ライフサイエンスコーパス: warm ischemia

1 ve endothelial structure and function during warm ischemia.

2 lly relevant 2-hour cold ischemia and 1-hour warm ischemia.

3 HBD), thereby improving function with longer warm ischemia.

4 roups were subjected to approximately 70 min warm ischemia.

5 use liver dysfunction after cold storage and warm ischemia.

6 important roles in mitigating the effects of warm ischemia.

7 an shortage, but they inherently suffer from warm ischemia.

8 volume before and after a 7-minute period of warm ischemia.

9 lipid peroxidation occurs in this model with warm ischemia.

10 ection of DCD grafts and clear definition of warm ischemia.

11 g systemic injury, hepatotoxin exposure, and warm ischemia.

12 of kidney grafts associated with substantial warm ischemia.

13 expression of VEGF in a mouse model of liver warm ischemia.

14 preservation of kidneys exposed to 60 min of warm ischemia.

15 Rats underwent bilateral renal warm ischemia (15-60 min) then reperfusion (20 or 80 min

16 ular EVLP for 2 hours after a combination of warm ischemia (20-420 min) and cold ischemia (120-600 mi

17 l allografts were subjected to 30 minutes of warm ischemia, 3.5 hours of cold ischemia, and then perf

18 were exposed to 0, 60, or 75 min of in situ warm ischemia (37 degrees C), followed by 24 to 72 hr pr

19 role of TIM-4 signaling in a model of liver warm ischemia (90 minutes) and reperfusion.

20 WT) controls were subjected to partial liver warm ischemia (90 minutes) followed by reperfusion (1-6

21 an established mouse model of partial liver warm ischemia (90 minutes) followed by reperfusion (6 ho

22 With a partial lobar liver warm ischemia (90 minutes) model, ASC-deficient and wild

23 (PACAP) in a murine model of partial liver "warm" ischemia (90 minutes) followed by reperfusion.

24 eath leads to vascular damage as a result of warm ischemia, affecting renovascular circulating volume

25 kidney graft, revascularized after 35 min of warm ischemia, also functioned immediately.

26 underwent sham operation (n=9), or 45 min of warm ischemia and 10 min of reperfusion with U74389G (6

27 5% survival) in kidneys exposed to 75 min of warm ischemia and 24 hr machine perfusion.

28 suscitate porcine livers after 60 minutes of warm ischemia and 4 hours of cold preservation.

29 ce of delayed graft function attributable to warm ischemia and cold ischemia (CI).

30 awley rats were subjected to 75 min of renal warm ischemia and contralateral nephrectomy.

31 awley rats were subjected to 75 min of renal warm ischemia and contralateral nephrectomy.

32 -1 (PSGL-1) in rat models of hepatic in vivo warm ischemia and ex vivo cold ischemia.

33 Porcine kidneys were retrieved after 10-min warm ischemia and flushed with 500 mL hyperosmolar citra

34 here the donor organ undergoes both cold and warm ischemia and global ischemic insult.

35 in a well-established model of liver partial warm ischemia and in situ reperfusion.

36 Criteria for matching included duration of warm ischemia and key confounders summarized in the bala

37 sed in two distinct animal models of hepatic warm ischemia and orthotopic liver transplantation (hypo

38 om male Lewis rats were subjected to 1 hr of warm ischemia and preserved with 5 hr of SCS or NELP, an

39 livers were exposed to 55 minutes prolonged warm ischemia and reperfused for 3 days (n = 6).

40 Hepatic warm ischemia and reperfusion (I/R) injury and inflammat

41 mucosal damage that occurs after intestinal warm ischemia and reperfusion and its recovery, little i

42 Liver injury from warm ischemia and reperfusion was attenuated with all la

43 ENT2 transcript and protein levels following warm ischemia and reperfusion.

44 cell-derived IL-22 in liver injury caused by warm ischemia and reperfusion.

45 ceived normal saline, the sham group without warm ischemia and the experimental groups, which receive

46 rcine livers were subjected to 60 minutes of warm ischemia and then assigned to the following groups:

47 t the immediate-function kidneys had shorter warm ischemia and total preservation times compared with

48 C57Bl/6J mice underwent bilateral warm ischemia and were sacrificed after 30 minutes or 24

49 th ischemia-reperfusion injury (IRI) (45-min warm ischemia), and rats subjected to acute cyclosporine

50 rfused hearts were subjected to 5 minutes of warm ischemia, and at 5, 10, and 15 minutes after initia

51 Vascular clamping confers warm ischemia, and attempts at renal hypothermia include

52 Mice underwent euthanasia and 60 minutes warm ischemia, and lungs were flushed with Perfadex and

53 e II NKT cells in mice with partial hepatic, warm ischemia, and reperfusion injury.

54 Mean console, warm ischemia, and rewarming times were 130.8 minutes, 2

55 of AP-1 was dramatically increased following warm ischemia at 1 to 3 hours postreperfusion.

56 donors after circulatory death (DCD) suffer warm ischemia before cold storage which may prejudice gr

57 f donor liver grafts to prolonged periods of warm ischemia before procurement causes injuries includi

58 Organs were subjected to 60 min of warm ischemia before the hypothermic machine preservatio

59 ole in signalling liver tissue damage due to warm ischemia before transplantation.

60 erformed in 15 patients without the need for warm ischemia by utilizing pharmalogically induced hypot

61 After warm ischemia, cardiac output in EC-SOD was significantl

62 late that this is caused by a combination of warm ischemia, cold ischemia, and hypertonic citrate dur

63 g) underwent left nephrectomy with 30 min of warm ischemia, Collins C-4 flush, and 24 hr of cold stor

64 n (HPP) of kidneys subjected to preretrieval warm ischemia compared with nonischemic controls.

65 etting of a solitary kidney, every minute of warm ischemia counts and ischemia is an important modifi

66 o (odds ratio, 0.20; P = 0.008) and arterial warm ischemia duration (odds ratio, 1.05; P = 0.008).

67 For the DCD donors, the median donor warm ischemia duration was 24 minutes.

68 undergo apoptosis after 60 to 120 minutes of warm ischemia followed by 0 to 24 hours of reperfusion.

69 Porcine kidneys were subjected to 10 min of warm ischemia followed by 18 hr of static cold storage w

70 Kidneys were subjected to 20 min warm ischemia followed by 2 or 18 hr of cold storage (n=

71 Ninety minutes of warm ischemia followed by 6 hours of reperfusion induced

72 njury induced by 90 minutes of liver partial warm ischemia followed by 6 hours of reperfusion.

73 served livers that had experienced 30 min of warm ischemia followed by a 10 hr preservation period.

74 erved tissues that had experienced 30 min of warm ischemia followed by a 5-hr preservation period wit

75 nephrectomized rats that underwent 60 min of warm ischemia followed by a 72-hr reperfusion interval w

76 stem in an established murine model of liver warm ischemia followed by reperfusion.

77 he slight deterioration seen when increasing warm ischemia from 1 to 2 hr, significantly improving tr

78 ) in the control to 0.82 (0.1) in the 60-min warm ischemia group (P<0.01).

79 -hr preservation of kidneys not subjected to warm ischemia (heart-beating donor model), but there was

80 However, all rats with 120 min (n=8) liver warm ischemia in splenic-caval shunt group survived for

81 ecipient age + 0.816 log creatinine + 0.0044 warm ischemia (in minutes) + 0.659 (if second transplant

82 ury and to enhance the tolerance of liver to warm ischemia injury with portosystemic shunt.

83 In the first model (warm ischemia), IPC significantly decreased serum aminot

84 Using a partial lobar warm ischemia model, groups of wild-type (WT), T cell-de

85 In an in vivo warm ischemia model, hepatic injury was assessed by seru

86 ponse were studied in a murine partial liver warm ischemia model.

87 A total of 67% of rats with 45 min liver warm ischemia (n=6) and 100% of rats with 60 min liver w

88 mia (n=6) and 100% of rats with 60 min liver warm ischemia (n=6) died within 1 day.

89 Controlled donors with a warm ischemia of <30 minutes were considered.

90 n Lewis and Fischer 344 rats after 45 min of warm ischemia of a single kidney and with or without con

91 of lipopolysaccharide in the rats with liver warm ischemia plus splenic-caval shunt.

92 After 30 min of warm ischemia, porcine kidneys were randomly assigned to

93 ction associated with 30 min of preretrieval warm ischemia (pre-WI).

94 vestigated in an experimental model of renal warm ischemia reperfusion injury.

95 steatotic livers in a model of total hepatic warm ischemia-reperfusion (I/R).

96 reconditioned with whole liver radiation and warm ischemia-reperfusion followed by intrasplenic trans

97 rge animals for protecting the liver against warm ischemia-reperfusion injury but not injury associat

98 hat calpain proteases play a pivotal role in warm ischemia-reperfusion injury of the rat liver throug

99 rough repeated CI during torpor, followed by warm ischemia/reperfusion (WI) during interbout arousal

100 d play an important role in limiting hepatic warm ischemia/reperfusion (WI/Rp) injury, probably throu

101 the role of IL-6 in rodent models of hepatic warm ischemia/reperfusion (WI/Rp) injury.

102 meliorates fatty livers and protects against warm ischemia/reperfusion fatty liver injury, suggesting

103 nd injury in a murine model of liver partial warm ischemia/reperfusion injury (IRI).

104 Further, after warm ischemia/reperfusion injury, we show that rats expr

105 vented the susceptibility of fatty livers to warm ischemia/reperfusion injury.

106 ble to phospholipid depletion in response to warm ischemia/reperfusion than normal livers.

107 ing HPP of kidneys subjected to preretrieval warm ischemia resulted in a normalization of GFR measure

108 Both 10 and 30 min warm ischemia resulted in a rise in TACE expression whic

109 ys of C57BL/6 mice that underwent unilateral warm ischemia revealed nine miRNAs (miR-21, miR-20a, miR

110 After 30 minutes of warm ischemia, right kidneys were removed from 30-kg Yor

111 mic shunt enhances the tolerance of liver to warm ischemia through the protective role of iNOS and nu

112 Donor age >50 years, BMI >30, warm ischemia time >25 minutes, ITU stay >7 days and ALT

113 cCrCl <60 mL/min/1.73m, PELD >25 points, and warm ischemia time >60 minutes.

114 5 days), cold ischemia time (>10 hours), and warm ischemia time (>40 minutes).

115 me (mean, 159 vs. 188 min; P<0.001), shorter warm ischemia time (2 vs. 5 min; P<0.001) and a lower in

116 status at transplantation, donor age, donor warm ischemia time (DWIT), and cold ischemia time (CIT).

117 In patients with embolization, the warm ischemia time (from embolization to removal of the

118 ntified recipient BMI (P = 0.046), recipient warm ischemia time (odds ratio, OR, 1.032; 95% CI, 1.008

119 " such as cold ischemia time (CIT) recipient warm ischemia time (WIT) and the use of thrombolytic flu

120 ischemia time (CIT) at 2-hour intervals and warm ischemia time (WIT) at 10-minute intervals showed t

121 In the HCV+ cohort, recipient race, warm ischemia time (WIT), and diabetes also independentl

122 sults are as follows: operative time 4.5 hr, warm ischemia time 25 min, and blood transfused (packed

123 es, estimated blood loss 344.2 +/- 690.3 mL, warm ischemia time 4.9 +/- 3.4 minutes, and donor length

124 n after circulatory death (DCD, n = 36, mean warm ischemia time = 2 min) and donation after brain dea

125 and donation after brain death (DBD, n = 76, warm ischemia time = none) were collected.

126 The donor organ was subjected to 1 hour of warm ischemia time after circulatory cessation, then flu

127 s well as clinical factors, such as cold and warm ischemia time and HLA mismatch.

128 cases showed no significant differences for warm ischemia time and other donor outcomes, delayed gra

129 um level, donor length of hospital stay, and warm ischemia time approached significance.

130 perform this type of anastomosis may reduce warm ischemia time as well.

131 atients, retransplant recipients, donor age, warm ischemia time greater than 30 minutes and cold isch

132 last 5 years with a nearly 50% reduction of warm ischemia time in experienced hands.

133 onor-specific antibody, negative crossmatch, warm ischemia time less than 60 min, absence of recipien

134 a mean estimated blood loss of 85.7 mL and a warm ischemia time of 116.0 seconds.

135 Mean warm ischemia time of the pancreas graft was 34 min.

136 n to asystole was 15.9+/-1.9 min and overall warm ischemia time was 12.5+/-1.0 min.

137 n, mean hospital stay was 3.2 days, and mean warm ischemia time was 123.3 seconds.

138 Mean warm ischemia time was 14.7 minutes (range, 7-40 minutes

139 The warm ischemia time was 21 minutes, and the cold ischemia

140 Mean warm ischemia time was 3 minutes after laparoscopic harv

141 let isolation time was 185 (37) minutes, and warm ischemia time was 51 (62) minutes.

142 Average warm ischemia time was 76 minutes.

143 /-0.7 vs. 3.0+/-0.7 hours, P <0.04), whereas warm ischemia time was shorter (3:55+/-1:47 vs. 4:55+/-0

144 Per minute increase in warm ischemia time was the only significant risk factor

145 hospitalization at time of OLT, and cold and warm ischemia time were independent predictors of surviv

146 s, improving renal cooling or shortening the warm ischemia time will expand its indications further.

147 After remaining in situ for 120 min (30-min warm ischemia time, 90-min cold ischemia time), the seco

148 rgical demographics included operative time, warm ischemia time, and estimated blood loss.

149 Graft survival is affected by donor gender, warm ischemia time, and pretransplant patient condition.

150 etwork for Organ Sharing (UNOS) status, cold/warm ischemia time, intraoperative blood loss, and occur

151 cluded operative time, islet isolation time, warm ischemia time, islet equivalent (IE) counts, estima

152 sis, panel-reactive antibodies, and cold and warm ischemia time, the odds of oliguria were 1.60 (1.14

153 prove perioperative characteristics, such as warm ischemia time, to levels comparable to open surgery

154 system closure and hemostasis with a limited warm ischemia time.

155 transaminase, UNOS status, donor gender, and warm ischemia time.

156 also enriched in DCD donors after the first warm ischemia time.

157 quality of life, shorter operating time, and warm ischemia time.

158 (LPN), particularly in regards to decreased warm ischemia time.

159 ), durations of perfusion (1 and 24 hr), and warm ischemia times (15 and 45 min).

160 d hypothermia should be considered if longer warm ischemia times are anticipated (i.e. >25 min).

161 nephrectomy group had shorter operative and warm ischemia times by 52 minutes (P < 0.001) and 102 se

162 Mean cold and warm ischemia times were 9:08 +/- 2:57 hr and 51 +/- 9 m

163 Outcomes evaluated were operative and warm ischemia times, blood loss, donor complications, le

164 ve complications, conversions, operative and warm ischemia times, blood loss, length of hospital stay

165 may be associated with shorter operative and warm ischemia times, patients undergoing laparoscopic ne

166 kidneys, which is susceptible to changes in warm ischemia times.

167 ime, and significantly decreased with longer warm ischemia times.

168 he open group but nonsignificantly different warm ischemia times.

169 o kidneys during reperfusion after 1 hour of warm ischemia using a mouse model.

170 owing a lethal 90 minutes of partial in vivo warm ischemia was examined.

171 Partial hepatic warm ischemia was induced in C57Bl/6 wild-type (WT) and

172 Local warm ischemia was induced in groups wild-type (WT) and t

173 A 30-min period of preretrieval warm ischemia was induced.

174 Partial warm ischemia was produced in hepatic lobes for 90 min f

175 METHODS.: Partial warm ischemia was produced in the left and middle hepati

176 -two porcine kidneys presenting up to 90 min warm ischemia were perfused with oxygenation at 4 degree

177 liver tissue that has experienced 30 min of warm ischemia when compared with SCS tissues.

178 e (GFR) of kidneys subjected to preretrieval warm ischemia when measured in situ at 2 weeks after tra

179 liver tissue that has experienced 30 min of warm ischemia, when compared with simple cold storage.

180 DCD kidneys have increased caspase-1 due to warm ischemia (WI) and increased caspase-3 and apoptosis

181 Control of warm ischemia (WI) lesions that occur with donation afte

182 Donor lungs obtained after prolonged warm ischemia (WI) may be unsuitable for transplantation

183 on reperfusion in line with the duration of warm ischemia with a concomitant rise in the vasoconstri

184 subjected to 45, 60, 120, and 150 min liver warm ischemia with or without portosystemic shunt (splen

185 gly increased in the hepatocytes after liver warm ischemia with portosystemic shunt, compared with li

186 t kidneys were exposed to 30 minutes in situ warm ischemia, without application of heparin.