue injury in the allograft setting.

229 cytometry (iFCM) to explore the kinetics of allograft sEV release and the extent to which donor sEVs

230 Concordance between allograft skin and mucosa biopsy grades increased with a

231 c polyomavirus replication while maintaining allograft-sparing immune suppression.

232 owever, the very same mechanisms that induce allograft-specific T-cell suppression are also important

233 The three allograft specimens showed grade 2A acute T cell-mediate

234 splants became tolerant and showed long-term allograft survival (>100 d).

235 nor and recipient genotyping exhibited worse allograft survival (P=0.02).

236 DSA) has been associated with improved renal allograft survival after antibody-mediated rejection (AM

237 development of novel cell therapy to improve allograft survival after transplantation.

238 fined acute kidney injury (AKI) have similar allograft survival as non-AKI kidneys but are discarded

239 and recipients were analyzed for patient and allograft survival as well as renal outcomes following C

240 y activity in vivo, promoting long-term skin allograft survival in a stringent transplantation model.

241 t leads to significant prolongation of islet allograft survival in allosensitized recipients.

242 sed neovascularization and prolonged corneal allograft survival in an inducible nitric oxide synthase

243 The better allograft survival in the BK group over acute rejection

244 er se were not significantly associated with allograft survival in the entire study sample.

245 Corneal allograft survival is mediated by the variety of immunol

246 discarded kidneys would be expected to have allograft survival of 93.1% at 1 year, 80.7% at 5 years,

247 Two-year allograft survival was 91% and 55% in the 2 groups, resp

248 Allograft survival was analyzed employing the Kaplan-Mei

249 cted therapies have the potential to improve allograft survival while minimizing patient harm related

250 ation induces MDSCs and these cells regulate allograft survival, C57BL/6 donor hearts were transplant

251 ed-coil protein kinase inhibitor, on corneal allograft survival.

252 S13) treatment of graft recipients increased allograft survival.

253 hat promote long-term immunosuppression-free allograft survival.

254 nsplanted in Europe and calculated predicted allograft survival.

255 heart transplantation resulted in prolonged allograft survival.

256 heterotopic heart transplantation to assess allograft survival.

257 mune encephalitis and enabled long-term skin allograft survival.

258 nce of AMR, graft histological features, and allograft survival.

259 matched skin allograft resulted in prolonged allograft survival.

260 3 weeks significantly prolonged human islet allograft survival.

261 , with no difference in long-term patient or allograft survival.

262 otypes and to determine factors that predict allograft survival.

263 Five-year liver and kidney allograft survivals were 67% and 64% in the T-cell group

264 ) and 3179 (95%) who did and did not receive allografts that had undergone EVLP, respectively.

265 s I can enhance tolerance to subsequent skin allografts through indirectly expanded nTreg leading to

266 ly increase the available pool of donor lung allografts through the reconditioning of "marginal" orga

267 on lymphatic drainage from the tolerant lung allograft to the periphery.

268 netic loss of CoREST in Tregs impaired organ allograft tolerance and unleashed antitumor immunity via

269 Here, we demonstrate a dominant skin-allograft tolerance model induced by a single DST across

270 erestingly, disruption of coronin 1 promotes allograft tolerance while immunity towards a range of pa

271 ucidate mechanisms of antitumor immunity and allograft tolerance, and inform updates to transplant de

272 T cells, is important for the maintenance of allograft tolerance.

273 Subcutaneous allograft tumors with overexpression or knock-down of VC

274 ising the inflammatory infiltrates in kidney allografts undergoing acute and/or chronic rejection are

275 Third-party vascular allografts (VAs) are an invaluable resource in kidney an

276 Coronary allograft vasculopathy (CAV) assessed by coronary intrav

277 Cardiac allograft vasculopathy (CAV) is a major contributor of h

278 Cardiac allograft vasculopathy (CAV) is an increasingly importan

279 Cardiac allograft vasculopathy (CAV) is associated with intragra

280 cytomegalovirus (CMV) infection and cardiac allograft vasculopathy (CAV) were conducted on patients

281 this approach include attenuation of cardiac allograft vasculopathy (CAV), improvement in glomerular

282 after HTx and future development of cardiac allograft vasculopathy (CAV).

283 lar ejection fraction (n=104, 85%), coronary allograft vasculopathy (n=86, 70%), prior rejection (n=7

284 graphy angiography (CTA) to rule out cardiac allograft vasculopathy versus 16 patients without transp

285 exhibited early onset or accelerated cardiac allograft vasculopathy.

286 ate chronic allograft rejection and coronary allograft vasculopathy.

287 e rejection in vascularized composite tissue allograft (VCA) have been established by the Banff 2007

288 g vascularized composite allotransplantation/allografts (VCA) in the United States.

289 Consequently, a second same-donor islet allograft was rejected in an accelerated fashion by thes

290 Indeed, survival of the heart allografts was dependent on lymphatic drainage from the

291 The rate of BPAR of kidney allografts was low in both control (9.5%) and investigat

292 e kidneys, and spontaneously accepted kidney allografts were analyzed using flow cytometry and immuno

293 Lama5 and Lama4/Lama5 ratios in allografts were associated with the rejection severity.

294 Allografts were rapidly infiltrated by recipient leukocy

295 usion and reduced cellular infiltrate in the allograft, when compared with conventional prednisolone.

296 ived XOR inhibitor therapy pretransplant (11 allografts), while 8 patients did not receive such treat

297 treatment strategies for the recipient of an allograft with CMV reactivation based on prior use of an

298 asty, bone grafting using a mixture of human allograft with demineralized bone matrix human allograft

299 a deceased-donor small intestinal and colon allograft with standard immunosuppressive treatment, ach

300 ted B cell clonal expansion in human cardiac allografts with CAV.