ライフサイエンスコーパス: liver graft

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

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

3 inhibitor for patients receiving their first liver graft.

4 ansient infiltrate within the first accepted liver graft.

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

6 hase and was repeated postreperfusion of the liver graft.

7 iscovered during back table preparation of a liver graft.

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

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

10 patient survival while candidates wait for a liver graft.

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

12 in chimpanzees and in mice containing human liver grafts.

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

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

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

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

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

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

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

20 affect the progression of HCV recurrence in liver grafts.

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

22 o fully restore accelerated rejection of TBI liver grafts.

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

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

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

26 lets cause SEC apoptosis upon reperfusion of liver grafts.

27 nged survival of both cardiac and orthotopic liver grafts.

28 viral gene delivery method to cold preserved liver grafts.

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

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

31 n the survival of the spontaneously accepted liver grafts.

32 , facilitating transplantation of very small liver grafts.

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

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

35 reduced size liver grafts compared to whole liver grafts.

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

37 therapy to stimulate regeneration of partial liver grafts.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 Mouse liver grafts are accepted across major histocompatibilit

60 Liver grafts are accepted across major histocompatibilit

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

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

63 Steatotic liver grafts are excluded for partial liver transplantat

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

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

66 All liver grafts are well and functioning.

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

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

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

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

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

72 een 1990 and 1994, 209 patients received 223 liver grafts at our institution.

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

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

75 Liver graft but not recipient IFNAR deficiency was requi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Liver grafts from CA donors function similarly to grafts

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

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

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

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

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

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

113 Liver grafts from ECD can be used to dramatically reduce

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Early liver graft function, as assessed by lactate dehydrogena

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

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

133 an be pharmacologically modulated, improving liver graft function.

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

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

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

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

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

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

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

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

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

143 survival, we recommend cautious use of older liver grafts in healthier recipients.

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

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

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

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

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

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

150 rther clinical development for prevention of liver graft infection.

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

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

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

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

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

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

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

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

159 Procurement-related injury to the liver graft is minimized without compromising pancreas g

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

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

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

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

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

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

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

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

168 ake was evaluated in six study groups: fresh liver grafts, livers preserved for 12 hr, 24 hr, 30 hr a

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

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

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

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

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

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

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

176 s present a clinicopathologic study of small liver grafts obtained from living donors.

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

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

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

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

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

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

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

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

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

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

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

188 Liver grafts procured from heart-beating donors and pres

189 These liver grafts produced high levels of C6 that reconstitut

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

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

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

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

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

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

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

197 on, resulting in second-set or "accelerated" liver graft rejection, within 4-5 days.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Apoptotic activity within liver grafts was determined by terminal deoxynucleotidyl

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

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

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

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

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

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

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

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

233 The liver grafts were comprised on 155 whole-organ, 24 reduc

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

235 The liver grafts were orthotopically transplanted after 48 h

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

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

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

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

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

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

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

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

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

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

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

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

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

249 The liver graft with severe macrovesicular steatosis was don

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

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

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

253 Recipients of liver grafts with ischemic preconditioning had significa

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

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

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

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

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

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

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

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

262 Twenty-four whole liver grafts (WLG) and 49 reduced size grafts (3 right l

263 rus mediated gene transfer of TGF-beta1 into liver grafts would enhanced local expression of this rec