ライフサイエンスコーパス: liver allograft

1 issue, indicating an ectopic origin from the liver allograft.

2 intains the celiac trunk with the left-sided liver allograft.

3 This, in turn, may adversely affect the liver allograft.

4 e to Gilbert's syndrome acquired through the liver allograft.

5 stula with cholestatic damage to the reduced liver allograft.

6 jects who received a heart, lung, kidney, or liver allograft.

7 e reported immunoprotection conferred by the liver allograft.

8 plantation patients that received an HLA-A2+ liver allograft.

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

10 m mononuclear cells infiltrating a rejecting liver allograft.

11 le of inflammation and fibrosis in long-term liver allografts.

12 ession in the hepatocytes and lymphocytes of liver allografts.

13 tes in both acute rejection and tolerance of liver allografts.

14 0) may reduce the extent of IRI in steatotic liver allografts.

15 ution are both used for cold preservation of liver allografts.

16 , may play a role in the immune privilege of liver allografts.

17 50 consecutive PSC patients who received 174 liver allografts.

18 luence both short- and long-term survival of liver allografts.

19 ing-related donor, and 36 were in situ split-liver allografts.

20 proliferating naive T lymphocytes in situ in liver allografts.

21 n activity recently has been demonstrated in liver allografts.

22 s well as preservation-reperfusion injury of liver allografts.

23 posttransplant complications and underuse of liver allografts.

24 d States to address the increased demand for liver allografts.

25 of intralobular immune synapse formation in liver allografts.

26 applicability to prevent HCV reinfection of liver allografts.

27 led to increased utilization of higher risk liver allografts.

28 infiltration after reperfusion of cadaveric liver allografts.

29 tic role in preventing biliary strictures in liver allografts.

30 laxis in recipients of HBsAg(-), anti-HBc(+) liver allografts.

31 -liver procurements resulted in 24 segmental liver allografts; 11 right trisegments, 11 left lateral

32 e of recurrent hepatitis C is seen in 90% of liver allografts; (2) Histologic hepatitis C recurs with

33 Eligible patients received liver allografts 6-144 months previously and maintenance

34 Liver allograft (93.3% vs 93.1%, P = .29), kidney allogr

35 These results indicate that spontaneous rat liver allograft acceptance is associated with the presen

36 normal recipients abrogated the spontaneous liver allograft acceptance normally observed and resulte

37 gulation, may be responsible for spontaneous liver allograft acceptance.

38 Hepatitis C virus (HCV) reinfection of the liver allograft after transplantation is universal, with

39 steatotic donor livers, and reutilization of liver allografts after brain death of the first recipien

40 entially accumulate within the donor pool in liver allografts, among hepatic virus-specific and tumou

41 year OS rate was 45.3% for those receiving a liver allograft and 12.5% for those treated with PVE and

42 s bone marrow infusion or a Lewis orthotopic liver allograft and a short course of immunosuppression.

43 Overall liver allograft and patient survival rates of LTA patien

44 LKT is preferable to LTA because it improves liver allograft and patient survival.

45 ibility that hemochromatosis recurred in the liver allograft and review possible factors contributing

46 noninvasive means of diagnosing AR in human liver allografts and for discriminating AR from intragra

47 to result in improved function of steatotic liver allografts and increased survival of recipients an

48 putative activation receptor is expressed in liver allografts and may participate in the innate immun

49 ngs demonstrate that long-term acceptance of liver allografts and tolerance induction is not dependen

50 ose observed for recipients of cadaver donor liver allografts and vertebral body marrow infusions.

51 s according to the immunologic status of the liver allograft, and hepatocyte-derived NO may be protec

52 us inflammation and cellular infiltration in liver allografts, and a mean graft survival time (MST) o

53 and consensus criteria for the diagnosis of liver allograft antibody-mediated rejection and provide

54 Liver allografts are accepted across major histocompatib

55 he liver is an immunologic privileged organ; liver allografts are accepted across major histocompatib

56 tible DA (RTl(a)) to Lewis (RT1(1), LEW) rat liver allografts are acutely rejected, the reciprocal LE

57 In the MELD era, liver allografts are first allocated to recipients with

58 4(+) regulatory T cells was increased in the liver allograft as well as in the peripheral blood.

59 s play an important role in the rejection of liver allografts, as is true for other vascularized graf

60 ng the lobular inflammation within long-term liver allografts assists in identifying those patients i

61 lant centers to truly optimize the number of liver allografts available from the cadaveric pool.

62 analysis, the ratio of listed candidates to liver allografts available had a significant effect on w

63 ty metric, the ratio of listed candidates to liver allografts available varied from 1.3 (region 11) t

64 isted for liver transplantation: 5,285 adult liver allografts became available, and 5,471 adult recip

65 to adult intestinal transplantation without liver allograft between 2015 and 2018.

66 onsecutive patients who received their first liver allograft between January 1 and December 31, 1993,

67 dose Tac to 40 adult recipients of cadaveric liver allografts between December 2001 and April 2003.

68 Median survival of technically successful liver allografts between pairs of outbred pigs (n=20) wa

69 The progression of parenchymal changes in liver allograft biopsies due to preservation-reperfusion

70 oarray profiling of RNA from sera matched to liver allograft biopsies from patients with nonimmune, n

71 rved centrilobular necrosis (CLN) in several liver allograft biopsies in our pediatric liver transpla

72 and 3.6 +/- 3.1) compared to BECs in normal liver allograft biopsies or those with nonspecific chang

73 informative miRNAs in 91 sera matched to 91 liver allograft biopsies were quantified using customize

74 f grading was prospectively applied to 2,038 liver-allograft biopsies from 901 adult tacrolimus-treat

75 We examined protocol annual review liver allograft biopsy specimens in consecutive adult pa

76 in both rejected and spontaneously accepted liver allografts, but not in syngeneic or cyclosporine A

77 Examination of the liver allografts by in situ terminal deoxynucleotidyltra

78 the syngeneic parenchymal environment of the liver allografts constitutes a privileged site for persi

79 performed to investigate whether an existing liver allograft could protect a kidney allograft from im

80 this study, we investigated the rejection of liver allografts deficient in the IFN-gamma receptor and

81 flow cytometry, and we examined the fate of liver allografts depleted of passenger B cells in either

82 an OPO surgeon was associated with decreased liver allograft discard and increased utilization of mar

83 mployed, organ-procurement specialist has on liver allograft discard rate, marginal organ utilization

84 During the first 3 days after liver allografting, donor B cells rapidly migrated from

85 The patterns of chemokine expression in liver allografts during rejection suggest that the recru

86 hich characterize the various causes of late liver allograft dysfunction.

87 aft FFPE C4d staining: (a) can help classify liver allograft dysfunction; (b) substantiates antibody

88 d determines the impact of extended criteria liver allografts (ECD).

89 matic utilization of extended donor criteria liver allografts (EDC), including living donor allograft

90 CV)-positive patients receiving HCV-positive liver allografts either the donor or recipient strain ov

91 was a significant risk factor for kidney and liver allograft failure and patient mortality.

92 prolonged cold ischemia interact to increase liver allograft failure at 90 days.

93 itive diagnosis and 21 days later, died from liver allograft failure because of recurrent lymphoma.

94 y associated with composite risk of death or liver allograft failure.

95 community remains that elderly recipients of liver allografts fare as well as their younger counterpa

96 Liver allograft FFPE C4d staining: (a) can help classify

97 Fibrosis was assessed by the Liver Allograft Fibrosis Semiquantitative score, inflamm

98 tissue staining and interpretation, staging liver allograft fibrosis, and findings related to immuno

99 Liver allografts for eight adult recipients were procure

100 Adequate preservation of liver allografts for transplantation is essential for su

101 eographic inequities mar the distribution of liver allografts for transplantation.

102 We report a novel case of the use of a liver allograft from a donor whose oxygen delivery was m

103 arity is needed on the impact of receiving a liver allograft from a donor with diabetes on post-LT ou

104 re grouped as having received a living donor liver allograft from either an offspring or a nonoffspri

105 The use of liver allografts from an older donor (OD) (age>50 years)

106 eived donation after circulatory death (DCD) liver allografts from donors aged >60 y.

107 The use of liver allografts from elderly donors (>/=70 years) has i

108 results was 1.5% in HCV NAT - recipients of liver allografts from HCV Ab + /NAT - donors.

109 cleic acid test (NAT) negative recipients of liver allografts from HCV antibody-positive/NAT-negative

110 OS database suggests that transplantation of liver allografts from HCV+ donors to HCV+ recipients res

111 resulted in the most effective protection of liver allografts from IRI, as measured by serum transami

112 ed production of TGF-beta2 by BEC can modify liver allograft function by enhancing the de-differentia

113 hypertension and liver disease can influence liver allograft function over time.

114 left ventricular ejection fraction and good liver allograft function were demonstrated.

115 of adults and 64% of children with excellent liver allograft function, on minimal or dual immunosuppr

116 ated rejection, attention should be given to liver allograft function, previous failed transplants, a

117 Female recipients of offspring liver allografts had both inferior 10-year graft (52% ve

118 In total 869 OPO-Present liver allografts had similar rates of discard (5.2%) com

119 Use of living-related and in situ split-liver allografts has dramatically reduced waiting times

120 Liver allografts have been thought to be immunoprotectiv

121 mmunoinhibitory effects that could influence liver allograft immunogenicity.

122 al vein were maintained with the right-sided liver allograft in all cases.

123 iac trunk was maintained with the left-sided liver allograft in nine cases.

124 ansplantation may be an unnecessary use of a liver allograft in these patients.

125 and -13) induced indefinite survival of ACI liver allografts in Lewis (RT1l) recipients ( > 250 days

126 by transplantation of CTLA4Ig-transduced ACI liver allografts in Lewis recipients.

127 ly demonstrated by spontaneous acceptance of liver allografts in many species, results from an immune

128 recognized by the spontaneous acceptance of liver allografts in many species.

129 This is the case in animal models; liver allografts in mice are spontaneously accepted with

130 Strategies to increase the number of liver allografts include liver splitting, use of donors

131 optimize the utilization and outcomes of DCD liver allografts, including donor-recipient matching, pe

132 fter a short course of tacrolimus, Lewis rat liver allografts induce donor-specific nonreactivity in

133 lammatory cytokines, and protects from early liver allograft injury.

134 ing in almost 50% of patients with a failing liver allograft, is costly and uses scarce donor organs

135 ed hemodynamics, decreased bleeding, reduced liver allograft ischemic time, and may result in reduced

136 were slightly higher in the DSA + group, but liver allograft, kidney allograft, and patient survival

137 Expanded regional sharing of liver allografts may increase cold ischemia and allograf

138 Patients with chronic rejection of liver allografts may show persistently high cyclosporine

139 e perfusion (NMP) preservation of kidney and liver allografts minimizes CS-associated IRI; however, i

140 g allo-antibody-mediated injury; and (b) how liver allografts modulate immune reactions.

141 Human liver allografts (n = 8) were then exposed to 6-h of NMP

142 t HCC (most frequently in lungs [n = 18] and liver allograft [n = 16]) in a single site in 19 patient

143 n, outcomes, and retransplantation (ReTx) of liver allografts obtained by donation after cardiac deat

144 have shown that rejection and loss of human liver allografts occurs despite immunosuppression.

145 nd the appearance of AAT globules within the liver allograft of a heterozygous donor may be related.

146 dies, were administered in 101 recipients of liver allografts (OLTX).

147 e evidence comparing preservation fluids for liver allografts on transplant outcomes.

148 17 pretransplantation variables on long-term liver allograft outcome was analyzed.

149 lation of hepatic inflammatory responses and liver allograft outcome.

150 hat were obtained from children who received liver allografts over a 4-year period were reviewed.

151 < 0.001), and a higher utilization rate for liver allografts (P = 0.007).

152 The Banff Working Group on Liver Allograft Pathology met in September 2022.

153 The Banff Working Group on Liver Allograft Pathology reviewed and discussed literat

154 The Banff Working Group on Liver Allograft Pathology undertook a study to determine

155 se, and decreased Treg response in renal and liver allograft patients.

156 iving heart grafts from the Lewis orthotopic liver allograft pretreated group are near normal and fre

157 ctor was used to perfused cold preserved ACI liver allograft prior to transplantation into Lewis reci

158 Liver allograft provided renal graft immunoprotection if

159 Liver allografts rarely undergo hyperacute rejection, bu

160 Lewis recipients of DA liver allografts received immunosuppressive agents after

161 and titer of cold agglutinins in 327 primary liver allograft recipients and analyzed their relationsh

162 phylaxis is recommended in anti-HBc-positive liver allograft recipients and anti-HBc alone individual

163 d from the prospective database of all adult liver allograft recipients and compared to matched data

164 demia and hypertension have been reported in liver allograft recipients and contribute to an increase

165 n conclusion, ICV occurs in 16% of pediatric liver allograft recipients and does not appear to be rel

166 allograft recipients prompted study of DSA+ liver allograft recipients as measured by lymphocytotoxi

167 median follow-up, 35 (3.3%) of 1049 primary liver allograft recipients first developed CR between 16

168 en sporadically discontinued by noncompliant liver allograft recipients for whom an additional 4 1/2

169 acrolimus were studied retrospectively in 94 liver allograft recipients from a North American and a E

170 Liver allograft recipients have a greater risk of cardio

171 up to 2 years in a prospective cohort of 27 liver allograft recipients showed only two patients to b

172 Nineteen orthotopic liver allograft recipients were converted from azathiopr

173 One hundred fifty liver allograft recipients were prospectively monitored

174 Lastly, we also report that liver allograft recipients with plasma cell hepatitis ha

175 virin are effective in a small proportion of liver allograft recipients with recurrent hepatitis C.

176 evels correlate with active CMV infection in liver allograft recipients.

177 nd could be used in a preemptive strategy in liver allograft recipients.

178 onic rejection in a large group of pediatric liver allograft recipients.

179 atient, their family, or the other potential liver allograft recipients.

180 Th2 cytokine profiles were characterized in liver allograft recipients.

181 n of oral tacrolimus disposition in 8 stable liver allograft recipients.

182 rus (R-HCV) are significant complications in liver allograft recipients.

183 say of T-cell function to study 71 long-term liver allograft recipients.

184 Early chronic liver allograft rejection (CR) is characterized by disti

185 The development of liver allograft rejection across non-MHC differences is

186 changes in the phenotype of BEC during acute liver allograft rejection and the mechanism driving thes

187 erature evidence regarding antibody-mediated liver allograft rejection at the 11th, 12th, and 13th me

188 Inhibition of acute liver allograft rejection by CTLA4Ig, linked to restorat

189 soluble Fas diminish in patients undergoing liver allograft rejection in contrast to patients with s

190 al immune reactivity and inhibits second-set liver allograft rejection in presensitized recipients.

191 lone was also tested to block small bowel or liver allograft rejection in rats.

192 r corticosteroids for the treatment of acute liver allograft rejection is associated with severe toxi

193 Liver allograft rejection is mediated by a primary respo

194 Early chronic liver allograft rejection is potentially reversible and

195 er, survival was significantly shortened and liver allograft rejection was accelerated in SLA-mismatc

196 When acute liver allograft rejection was induced by administration

197 significantly reduce the incidence of acute liver allograft rejection, allow a significant reduction

198 as lethal TBI in preventing mouse second-set liver allograft rejection, and to evaluate the role of p

199 ition, effector cells and pathways mediating liver allograft rejection, the role of regulatory T cell

200 s involved in the hepatocyte loss of chronic liver allograft rejection.

201 olecule expression is increased during acute liver allograft rejection.

202 ng viral and autoimmune hepatitis as well as liver allograft rejection.

203 did not reverse renal dysfunction nor cause liver allograft rejection.

204 x PTPN22 SNPs on the susceptibility to acute liver allograft rejection.

205 tionally accepted standard for grading acute liver-allograft rejection, but it has not been prospecti

206 nsfer to MMF should be considered to prevent liver-allograft rejection.

207 Moreover, recipients of human liver allografts require less immunosuppression than do

208 thymus by direct DNA injection, followed by liver allografting, results in donor-specific unresponsi

209 chnique to retrieve intestine, pancreas, and liver allografts safely from the same donor and to trans

210 Liver allograft sections showed a positive correlation (

211 ogressive fibrosis suggests that a subset of liver allografts seem resistant to the chronic injury th

212 n patients with CRLMs, but in North America, liver allograft shortages make the use of deceased-donor

213 If indeed as a community we feel that liver allografts should not be distributed to patients w

214 LRD liver allografts showed minimal changes postreperfusion.

215 Results of studies in adult recipients of liver allograft suggest that tacrolimus is more efficaci

216 lerance in pediatric and adult recipients of liver allografts, suggesting a high incidence of a pro-t

217 We found significant differences in liver allograft supply and demand--but these differences

218 Recipients with long-term liver allograft survival accepted ACI but not PVG skin g

219 ocytes secreting alloantigen showed extended liver allograft survival and decreased cytotoxic T lymph

220 reactive T cell population, is important for liver allograft survival and tolerance induction.

221 antation variables associated with long-term liver allograft survival in 278 children who underwent t

222 Posttransplant TLI prolonged ACI (RT1(a)) liver allograft survival in Lewis (RT1(b)) hosts, with 5

223 Prolongation of liver allograft survival in presensitized recipients was

224 of antibodies failed to alter the outcome of liver allograft survival in the tolerogenic or immunogen

225 rome showed significantly higher patient and liver allograft survival rates.

226 Overall 1- and 3-year actuarial patient and liver allograft survival was 88% and 71% (after renal tr

227 Liver allograft survival was superior among CLKT patient

228 antibodies are not deleterious to patient or liver allograft survival.

229 survival time, 5 days), whereas control B10 liver allografts survived >100 days.

230 ntestinal-pancreatic, or 14 whole or partial liver allografts sustained serious ischemic injury or we

231 Utilization of liver allografts that do not meet traditional donor crit

232 ts into key molecular mechanisms in marginal liver allografts that might provide therapeutic targets.

233 Pretreatment with a liver allograft (the orthotopic liver transplant [OLTx]

234 chimerism with spontaneous acceptance of rat liver allografts, the active role and the identity of ch

235 chimeric B cells proliferated in tolerogenic liver allografts, their clonal expansion does not seem t

236 DNA was extracted from paraffin-embedded liver allograft tissue and peripheral lymphocytes and wa

237 m was found in the DNA obtained from 2 of 14 liver allograft tissues (14.2%) but not in the DNA from

238 We demonstrate that anastomosis of liver allograft to a Dacron vena cava graft can be a fea

239 encountered during reduction of a cadaveric liver allograft to a left lateral segmental graft from a

240 ential for immunological protection from the liver allograft to a simultaneously transplanted kidney

241 dressed these questions using HLA-mismatched liver allografts to discriminate the liver-resident (don

242 Given the different clinical behavior of liver allografts to preformed antibody, we felt that suc

243 and the identity of chimeric cells mediating liver allograft tolerance are unknown.

244 ot seem to be essential for the promotion of liver allograft tolerance.

245 rom the grafted liver may be responsible for liver allograft tolerance.

246 e patients who successfully bridged to whole liver allograft transplant are alive, home, and normal w

247 Recent reports have shown that liver allografts transplanted against a positive lymphoc

248 monstrated among the nonparenchymal cells of liver allografts up to 100 days.

249 Types of liver allografts used included cadaveric, 85% (reduced s

250 h (DCD) and donation after brain death (DBD) liver allografts using days alive and out of hospital (D

251 that posttransplant TLI induces tolerance to liver allografts via a mechanism involving apoptotic cel

252 ression of chemokines and receptors in human liver allografts was studied by immunohistochemistry of

253 One of the liver allografts was successfully transplanted; the othe

254 of CD4 T cells in the pathogenesis of IRI in liver allografts were determined using a depleting anti-

255 A total of 144 primary liver allografts were performed from 1991 to 1996.

256 ACI liver allografts were permanently accepted by Lewis reci

257 , when exogenous rhIL-2 was given daily, LEW liver allografts were rejected by the DA recipients.

258 The remaining five liver allografts were shared with regional liver transpl

259 Eighty liver allografts were studied to determine the predictiv

260 Nineteen of the 24 split-liver allografts were transplanted at our center.

261 The protective effect of the liver allograft when simultaneously transplanted with a

262 immunological and regenerative properties of liver allografts, which lead to a low incidence and reve

263 r findings suggest that patients receiving a liver allograft with no HLA-B mismatched antigens are at

264 ceived cadaveric (n=53) or live donor (n=25) liver allografts with rabbit anti-human thymocyte globul

265 We conclude that liver allografts with up to 30% fat lead to diminished o

266 ntroversy, we reexamined the fate of outbred liver allografts without immunosuppression and used part

267 is evidence of complement activation in the liver allograft, without significant clinical impact in