ライフサイエンスコーパス: liver graft

1 patient survival while candidates wait for a liver graft.

2 one according to the biliary anatomy of the liver graft.

3 uate I/R-induced apoptotic cell death in the liver graft.

4 inhibitor for patients receiving their first liver graft.

5 ansient infiltrate within the first accepted liver graft.

6 e levels and also increased apoptosis in the liver graft.

7 hase and was repeated postreperfusion of the liver graft.

8 iscovered during back table preparation of a liver graft.

9 treatment, and 20 of them required a second liver graft.

10 tatus and degree of steatosis of a potential liver graft.

11 cell mobilizer, salvaged 5 of 10 whole fatty liver grafts.

12 reduced size liver grafts compared to whole liver grafts.

13 HCV genotype 1b infection in mice with human liver grafts.

14 therapy to stimulate regeneration of partial liver grafts.

15 hages as major sources of MMP-9 in steatotic liver grafts.

16 in chimpanzees and in mice containing human liver grafts.

17 r function to the level achieved using whole liver grafts.

18 xpression in NK cells, multiple tissues, and liver grafts.

19 CA triggers ischemic preconditioning (IP) in liver grafts.

20 ents in ischemia/reperfusion injury (IRI) to liver grafts.

21 ggesting that VEGF may have a role in IRI to liver grafts.

22 intervention to enhance the function of aged liver grafts.

23 n-is a major priority to optimize the use of liver grafts.

24 in both allogeneic and CD8+ T cell-depleted liver grafts.

25 affect the progression of HCV recurrence in liver grafts.

26 o fully restore accelerated rejection of TBI liver grafts.

27 el, creatinine level, and reduced-size/split liver grafts.

28 an, and increase the safer use of "marginal" liver grafts.

29 defense, and graft metabolic function in old liver grafts.

30 lets cause SEC apoptosis upon reperfusion of liver grafts.

31 nged survival of both cardiac and orthotopic liver grafts.

32 viral gene delivery method to cold preserved liver grafts.

33 n the rats that received long-term-preserved liver grafts.

34 rvival of rats that received 16-hr-preserved liver grafts.

35 n the survival of the spontaneously accepted liver grafts.

36 it is critical to improve the quality of DCD liver grafts.

37 e substantially increase safe utilization of liver grafts.

38 ut judicious use of extended criteria donors liver grafts.

39 increased usage of "higher risk" kidney and liver grafts.

40 All patients in era II received tPA flushed liver grafts.

41 , facilitating transplantation of very small liver grafts.

42 rtant benefits in preserving higher-risk DCD liver grafts.

43 e DA liver recipients from days 1 to 7 after liver grafting.

44 adenoviral infection (intestinal graft, 13; liver graft, 1).

45 ollowing recommendations for handling orphan liver grafts: (1) obtain predonation informed consent fr

46 tcomes were worse for NASH, HCV, and HCC for liver graft (72%, 66%, and 72% vs. 82%; hazard ratio, HR

47 imilar comparing group II versus group I for liver graft (78 vs 74%, P = 0.14) and patient survival (

48 Ten months after reappearance of LCH in the liver graft a follow-up cholangiography in one of the gi

49 In an attempt to reverse LEW liver graft acceptance, 180,000 units human IL-2 (hIL-2)

50 xpression and neutrophil accumulation in the liver graft after OLT compared with untransfected or AdL

51 ne triphosphate (ATP) content decay of mouse liver grafts after cold ischemia, warm ischemia, and com

52 d to quantify glycocalyx damage within human liver grafts after organ preservation and correlate the

53 ith antiinflammatory functions, will protect liver grafts after prolonged cold ischemia.

54 In viable liver grafts, all cell types recover from preservation/r

55 period with independent predictors of split-liver graft and recipient survival identified by multiva

56 Sirtuin1 expression is diminished in old liver grafts and correlates with mitochondrial and metab

57 status of dynamic preservation of kidney and liver grafts and describes ongoing research and emerging

58 It has been reported previously that liver grafts and liver cells seem to be tolerogenic, bas

59 (PTLD) in pediatric patients receiving first liver grafts and primarily immunosuppressed with tacroli

60 of glycocalyx degradation in effluents of 38 liver grafts and serum of patients undergoing OLT.

61 G levels track with operational tolerance of liver grafts and support favorable outcomes in pediatric

62 However, depletion of B cells from liver grafts and the absence of antibodies failed to alt

63 rtuin-1 expression/activity in old vs. young liver grafts and to determine correlations with mitochon

64 europathy (FAP) received an orthotopic split liver graft, and her explanted liver was donated to anot

65 ction/histological preservation of steatotic liver grafts, and extended their 14-day survival in lean

66 lization of cut down "reduced" livers, split liver grafts, and living-related donors has provided mor

67 s of ischemic injury of experimental partial liver grafts, and that its therapeutic targeting within

68 e donor mouse; back-table preparation of the liver graft; and transplant of the liver into the recipi

69 Mouse liver grafts are accepted across major histocompatibilit

70 Liver grafts are accepted across major histocompatibilit

71 MHC-mismatched liver grafts are accepted spontaneously between many mou

72 onate, pH, and glucose during ex situ NMP of liver grafts are accurate biomarkers of BDI and can be e

73 ic criteria for primary nonfunction (PNF) of liver grafts are based on clinical experience rather tha

74 Steatotic liver grafts are excluded for partial liver transplantat

75 Donation after circulatory death (DCD) liver grafts are known to be predisposed to primary nonf

76 e acutely rejected, the reciprocal LEW to DA liver grafts are spontaneously accepted.

77 or weight, and the use of reduced-size/split liver grafts are the most important factors affecting su

78 All liver grafts are well and functioning.

79 d multiple ducts, particularly in right lobe liver grafts, are major factors that contribute to bilia

80 We used acute infection of liver graft as a model to investigate the molecular mech

81 ciple for the generation of a transplantable liver graft as a potential treatment for liver disease.

82 of ESLD mandates simultaneous inclusion of a liver graft as well.

83 GFP(+) host cells were found in untreated WT liver grafts at 1 hour and included nucleated CD45(+) le

84 Because of the shortage of liver grafts available for transplantation, the restrict

85 Normothermic perfusion of liver grafts before transplantation effectively reduced

86 tive OLT in 1045 adult patients who received liver grafts between April 1985 and August 1995 were rev

87 ons that not only affect the function of the liver graft but may risk the life of the patient.

88 Liver graft but not recipient IFNAR deficiency was requi

89 iltrating T cells and why this occurs within liver grafts, but not heart or skin grafts, remain to be

90 IRF-1 deficiency in liver grafts, but not in recipients, resulted in signifi

91 ssing, the spontaneous acceptance of the LEW liver grafts by DA recipients was unaffected.

92 ether IP attenuates injury of small-for-size liver grafts by preventing free radical production and m

93 AdLacZ was delivered to cold preserved rat liver grafts by: (1) continuous perfusion via the portal

94 The recellularized liver grafts can be transplanted into rats, supporting h

95 Microsteatotic or 30% or less macrosteatotic liver grafts can be used safely up to BAR score of 18 or

96 transplantation when hepatopetal flow to the liver graft cannot be established by other techniques.

97 Compared to WT liver grafts, CD39(-/-) grafts exhibited enhanced inters

98 were significantly increased in reduced size liver grafts compared to whole liver grafts.

99 h the prognosis of cirrhosis and severity of liver graft damage after transplantation.

100 The mechanisms by which small-for-size liver grafts decrease survival remain unclear.

101 nearly all CD4+ thymocytes from human thymus/liver grafts, despite the fact that fewer than 5% of the

102 of 0.4), transduction rate in 3-hr preserved liver grafts, determined by 5-bromo-4-chromo-3-indolyl-b

103 In patients with end-stage liver graft disease and CKD, liver retransplantation ass

104 The development of liver graft disease is partially determined by individua

105 The use of anti-HBc+ liver grafts does not affect graft or patient survival.

106 Forty-three consecutive liver-graft donor/recipient pairs performed at our cente

107 that the glycocalyx is damaged within human liver grafts during preservation and the extent of glyco

108 e enables continuous oxygenated perfusion of liver grafts during procurement, splitting, and implanta

109 teria donation after brain death (DBD) human liver grafts during the last 7 years.

110 graft Function (MEAF) grades the severity of liver graft dysfunction.

111 irus disease 21 months after PTLD treatment (liver), graft dysfunction 25 months after PTLD (heart).

112 istent shortage and heterogeneous quality of liver grafts encourages the optimization of donor-recipi

113 [aHR] 2.63, P < 0.001), 1.6-fold increase in liver graft failure (aHR 1.62, P < 0.001), and 1.6-fold

114 ute rejection (13.3% vs 10.5%, P = 0.36) and liver graft failure requiring re-transplantation (3.2% v

115 sociation between race/ethnicity and sex and liver graft failure risk, accounting for DRI.

116 c allografts, also seen in chronic renal and liver graft failure, is luminal stenosis of blood vessel

117 ent and donor TM6SF2 rs58542926 genotypes on liver graft fat content after liver transplantation.

118 ted data on 827 patients receiving a primary liver graft for chronic liver disease, we used a self-or

119 A total of 64 adult patients receiving first liver grafts for a variety of indications were randomize

120 sions made by transplant surgeons to decline liver grafts for local use are based on both objective a

121 A shortage in appropriate-sized liver grafts for pediatric patients led to the use of se

122 generate a significant number of additional liver grafts for transplantation every year, thus greatl

123 isms underlying the failure of fatty partial liver grafts (FPG) remain unknown.

124 s who underwent liver transplantation with a liver graft from a brain-dead donor whose cause of death

125 control group of 54 patients who received a liver graft from donors aged 20 to 49 years (D20-49 grou

126 w that ischemic preconditioning protects the liver graft from subsequent long-term cold preservation-

127 Liver grafts from C57B1/6 mice were procured and preserv

128 Liver grafts from CA donors function similarly to grafts

129 After 1998, 40 liver grafts from cadaveric donors were divided, and all

130 about using such an approach for division of liver grafts from cadaveric donors, and many teams prefe

131 orts describing the national experience with liver grafts from donation after cardiac death (DCD) don

132 Whole liver grafts from donors age less than or equal to 13 ye

133 as to analyze our experience with the use of liver grafts from donors whose cause of death is suicida

134 CD4+ T cells, but not iNKT cells, protected liver grafts from early IRI.

135 Liver grafts from ECD can be used to dramatically reduce

136 finding may have high clinical relevance, as liver grafts from extended DBD or DCD donors carry consi

137 Survival of liver grafts from FL donors was markedly prolonged by CT

138 C3H (H2k) recipients of orthotopic liver grafts from FL-treated B10 (H2b) donors were given

139 Therefore, C3H (H2(k)) recipients of liver grafts from Flt3 ligand-treated B10 donors were gi

140 We reviewed our experience with liver grafts from hepatitis-B surface antigen (HBsAg)(-)

141 ficacy of the HMP Airdrive system to protect liver grafts from lethal ischemic damage before transpla

142 rolimus (1 mg/kg), whereas in a third group, liver grafts from Lewis rats underwent HOPE or deoxygena

143 ugust 1998 and July 2000, 48 adults received liver grafts from living donors.

144 ility of ischemic preconditioning to protect liver grafts from long-term preservation-reperfusion inj

145 Use of liver grafts from non-heart-beating donors (NHBDs) warra

146 he period June 1, 2005 to December 31, 2014, liver grafts from ODAT donors had a significantly higher

147 In our preliminary experience, recipients of liver grafts from older CNHBDs had an outcome equivalent

148 rict evaluation of the donors and brief CIT, liver grafts from older CNHBDs may be used to expand the

149 Here, we report our experience using liver grafts from older CNHBDs.

150 and unperfused DCD livers were compared with liver grafts from standard brain dead donors (n = 50), a

151 ransplantation was performed using steatotic liver grafts from Zucker rats transplanted into lean rec

152 the perfusate provides a fast prediction of liver graft function and loss during ex situ MP before i

153 and (ii) effects of inhibition of calpain on liver graft function using the isolated perfused rat liv

154 Liver graft function, injury, and IP benefit were examin

155 an be pharmacologically modulated, improving liver graft function.

156 of severe I/R injury and a predictor of poor liver graft function.

157 wever, use of moderate or severely steatotic liver grafts (>30% macrosteatosis) resulted in acceptabl

158 e absence of cardiac arrest in donors, older liver grafts (>75 years) may be safely attributed to non

159 Older liver grafts have been considered in the past decade due

160 Small-for-size liver grafts have decreased survival compared to full-si

161 hanisms underlying impaired function of aged liver grafts have not been fully elucidated, but mitocho

162 ing cold-ischemic storage and reperfusion of liver grafts, HSCs can interact directly with cells of t

163 ediatric recipients of parental living donor liver grafts, identified as operationally tolerant throu

164 ediatric recipients of parental living donor liver grafts, identified as operationally tolerant throu

165 IRF-1 was induced in liver grafts immediately after reperfusion in both human

166 n by pure laparoscopic total hepatectomy and liver graft implantation using a preexisting midline inc

167 ents, and resulted in acute rejection of the liver grafts in 9-20 days.

168 ession is upregulated in young, but not old, liver grafts in response to cold storage and reperfusion

169 e seen, exists for HIV-1 infection of thymus/liver grafts in SCID-hu mice.

170 arly relevant for transplantation of partial liver grafts in the living donor setting.

171 transplantation recipients who received NMP liver grafts in the QEHB between 2013 and 2016 were comp

172 Histologically, the liver grafts in treated animals demonstrated more injury

173 followed by transplantation, the survival of liver grafts increased from 50% in Ad-beta-gal untreated

174 entry inhibitors have been shown to prevent liver graft infection in animal models and delay graft i

175 challenges and pathology associated with HCV liver graft infection, highlight current and future stra

176 rther clinical development for prevention of liver graft infection.

177 renewed hope for prevention and treatment of liver graft infection.

178 Freshly isolated liver graft-infiltrating cells harvested on days 4 and 7

179 Plant polyphenols decrease liver graft injury and increase survival of small-for-si

180 nor pretreatment with AdiNOS led to improved liver graft injury and posttransplantation survival.

181 r transplantation, it is unclear whether the liver graft is colonized by virions present in the circu

182 CV-positive liver transplant recipients, the liver graft is colonized primarily by liver-derived viru

183 Since 1998, in our center, when a donor-liver graft is divided we prefer retaining the main vess

184 n the IFN-gamma receptor and reveal that the liver graft is equipped with machineries capable of coun

185 The estimation of steatosis in a liver graft is mandatory prior to liver transplantation,

186 mited the development of a tissue-engineered liver graft is oxygen and nutrient transport.

187 However, reinfection of the liver graft is still common, especially in patients with

188 main selection criteria of the quality of a liver graft is the degree of steatosis, which will deter

189 In many countries, the allocation of liver grafts is based on the Model of End-stage Liver Di

190 CMV) on recurrent hepatitis C virus (HCV) in liver grafts is controversial.

191 Normothermic machine perfusion (NMP) of liver grafts is increasingly being incorporated in clini

192 ic oxygenated perfusion (HOPE), used for DCD liver grafts, is based on cold perfusion for 1 hour by a

193 above the median, and the presence of severe liver graft ischemia-reperfusion damage.

194 and transplanted into WT recipients chimeric liver grafts lacking B7-H1 on parenchymal cells or BMDCs

195 hese patients, odds of patient mortality and liver graft loss were about 1.2-fold and twofold higher

196 domized trials report cellular rejection and liver graft loss when mycophenolate mofetil (MMF) monoth

197 Low-grade macrosteatotic liver grafts (</=30% macrosteatosis) resulted in 5-year

198 hepatic steatosis causes failure of partial liver grafts, most likely by increasing RNS that leads t

199 jury and increase survival of small-for-size liver grafts, most likely by scavenging free radicals.

200 d with untreated Lewis recipients of hamster liver grafts, MST=6.0 days, n=6).

201 lly preserved (static cold preservation) DCD liver grafts (n = 50) from 2 well-established European p

202 Old and young rat liver grafts (N = 7 per group) were exposed to 12 h of s

203 CD) donation in 1 participating center, each liver graft of this center was pretreated with the new m

204 e humoral immune response and reinfected the liver graft of transplant patients, it may be a valuable

205 ever, immediately after transplantation, the liver graft of viremic patients universally becomes infe

206 ained the Y chromosome in syngeneic XX to XY liver grafts or when the hosts of Lewis XX to DA XY allo

207 , B, and AB (P<0.03), and reduced-size/split liver grafts (P<0.02).

208 Liver graft perfusate-derived KCs and in vitro-generated

209 and improves regeneration of small-for-size liver grafts, possibly by increasing mitochondrial Mn-SO

210 Donor brain death and prolonged liver graft preservation do not interact significantly t

211 Our results demonstrate that cDCD liver grafts preserved with NRP appear far superior to t

212 erventions could decrease the fat content of liver grafts prior to transplantation.

213 Use of liver grafts procured after circulatory death is an effe

214 ed retrospectively to assess the survival of liver grafts procured from HCV+ donors.

215 Liver grafts procured from heart-beating donors and pres

216 th prolonged ex vivo cold storage to explore liver graft protection.

217 times of organ scarcity and extended use of liver grafts, protective strategies in transplantation a

218 This study shows that while liver graft quality differed significantly by recipient

219 One hundred seventy-nine (6.2%) of 2908 liver graft recipients and 944 (6.1%) of 15520 kidney gr

220 Four hundred eighty-six liver graft recipients were genotyped for TGF-beta1 codo

221 Right lobe liver graft recipients who have variant right biliary an

222 easured TGFbeta levels in blood samples from liver graft recipients who were of known TGFbeta1-respon

223 Both adult and pediatric liver graft recipients will be studied, in comparison to

224 at an elevated MDC:PDC ratio associates with liver graft rejection, which occurs after first year in

225 have a deleterious effect on the recovery of liver grafts requiring significant regeneration.

226 In this study, we have shown that NMP liver grafts return better coagulation profiles intraope

227 interval [CI] 1.53-5.51); reduced-size/split liver grafts (RR 2.53, CI 1.30-5.64); and UNOS status I

228 d mice implanted with human fetal thymus and liver grafts (SCID-hu Thy/Liv mice) to KSHV infection.

229 However, LTx with chimeric liver grafts showed that grafts lacking hepatocellular I

230 499A allele is an independent risk factor of liver graft steatosis after liver transplantation that i

231 ient survival at 1 and 2 years was 100%, the liver graft survival 100%, and the bowel graft survival

232 eir effects on sensitization, rejection, and liver graft survival are not well known.

233 Data on patient and liver graft survival comparing liver transplantation alo

234 te an increase in overall 1-year patient and liver graft survival only in those patients on long-term

235 Kaplan-Meier methods were used to calculate liver graft survival rates, Cox proportional hazard mode

236 BV/HCV coinfection was associated with worse liver graft survival than HBV or HCV mono-infection.

237 Liver graft survival within 90 days of OLT and early pos

238 seven recipients of reduced sized alcoholic liver grafts survived long term.

239 s were examined in 121 recipients of primary liver grafts, surviving > or = 30 days.

240 The full liver graft that underwent NMP via the umbilical vein fo

241 died in a series of 53 consecutive cadaveric liver grafts that were divided for transplantation.

242 tution has offered all children with failing liver grafts the option of retransplantation regardless

243 adults undergo transplantation with partial liver grafts, the unique features of these segments and

244 s been applied to hepatic bile from selected liver grafts to evaluate its potential role in graft ass

245 Exposure of donor liver grafts to prolonged periods of warm ischemia befor

246 as not solved the problem, because steatotic liver grafts tolerate ischemia-reperfusion (I/R) injury

247 in the sera from Lewis recipients of hamster liver grafts treated with anti-CD4 mAb and hCTLA4Ig was

248 (NMP-L) is a novel technique that preserves liver grafts under near-physiological conditions while m

249 h could be attributed to the preservation of liver grafts under physiological conditions.

250 d with hypothermic machine perfusion, 1 full liver graft underwent NMP for 4 hours, and 1 left latera

251 stigated the possible role of VEGF in IRI to liver grafts using a syngeneic rat orthotopic liver tran

252 a novel approach to generate transplantable liver grafts using decellularized liver matrix.

253 were used as recipients of hamster heart or liver grafts using different regimens of FK506 and Lef.

254 Liver graft viability assessment has long been considere

255 increasing numbers of patients on kidney and liver graft waiting lists.

256 The volume of the liver graft was doubled 2 weeks after the first procedur

257 The liver graft was reduced and latero-lateral caval anastom

258 the four patients receiving the extra split-liver graft was reduced significantly to 37 days (range

259 Apoptotic activity within liver grafts was determined by terminal deoxynucleotidyl

260 ide, activation of inflammatory mediators in liver grafts was significantly inhibited.

261 Interestingly, MMP-9 activity in steatotic liver grafts was, to a certain extent, independent of th

262 ansplantation, using whole or partial murine liver grafts, was performed following cold preservation

263 ic I/R injury, and using B7-H1 knockout (KO) liver grafts, we tested this hypothesis in the mouse LT

264 tive mortality rates after 3rd, 4th, and 5th liver graft were 25%, 14%, and 50%, respectively.

265 l organs other than one kidney and one split liver graft were functioning at 1 yr post-transplant.

266 Consecutive pediatric recipients of a first liver graft were immunosuppressed with oral tacrolimus (

267 However, early results with DCD liver grafts were associated with a greater incidence of

268 pic liver transplant recipients receiving 89 liver grafts were evaluated.

269 Until March 2018, liver grafts were offered to a center and allocated to a

270 increase blood inflow, arterialized partial liver grafts were performed without changing the outcome

271 Of the 70 donors, 66 (94%) liver grafts were procured by laparoscopy, whereas 4 (6%

272 Ten donor liver grafts were procured, four (40%) from donation aft

273 e, and MHV tributaries of the 640 right lobe liver grafts were reconstructed with AVG.

274 een hours after confirmation of brain death, liver grafts were retrieved.

275 Twenty-one deceased liver grafts were split into full right and full left lo

276 A total of 132 and 93 liver grafts were transplanted after NRP and HOPE, respe

277 Either Lewis or dark agouti rat liver grafts were transplanted into Lewis recipients to

278 When B7-H1 KO liver grafts were transplanted into WT recipients, serum

279 diatric patients led to the use of segmental liver grafts, which became the predominant graft used in

280 ent of syngeneic rats (n=10) that received a liver graft with a 16-hr cold ischemia time in Euro-Coll

281 ncrease the survival of rats that received a liver graft with a 16-hr cold ischemia time, and the sur

282 e possibility of genetic modification of the liver graft with a recombinant adenovirus vector encodin

283 In this case report, we present a liver graft with abnormal left hepatic vein draining dir

284 ontrast, 87.5% of rats (n=8) that received a liver graft with ischemic preconditioning (10-10 group)

285 The liver graft with severe macrovesicular steatosis was don

286 val, 12.64-310.19; P < 0.001) and the use of liver grafts with a graft-to-recipient weight ratio less

287 The authors found that liver grafts with absent carcinoembryonic antigen-relate

288 cy using three different delivery methods to liver grafts with adenoviral vector encoding the LacZ ma

289 There were 14 liver grafts with documented HAT (2.62%) in 13 patients.

290 Recipients of liver grafts with ischemic preconditioning had significa

291 cal trial (n = 6) to identify transplantable liver grafts with low BDI.

292 ed safely up to BAR score of 18 or less, but liver grafts with more than 30% macrosteatotis should be

293 amethasone at the time of transplantation of liver grafts with prolonged cold storage (16 hours).

294 , we treated recipients of lean or steatotic liver grafts with saline or CR2-Crry.

295 roach to reducing the preservation injury to liver grafts with the human Bcl-2 gene.

296 of creating fully functional transplantable liver grafts with this whole liver engineering approach.

297 Liver division can be performed safely in liver grafts with variant LHV anatomy, if appropriate te

298 Recipients of livers grafts with greater glycocalyx damage might be at

299 While untreated LEW recipients rejected DA liver grafts within 13 days, DA recipients accepted LEW

300 eased bile flow, compared with recipients of liver grafts without ischemic preconditioning.