ライフサイエンスコーパス: cold ischemia

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

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

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

4 aft CD11c(+)F4/80(+) renal macrophages after cold ischemia.

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

6 ere significantly altered by the duration of cold ischemia.

7 ver transplants despite prolonged periods of cold ischemia.

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

9 ospital length of stay despite longer kidney cold ischemia.

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

11 ge, donation after cardiac death, and longer cold ischemia.

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

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

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

15 ncrease glomerular pathology after prolonged cold ischemia.

16 d ischemia, warm ischemia, and combined warm+cold ischemia.

17 ograft glomerular injury caused by prolonged cold ischemia.

18 xpressed in human kidneys following extended cold ischemia.

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

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

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

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

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

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

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

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

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

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

29 NMP can enable the reduction or avoidance of cold ischemia and allows for pretransplant measurement o

30 miR expression in human lungs in response to cold ischemia and ex vivo reperfusion (CI/EVR).

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

32 fusates from Lewis rat livers as a result of cold ischemia and machine perfusion.

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

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

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

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

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

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

39 Cold ischemia and reversible ischemia-reperfusion injury

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

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

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

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

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

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

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

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

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

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

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

51 e of HLA mismatch, number of veins/arteries, cold ischemia, and travel times.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 Prolonged cold ischemia (CI) is a risk factor for acute kidney inj

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

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

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

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

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

72 neys; (2) donor kidneys subjected to ex vivo cold ischemia (CI); (3) donor kidneys subjected to kidne

73 Cold ischemia did not significantly affect the final gra

74 g islet function is exposure of pancreata to cold ischemia during unavoidable windows of preservation

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

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

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

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

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

80 -1 Ab prevented hepatic insult in a model of cold ischemia, followed by OLT, as assessed by 1) decrea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 To investigate effects of cold ischemia on donor-reactive immune responses and gra

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

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

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

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

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

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

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

111 After 4 hours of cold ischemia, physiologic function and vascular tone of

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

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

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

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

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

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

118 ntitative ultrasound scan, against prolonged cold ischemia-reperfusion injury (24 hours at 4 degrees

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

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

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

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

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

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

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

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

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

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

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

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

131 d MHC-mismatched BALB/c kidney allografts to cold-ischemia storage for 0.5 or 6 hours before transpla

132 llografts subjected to 6 versus 0.5 hours of cold-ischemia storage had increased levels of anti-MHC c

133 chanisms underlying the effects of prolonged cold-ischemia storage on kidney allografts are poorly un

134 arm ischemia (kidney clamping) and prolonged cold ischemia (syngeneic renal transplant).

135 After 4 hours of cold ischemia, the BACS group exhibited significantly hi

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

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

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

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

140 (>55 years), donor hospital stay (>5 days), cold ischemia time (>10 hours), and warm ischemia time (

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

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

143 l group, kidneys with diffuse GFT had longer cold ischemia time (34 versus 27 h), were more frequentl

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

145 ble to the effect of each hour of additional cold ischemia time (adjusted HR 1.04, 95% CI 1.02-1.05;

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

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

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

149 0.001) and kidneys with longer than 30 hr of cold ischemia time (CIT) (OR, 0.95; per 5% increment; 95

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

151 clinical findings, suboptimal biopsies, long cold ischemia time (CIT) and/or poor hypothermic perfusi

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

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

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

155 While the current maximum cold ischemia time (CIT) for donor lungs in clinical LTx

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

157 as 4% (40) and in multivariate analysis only cold ischemia time (CIT) longer than 8 hours (hazard rat

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

159 Cold ischemia time (CIT) was 10.8 +/- 4.1 hours and anas

160 The potential exists for an increase in cold ischemia time (CIT) with resulting increases in del

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

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

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

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

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

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

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

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

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

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

171 being from donors after brain death (median cold ischemia time 33 +/- 36.9 hours) and 5 being from d

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

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

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

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

176 Longer cold ischemia time and large droplet macrovesicular stea

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

178 for the standard FXM, potentially shortening cold ischemia time and providing clinicians with unambig

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

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

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

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

183 Improved patient selection and reduction in cold ischemia time appear to be contributing factors.

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

185 , African American ethnicity, donor age, and cold ischemia time as predictors of graft and patient su

186 , older donor age, male donors, and a longer cold ischemia time but not donor terminal creatinine wer

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

188 owed no-flow time, functional warm time, and cold ischemia time did not affect the risk of PNF or poo

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

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

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

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

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

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

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

196 3+/-14.6 years (range: 0.7-50), and the mean cold ischemia time in the cadaveric cases was 26.5+/-8.8

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

198 iver, and only 3% were listed as requiring a cold ischemia time less than 6 hours.

199 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

200 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

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

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

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

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

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

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

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

208 Cold ischemia time was 13.6 +/- 4.7 hours; anastomosis t

209 Mean cold ischemia time was 14 hours.

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

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

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

213 Mean cold ischemia time was 8.5 hr.

214 Cold ischemia time was a predictor of DGF independently

215 Cold ischemia time was longer in those with recurrent st

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 thnicity, cause of liver disease, donor age, cold ischemia time, and waiting time.

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

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

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

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

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

236 facilities emerged in donor selection (age, cold ischemia time, intensive care unit length, amylase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 prevalent in cadaveric allografts with long cold ischemia time.

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

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

259 ard or delayed allocation beyond 36 hours of cold ischemia time.

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

261 r wait times can impact logistics as well as cold ischemia time; our findings motivate an exploration

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

263 60 post-transplant, allografts with a 6 hour cold-ischemia time developed extensive glomerular injury

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

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

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

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

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

269 ate pathology in allografts with 0.5 hour of cold-ischemia time.

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

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

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

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

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

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

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

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

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

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

280 es in donor/recipient case-mix and increased cold ischemia times under the Kidney Allocation System (

281 Warm ischemia time and cold ischemia times were 38 and 466 minutes, respectivel

282 Mean cold ischemia times were less than 20 hr.

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

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

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

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

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

288 P) content decay of mouse liver grafts after cold ischemia, warm ischemia, and combined warm+cold isc

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

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

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

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

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

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

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

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

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

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

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

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