ライフサイエンスコーパス: liver allograft

1 d HLA-A2(-) individual received an HLA-A2(+) 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 issue, indicating an ectopic origin from the liver allograft.

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

8 e reported immunoprotection conferred by the liver allograft.

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

10 m mononuclear cells infiltrating a rejecting liver allograft.

11 ession in the hepatocytes and lymphocytes of liver allografts.

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

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

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

15 50 consecutive PSC patients who received 174 liver allografts.

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

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

18 proliferating naive T lymphocytes in situ in liver allografts.

19 n activity recently has been demonstrated in liver allografts.

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

21 applicability to prevent HCV reinfection of liver allografts.

22 led to increased utilization of higher risk liver allografts.

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

24 infiltration after reperfusion of cadaveric liver allografts.

25 tic role in preventing biliary strictures in liver allografts.

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

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

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

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

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

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

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

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

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

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

36 Overall liver allograft and patient survival rates of LTA patien

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

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

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

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

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

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

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

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

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

46 Liver allografts are accepted across major histocompatib

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

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

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

50 4(+) regulatory T cells was increased in the liver allograft as well as in the peripheral blood.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 Examination of the liver allografts by in situ terminal deoxynucleotidyltra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 Liver allografts for eight adult recipients were procure

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

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

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

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

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

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

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

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

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

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

95 Liver allografts have been thought to be immunoprotectiv

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 17 pretransplantation variables on long-term liver allograft outcome was analyzed.

117 lation of hepatic inflammatory responses and liver allograft outcome.

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

119 < 0.001), and a higher utilization rate for liver allografts (P = 0.007).

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

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

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

123 Liver allograft provided renal graft immunoprotection if

124 Liver allografts rarely undergo hyperacute rejection, bu

125 Lewis recipients of DA liver allografts received immunosuppressive agents after

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

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

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

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

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

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

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

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

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

135 Liver allograft recipients have a greater risk of cardio

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

137 Nineteen orthotopic liver allograft recipients were converted from azathiopr

138 One hundred fifty liver allograft recipients were prospectively monitored

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

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

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

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

143 Th2 cytokine profiles were characterized in liver allograft recipients.

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

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

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

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

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

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

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

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

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

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

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

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

156 Liver allograft rejection is mediated by a primary respo

157 Early chronic liver allograft rejection is potentially reversible and

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

159 When acute liver allograft rejection was induced by administration

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

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

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

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

164 olecule expression is increased during acute liver allograft rejection.

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

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

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

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

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

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

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

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

173 Liver allograft sections showed a positive correlation (

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

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

176 LRD liver allografts showed minimal changes postreperfusion.

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

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

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

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

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

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

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

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

185 Prolongation of liver allograft survival in presensitized recipients was

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

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

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

189 Liver allograft survival was superior among CLKT patient

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 ACI liver allografts were permanently accepted by Lewis reci

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

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

216 Eighty liver allografts were studied to determine the predictiv

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

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

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

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

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

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

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

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