ライフサイエンスコーパス: cold ischemia

1 and use of marginal livers, while minimizing cold ischemia.

2 Donor hearts were subjected to 2 hr of cold ischemia.

3 ver transplants despite prolonged periods of cold ischemia.

4 splantation (OLT) after prolonged periods of cold ischemia.

5 tissue exposed to a combination of warm and cold ischemia.

6 recipients of transplants with over 24 hr of cold ischemia.

7 id cardioplegia with greater than 8 hours of cold ischemia.

8 GAD developed in isografts undergoing 4-hour cold ischemia.

9 of hepatic in vivo warm ischemia and ex vivo cold ischemia.

10 th severe histological I/R injury and longer cold ischemia.

11 s as UW in our model of pig PT with 16 hr of cold ischemia.

12 e pigs underwent allogeneic PT with 16 hr of cold ischemia.

13 s, will protect liver grafts after prolonged cold ischemia.

14 kidney that had been subjected to 30 min of cold ischemia.

15 ombination of warm ischemia (20-420 min) and cold ischemia (120-600 min).

16 Isolated lungs were exposed to 6 hours of cold ischemia (4 degrees C), followed by 2 hours of warm

17 At early time points after cold ischemia (4 to 24 hours), allografts mismatched for

18 By day 7 post-transplant, both control and cold ischemia allografts showed comparable expression of

19 recipients with a clinically relevant 2-hour cold ischemia and 1-hour warm ischemia.

20 c death (DCD) kidneys before donation, after cold ischemia and after reperfusion.

21 nal sharing of liver allografts may increase cold ischemia and allograft failure, particularly with l

22 e collected every 2 min during the period of cold ischemia and hypothermic reperfusion (HtR).

23 These data demonstrate that cold ischemia and NK cells play critical roles in the de

24 fusion injury but not injury associated with cold ischemia and reperfusion (preservation injury).

25 In the ex vivo hepatic cold ischemia and reperfusion model, pretreatment with a

26 We characterized the effects of cold ischemia and reperfusion on expression of Na+/K+-AT

27 ned to counteract the detrimental effects of cold ischemia and reperfusion.

28 Donor hearts were subjected to 2 hr of cold ischemia and retrieved after 3 hr of reperfusion.

29 of protecting cadaver donor allografts from cold ischemia and subsequent reperfusion injury.

30 Following cold ischemia and syngeneic OLT, BV therapy extended ani

31 nditioning protects the liver from sustained cold ischemia and that tyrosine kinases are involved in

32 lationship was found between the duration of cold ischemia and the extent of complement-mediated tubu

33 or 7 days before being subjected to 2 hr of cold ischemia and then transplanted.

34 etic donors had lower serum creatinine, less cold ischemia and these kidneys were less likely to be p

35 use is warranted, including minimization of cold ischemia and use in stable recipients.

36 The injury resulting from cold ischemia and warm reperfusion during liver transpla

37 graftment of bone marrow-derived LSECs after cold ischemia and warm reperfusion.

38 is caused by a combination of warm ischemia, cold ischemia, and hypertonic citrate during in situ pre

39 kidney and liver donor risk indices, kidney cold ischemia, and inferior overall survival.

40 to 30 minutes of warm ischemia, 3.5 hours of cold ischemia, and then perfused with a humanized anti-C

41 rafts, but careful donor selection and short cold ischemia are mandatory.

42 fter harvest, the lungs underwent 6 hours of cold ischemia before being evaluated with EVLP for 4 hou

43 ween donor and recipient and the duration of cold ischemia before transplantation.

44 ntrast, in vessels exposed to more than 6 hr cold ischemia, both W6/32 antibody (30.4%+/-6.9%) and is

45 ntrast, in vessels exposed to more than 6 hr cold ischemia, both W6/32 antibody (30.4%T6.9%) and isot

46 d in human vessels exposed to more than 6 hr cold ischemia but only in the presence of antibody (P<0.

47 d in human vessels exposed to more than 6 hr cold ischemia but only in the presence of antibody (P<0.

48 f liver disease, retransplantation, warm and cold ischemia, but not graft type (whole, split, living-

49 Although prolonged cold ischemia can initiate mild GAD in isografts by tran

50 demonstrates that in the clinical situation, cold ischemia causes platelet deposition and neutrophil

51 Rat lungs obtained after 3 hours cold ischemia (CI group, control), or 1 hour WI plus 2 h

52 ccur at organ retrieval and during and after cold ischemia (CI) are sparse.

53 The effect of cold ischemia (CI) in vascularized composite allotranspl

54 Graft failure due to cold ischemia (CI) injury remains a significant problem

55 Prolonged cold ischemia (CI) is a risk factor for the development

56 We have previously shown that cold ischemia (CI) results in massive increases in caspa

57 Prolonged cold ischemia (CI) significantly reduced levels of cGMP

58 calpain activity during different periods of cold ischemia (CI), rewarming, or reperfusion, and (ii)

59 t function attributable to warm ischemia and cold ischemia (CI).

60 rats after 2 hours, 6 hours, or 10 hours of cold ischemia (CI).

61 Cold ischemia did not significantly affect the final gra

62 blished steatotic rat liver model of ex vivo cold ischemia followed by iso-transplantation.

63 hed steatotic rat liver model of ex vivo ice-cold ischemia followed by isotransplantation.

64 In a model of ex vivo cold ischemia followed by transplantation, the survival

65 schemia followed by reperfusion, and ex vivo cold ischemia followed by transplantation.

66 early PSGL-1 blockade in rat liver models of cold ischemia, followed by ex vivo reperfusion or transp

67 -1 Ab prevented hepatic insult in a model of cold ischemia, followed by OLT, as assessed by 1) decrea

68 tive mechanical ventilation, (3) donor organ cold ischemia > or =12 hr, (4) preoperative serum creati

69 tension as cause of end-stage renal disease, cold ischemia >or=30 hours, and use of tacrolimus each i

70 Prolonged cold ischemia has been suggested as a factor that will e

71 the importance of controlling the degree of cold ischemia in clinical transplantation in an effort t

72 increase in tyrosine phosphorylation before cold ischemia in preconditioned grafts only, but not in

73 ant) + 0.10 log bilirubin + 0.0087 PT + 0.01 cold ischemia (in hours).

74 Relative to control isografts, cold ischemia induced transiently enhanced endothelial e

75 Interestingly, cold ischemia-induced CAV posttransplantation was not se

76 ntage of a better immunologic match, reduced cold ischemia injury, and decreased waiting time.

77 s suggest that older donor age and prolonged cold ischemia interact to increase liver allograft failu

78 nd orthotopically transplanted after 1 hr of cold ischemia into syngeneic recipients.

79 Prolonged warm or cold ischemia is associated with poor survival of cardia

80 Even a short period of cold ischemia is significantly deleterious to the functi

81 Following cold ischemia/isotransplantation, HO-1 overexpression ex

82 come with little increase in the duration of cold ischemia justifies national sharing of HLA-matched

83 uded pretransplant dialysis duration, kidney cold ischemia, kidney donor risk index, and recipient hy

84 Sixteen pigs were transplanted with 26-hr cold ischemia kidneys.

85 f livers from donors older than 45 years and cold ischemia less than 12 hr.

86 y performed in a clinically relevant ex vivo cold ischemia model is the first to provide the evidence

87 the interaction of age 45 years or more and cold ischemia more than or equal to 12 hr reached statis

88 livers from donors aged 45 years or more and cold ischemia more than or equal to 12 hr showed an adju

89 We have found that cold ischemia of cardiac grafts induces CAV after transp

90 </= 7 d) events of warm and in situ perfused cold ischemia of native kidneys in uninephrectomized rat

91 hotopic lung transplantation after prolonged cold ischemia (OLT-PCI).

92 ted the influence of supplemental GSH during cold ischemia on early renal allograft function.

93 We therefore examined the effects of cold ischemia on GAD as well as adhesion molecule and cy

94 splants despite prolonged periods of warm or cold ischemia, or both.

95 One pancreas, with cold ischemia over 30 h, did not appear viable and was e

96 ncrease in the risk of DGF for every 6 hr of cold ischemia (P<0.001).

97 357), nor in lipid peroxidation during 16-hr cold ischemia (P=0.672), or reperfusion (P=0.185), but I

98 le grafts harvested after the same period of cold ischemia, partial grafts had eightfold more T-cell

99 -reperfusion injury, prolongs the acceptable cold ischemia period of lung grafts, and improves the fu

100 Cold-ischemia produced a rapid, unpredictable, and wides

101 standing of the mechanism by which prolonged cold ischemia reduces immediate graft survival but also

102 tion, there was no significant difference in cold ischemia, rejection episodes, or patient or graft s

103 ow concentration provides protection against cold ischemia-reperfusion (I/R) injury after kidney tran

104 signaling mediates early inflammation after cold ischemia-reperfusion (I/R).

105 cific functional state of mitochondria after cold ischemia-reperfusion in a rat heart transplant mode

106 with warm CRS before implantation diminishes cold ischemia-reperfusion injury and improves the functi

107 warm ischemic time in addition to subsequent cold ischemia-reperfusion injury may result in damage to

108 ated protein kinases (MAPK) is implicated in cold ischemia-reperfusion injury of donor organs.

109 Kidney damage caused by cold ischemia-reperfusion injury promotes adverse outcom

110 he pathogenesis of post-lung transplantation cold ischemia-reperfusion injury.

111 lar endothelial cell killing associated with cold ischemia-reperfusion injury.

112 -1) in steatotic rat liver models of ex vivo cold ischemia/reperfusion (I/R) injury.

113 partial grafts, and significantly decreased cold ischemia/reperfusion injury (P<0.05) and associated

114 Partial grafts showed more severe cold ischemia/reperfusion injury and greater inflammator

115 ive efficacy of inhaled CO during intestinal cold ischemia/reperfusion injury associated with small i

116 or 112% of normal following 1, 2, or 3 hr of cold ischemia, respectively; P < 0.05).

117 Gender, age, ABO blood-type, cold ischemia, splenectomy and allograft type were signi

118 Our study indicates that cold ischemia stimulates inflammatory pathways (chemokin

119 c preconditioning (10-10 group) and 16 hr of cold ischemia survived for more than 1 day and 75% for m

120 Under extreme conditions such as prolonged cold ischemia, these enzymes may be unable to adequately

121 ican race, Kidney Donor Profile Index > 50%, cold ischemia time > 24 hours) and low-risk (not having

122 HTLV reactive, donation after cardiac death, cold ischemia time >12 hours, ICU stay >5 days, 3 or mor

123 DGF was associated with cold ischemia time >24 hr (P = 0.0003) and Rej (P = 0.06

124 s: donor age >55 yr, non-heartbeating donor, cold ischemia time >36 h, and donor hypertension or diab

125 (>55 years), donor hospital stay (>5 days), cold ischemia time (>10 hours), and warm ischemia time (

126 ithin 3 months posttransplant were prolonged cold ischemia time (>36 hours, odds ratio [OR]=3.38 vs.

127 of HAT was 8 out of 73 transplants (11%).The cold ischemia time (14.3 +/- 3.03 hr) in this group was

128 wait-time (571 vs. 471 days, P<0.01), longer cold ischemia time (22 vs. 20 hr, P<0.01), and donor and

129 ed with recipients of kidneys with a shorter cold ischemia time (3.2%).

130 We found that a prolonged cold ischemia time (6-12 hr) alone did not induce IE.

131 ed with DDK with non-DGF after adjusting for cold ischemia time (alpha=0.001).

132 ), but this risk was limited to kidneys with cold ischemia time (CIT) >12 hours.

133 001), non-AA donor (HR 1.66, P < 0.001), and cold ischemia time (CIT) (HR 1.03 per hour >8 hours, P =

134 0.001) and kidneys with longer than 30 hr of cold ischemia time (CIT) (OR, 0.95; per 5% increment; 95

135 Prolonged cold ischemia time (CIT) affected BT rate significantly

136 Cadaveric kidneys experiencing longer cold ischemia time (CIT) are associated with higher leve

137 We used cold ischemia time (CIT) as an instrument to test the hy

138 Cumulative recurrence curves according to cold ischemia time (CIT) at 2-hour intervals and warm is

139 Prolonged cold ischemia time (CIT) is associated with a significan

140 ptimizing "modifiable risk factors," such as cold ischemia time (CIT) recipient warm ischemia time (W

141 The effect of this policy on cold ischemia time (CIT), delayed graft function (DGF),

142 covariates in both groups, while donor race, cold ischemia time (CIT), female to male transplants, an

143 Imported pancreata accumulate cold ischemia time (CIT), limiting utilization and worse

144 or age, donor warm ischemia time (DWIT), and cold ischemia time (CIT).

145 estigated in addition to causes of prolonged cold ischemia time (CIT).

146 l operating room time (207 vs. 200 min.), or cold ischemia time (excluding pancreas).

147 d a reduction in use of donors with extended cold ischemia time (p = 0.04) and private pay recipients

148 Bilirubin (P=0.006) and cold ischemia time (P=0.002) were predictive of graft lo

149 A negative association to DeltaCP/GCr was cold ischemia time (r=-0.330, P<0.001).

150 in the U.S. study had a significantly longer cold ischemia time (the time elapsed between procurement

151 Increased donor age and cold ischemia time additionally decreased graft survival

152 ations of kidneys with less than 12 hours of cold ischemia time and 74,997 dollars for those with mor

153 ible donors, and is associated with a longer cold ischemia time and a potentially higher rejection ra

154 risk factors for reduced graft survival are cold ischemia time and donor age.

155 uld be reallocated without delay to minimize cold ischemia time and maximize the utility of the graft

156 with intrahepatic strictures, and prolonged cold ischemia time and rejection were associated with st

157 When results were adjusted for cold ischemia time and sex, iNO significantly decreased

158 Non-treated allogeneic grafts without cold ischemia time and syngeneic grafts did not develop

159 The short tolerable cold ischemia time and the importance of other risk fact

160 prospective cross-match as a means to reduce cold ischemia time and the incidence of delayed graft fu

161 Prolonged cold ischemia time and use of a whole graft with recipie

162 Bilirubin and cold ischemia time are crucial for graft outcome post-LT

163 ansplantation model grafts subjected to long cold ischemia time developed severe TV with intimal hype

164 ), expanded criteria donor kidney (15%), and cold ischemia time exceeding 24 hr (27%).

165 The mean cold ischemia time for both groups was 11 +/-3 hr.

166 in start of surgery (25 vs. 77 min), shorter cold ischemia time for recovered pancreases (355 vs. 630

167 years (range, 1.0-50.0 years), and the mean cold ischemia time for the cadaveric kidneys was 27.0+/-

168 this group was significantly longer than the cold ischemia time for those without HAT (11.7 +/- 3.94

169 with donor body mass index >30 and pancreas cold ischemia time greater than 12 hr.

170 Recipients of kidneys with cold ischemia time greater than 24 hr also had a higher

171 For CAD kidney recipients, organ cold ischemia time greater than 24 hr increased the risk

172 tigen (HLA) mismatches, increased donor age, cold ischemia time greater than 24 hr, African American

173 xplant, donor age greater than 55 years, and cold ischemia time greater than 550 minutes were signifi

174 icant correlation between apoptosis rate and cold ischemia time in CAD (r=0.86, P<0.001) renal allogr

175 10) that received a liver graft with a 16-hr cold ischemia time in Euro-Collins solution survived for

176 3+/-14.6 years (range: 0.7-50), and the mean cold ischemia time in the cadaveric cases was 26.5+/-8.8

177 Older recipient age and prolonged cold ischemia time increase the risk of graft failure.

178 95% CI 1.23-2.02, P<0.001), and kidneys with cold ischemia time more than 24 hr (HR 1.31, 95% CI 1.04

179 95% CI 1.20-1.30, P=0.002) and kidneys with cold ischemia time more than 24 hr (HR 1.44, 95% CI 1.04

180 assessed using this technique after a median cold ischemia time of 13 h 19 min.

181 SSI: kidney from extended criteria donors, a cold ischemia time of more than 30 hr, time of surgical

182 vailability and thereby increase donor organ cold ischemia time that might then result in increased r

183 enal grafts were transplanted with a shorter cold ischemia time to more poorly HLA-matched recipients

184 Mean kidney cold ischemia time was 10 +/- 3 and 50 +/- 15 hours, for

185 The median cold ischemia time was 12 h 30 min (range 5 h 25 min-18

186 yte antigen (HLA) match was one; and average cold ischemia time was 12 hours.

187 In the marginal group, the cutoff value of cold ischemia time was 12.6 hr.

188 Mean cold ischemia time was 26.9+/-8.6 hr.

189 In cadaveric grafts, the mean cold ischemia time was 29.0 hours +/- 6.9 in those with

190 The mean cold ischemia time was 30.5+/-9.2 hr.

191 pancreatic excision was 34 minutes, whereas cold ischemia time was 6 hours and 40 minutes.

192 Mean cold ischemia time was 8.5 hr.

193 Cold ischemia time was a predictor of DGF independently

194 Cold ischemia time was longer in those with recurrent st

195 Cold ischemia time was not found to be an important fact

196 ets expressing either P-selectin or vWF, the cold ischemia time was significantly longer (885 +/- 123

197 experienced early acute rejection, the mean cold ischemia time was significantly longer than in allo

198 Cold ischemia time was strongly associated with DGF, wit

199 age difference, donor gender, donor type, or cold ischemia time were comparable.

200 percent) when the potential costs of longer cold ischemia time were considered.

201 gram, because the additional costs of longer cold ischemia time were greater than the advantages of o

202 Lactated Ringer's solution and 3-hr cold ischemia time were used for mechanistic investigati

203 iated with early transplant stressors (e.g., cold ischemia time) and donor aging.

204 r 120 min (30-min warm ischemia time, 90-min cold ischemia time), the second kidney was removed (NHBD

205 age Liver Disease score was 15 (IQR, 11-21); cold ischemia time, 8.0 hours (IQR, 6.4-9.7 hours); MEAF

206 ly significant factors such as HLA mismatch, cold ischemia time, and African-American or diabetic rec

207 ominal sepsis) and donor factors (donor age, cold ischemia time, and donor cytomegalovirus status), m

208 , human leukocyte antigen-B and DR mismatch, cold ischemia time, and double or en bloc transplant.

209 ransplanted, increment of insulin secretion, cold ischemia time, and exocrine tissue volume transplan

210 size, age of donor kidney, damage caused by cold ischemia time, and mode of donor death all had subs

211 t to include both nonimmunologic (donor age, cold ischemia time, and recipient race) and immunologic

212 RA), recipient and donor race and donor age, cold ischemia time, and the pretransplantation use of ei

213 ats that received a liver graft with a 16-hr cold ischemia time, and the survival rate was 83% after

214 he effects of this system on graft survival, cold ischemia time, and the transplantation of highly se

215 and acute rejection; and donor age and race, cold ischemia time, and year of transplant.

216 dictors, whereas donor age, gender and race, cold ischemia time, cadaveric versus living donor, delay

217 phenomena, such as donor death and possibly cold ischemia time, contributed to differences in comple

218 were used to measure the relationships among cold ischemia time, delayed graft function, acute reject

219 ntibody more than 0%, cytomegalovirus D+/R-, cold ischemia time, delayed graft function, induction wi

220 erences, including donor brain death, longer cold ischemia time, diabetogenic immunosuppression, and

221 No significant differences in donor age, cold ischemia time, digestion time, or weight of the pan

222 e, panel-reactive antibody level, HLA match, cold ischemia time, donor age, and expanded criteria don

223 Cadaveric transplants, prolonged cold ischemia time, elevated panel reactive antibody, an

224 matches, human leukocyte antigen antibodies, cold ischemia time, living donor, and preemptive transpl

225 There was no difference regarding cold ischemia time, model for end-stage liver disease sc

226 was unassociated with 0Pre biopsy findings, cold ischemia time, or peak PT values.

227 There was no difference in donor age, cold ischemia time, or recipient United Network for Orga

228 groups in recipient demographics, donor age, cold ischemia time, or total number of doses of Thymoglo

229 ting for recipient age, sex, race, diabetes, cold ischemia time, panel cross-reactivity, pretransplan

230 ties for planning surgery and also decreases cold ischemia time, potentially translating into a highe

231 , local origin of procurement team, pancreas cold ischemia time, recipient cerebrovascular disease.

232 Assuming no change is cold ischemia time, the potential number of 0 CREG, 0 DR

233 ring of 0-MM kidneys significantly increased cold ischemia time, the risk of graft loss was significa

234 l reactive antibody, delayed graft function, cold ischemia time, time since start of dialysis, etiolo

235 after adjusting for recipient and donor age, cold ischemia time, urine output, and Scr.

236 Within this range of cold ischemia time, UW and HTK demonstrate similar effic

237 milar among the groups with the exception of cold ischemia time, which was longer in the MP group com

238 al donors (n = 14) matched for age, BMI, and cold ischemia time.

239 ntigen mismatch, pretransplant dialysis, and cold ischemia time.

240 g donor type, HLA mismatches, donor age, and cold ischemia time.

241 ale donor, PRA as a continuous variable, and cold ischemia time.

242 n of CD14 mRNA correlated with the length of cold ischemia time.

243 diate-term graft survival despite increasing cold ischemia time.

244 nsitized patients in spite of similar length cold ischemia time.

245 prevalent in cadaveric allografts with long cold ischemia time.

246 variables included age, weight, gender, and cold ischemia time.

247 ps in terms of recipient sex, race, age, and cold ischemia time.

248 th University of Wisconsin solution and 6-hr cold ischemia time.

249 ree of sensitization, retransplantation, and cold ischemia time; however, EBK recipients were somewha

250 ction criteria and the requirement for short cold-ischemia time (CIT).

251 The cold-ischemia time of the donor hand was 310 minutes.

252 antibody titer, extent of HLA matching, and cold-ischemia time), and post-transplantation variables

253 Primary outcomes were discard, cold-ischemia time, delayed graft function, and 1-year g

254 pancreas after kidney recipients, prolonged cold-ischemia time, prolonged donor hypotension, non-hea

255 l with donor BMI >30 (P=0.06) and increasing cold-ischemia time.

256 nce of delayed graft function (38% vs. 26%), cold ischemia times (12.9 vs. 13.5 hr), and graft surviv

257 age Liver Disease score, and longer warm and cold ischemia times (C statistic, 0.75).

258 percentage of transplanted ECD kidneys with cold ischemia times (CIT) <12 hr increased significantly

259 Concerns remain over prolonged cold ischemia times (CIT) associated with shipping kidne

260 on for short (3 hr; control) or long (18 hr) cold ischemia times (CIT).

261 nal allocation variance designed to minimize cold ischemia times and encourage adoption of DCD protoc

262 ave focused on graft damage due to prolonged cold ischemia times and rewarming during the long benchi

263 early allograft dysfunction with increasing cold ischemia times and should be transplanted within 12

264 n those retrieved from cadaver donors, where cold ischemia times are significantly longer.

265 es, including those of cadaveric grafts with cold ischemia times of as long as 41 hr.

266 Mean cold ischemia times were less than 20 hr.

267 levels of panel-reactive antibodies, shorter cold ischemia times, a lower incidence of delayed graft

268 Cold ischemia times, donor age, and preoperative eGFR fo

269 he benefits of sustained euglycemia, shorter cold ischemia times, lower rates of sensitization, and e

270 n time (PT), retransplantation, and warm and cold ischemia times, were applied to the UNOS database.

271 om older, more mismatched donors with longer cold ischemia times.

272 seen in grafts from older donors and longer cold ischemia times.

273 tiplicity of infection of 0.4 with prolonged cold ischemia to 18 hr.

274 IE in human vessels that are injured through cold ischemia via interaction with Fc-receptor-positive

275 Cold ischemia/warm reperfusion (CI/WR) liver injury rema

276 ears, respectively, and the mean duration of cold ischemia was 23 hours and 22 hours, respectively.

277 Mean cold ischemia was 305 min (300-330 min), and revasculari

278 e warm ischemia time was 21 minutes, and the cold ischemia was 8 hours.

279 s defined as 45 years or more, and prolonged cold ischemia was defined as 12 hours or more.

280 Tolerance of the transplanted liver to cold ischemia was determined by survival time and liver

281 onmarginal populations, and the influence of cold ischemia was determined for each group.

282 estimated cost savings, when the duration of cold ischemia was taken into account.

283 The effects of PSGL-1 in cold ischemia were assessed using an isolated perfused r

284 action between older donor age and prolonged cold ischemia were performed.

285 Older recipient age and length of cold ischemia were significant predictors of graft failu

286 een an urgent need to minimize both warm and cold ischemia, which often necessitates more rapid remov

287 hils, significantly increased after 48 hr of cold ischemia with Collins flush and 1 hr of reperfusion

288 solated from rabbit kidneys after 1-48 hr of cold ischemia with or without transplantation-reperfusio

289 dominal wall allograft substantially reduces cold ischemia without imposing constraints on the intest

290 chemic tissue or mucosal tissue subjected to cold ischemia without reperfusion.