ライフサイエンスコーパス: rewarming

1 ours (before rewarming), and 96 hours (after rewarming).

2 hese temperature conditions for 6 hrs before rewarming.

3 ter followed by release of the occluders and rewarming.

4 maintained for 24 hours followed by passive rewarming.

5 auses Ca(2+) loading and reduced function on rewarming.

6 ere unsuitable candidates for OLT died after rewarming.

7 icrotubule network was observed after 60 min rewarming.

8 n = 94) followed by cardioplegic arrest and rewarming.

9 ct the brain through improved cooling and/or rewarming.

10 r 72 hours, followed by spontaneous, natural rewarming.

11 plegic arrest and subsequent reperfusion and rewarming.

12 ollowed by simulated cardioplegic arrest and rewarming.

13 dioprotection during cardioplegic arrest and rewarming.

14 rdial function after cardioplegic arrest and rewarming.

15 ion during simulated cardioplegic arrest and rewarming.

16 bjected to simulated cardioplegic arrest and rewarming.

17 ammatory upregulation in the graft by gentle rewarming.

18 ricular function were rapidly reversed after rewarming.

19 d to optimize the protocol and achieve liver rewarming.

20 er (100 W) and lower power (20 W) ultrasonic rewarming.

21 voiding damage caused by slow and nonuniform rewarming.

22 eizure occurred in 34 infants (11.5%) during rewarming.

23 ystals of LS3 and LS4 both convert to HS1 on rewarming.

24 ens protein alphaA-crystallin (CRYAA) during rewarming.

25 ilization, cryoprotectant agent loading, and rewarming.

26 yocardial infarction) followed by controlled rewarming.

27 l conditions, during cortical cooling and on rewarming.

28 followed by a slight ( approximately 2-3 K) rewarming.

29 ring 24 hours therapeutic hypothermia, until rewarming.

30 were obtained during cooling and again after rewarming.

31 very of normothermic homeostasis ensues upon rewarming.

32 mia, followed by a secondary increase during rewarming.

33 hypothermia and remained at this level after rewarming.

34 atures in a pig model of surface cooling and rewarming.

35 values of interleukin-10 were observed after rewarming.

36 urs followed by 12 to 24 hours of controlled rewarming.

37 in nonsurvivors (n=6) at admission and after rewarming.

38 lapse; and SEPs during hypothermia and after rewarming.

39 ents during mild therapeutic hypothermia and rewarming.

40 ests at room temperature, after cooling, and rewarming.

41 n, thereby normalizing drug metabolism after rewarming.

42 pact of hypothermia on drug metabolism after rewarming.

43 which contributes causally to the injury at rewarming.

44 ortening the time to achieve hypothermia and rewarming.

45 meters were restored to precooling levels on rewarming.

46 measured at the end of both hypothermia and rewarming (1 and 2 hrs after traumatic brain injury).

47 jury for 4 hours, 33 degrees C) with gradual rewarming (1 degrees C per hour) for the preservation of

48 posttraumatic hypothermia followed by rapid rewarming (15 mins) failed to decrease contusion volume,

49 re continued in both groups until the end of rewarming (2 hrs after traumatic brain injury).

50 = 8) were tested at 25 degrees C and during rewarming (30-34 degrees C).

51 In contrast to cold storage alone, rewarming (37 degrees C for 24 hr) of cold stored cells,

52 induced cord hypothermia (33 degrees C) then rewarming (37 degrees C).

53 es), DHCA (120 minutes at 18 degrees C), and rewarming (40 minutes).

54 : 48 hr cold: 2+/-0.6%, 48 hr cold and 24 hr rewarming: 54+/-17%), which was confirmed by the TEM bas

55 of synaptic contacts, which are reformed on rewarming, a form of structural plasticity.

56 ng whole-body hypothermia were randomized to rewarming after 48 or 72 hours of hypothermia.

57 jugular venous desaturation can occur during rewarming after cardiopulmonary bypass surgery.

58 l application suggests that controlled graft rewarming after cold storage is a feasible and safe meth

59 The recovery of cytoplasmic Ca2+ during rewarming after rapid cooling in lactate was slower than

60 , which are released into the cytoplasm upon rewarming allowing synthesis of specific clock proteins.

61 ange during mild therapeutic hypothermia and rewarming, although low values of interleukin-10 were ob

62 Specimens were harvested following rewarming and 2 hours of recovery.

63 c encephalopathy but data on seizures during rewarming and associated outcomes are scarce.

64 erve as a foundation for ultrasonic cryovial rewarming and demonstrates potential for scaling to larg

65 Hands were imaged to monitor rewarming and reperfusion.

66 that cold-induced wheals usually develop on rewarming and resolve within an hour and that anaphylaxi

67 hocardiography at 24 hours, 72 hours (before rewarming), and 96 hours (after rewarming).

68 hypothermic perfusion, controlled oxygenated rewarming, and normothermic perfusion (DHOPE-COR-NMP), o

69 demographics were collected during cooling, rewarming, and posttreatment periods (8 d).

70 onary bypass, decreased significantly during rewarming, and remained depressed 6 hrs after cardiopulm

71 rs cold ischemia durations, gradual recovery/rewarming, and risk of hemolysis.

72 appropriate inotropic support, attention to rewarming, and ventilator management are key components.

73 Cord hypothermia-rewarming, applied to awake patients, did not cause disc

74 This study aids in CPA development for EM rewarming approaches advancing organ cryopreservation.

75 A range of electromagnetic (EM) rewarming approaches are being studied with the potentia

76 igher odds of electrographic seizures during rewarming are associated with death or disability at 2 y

77 emperatures (2.5 or 5 degrees C) followed by rewarming at 20 degrees C.

78 25 degrees C, but returned to control during rewarming at 34-35 degrees C.

79 2-33 degrees C for 72 hours followed by slow rewarming at a rate compatible with maintaining intracra

80 After rewarming at approximately 12 degrees C/min and removal

81 dered and a minimum observation period after rewarming before brain death testing ensues should be es

82 creased permeability in the first hour after rewarming but had significantly increased permeability a

83 Myocyte contractility was measured after rewarming by videomicroscopy.

84 During rewarming, cardiovascular effects of dopamine at moderat

85 Cardioplegic arrest and rewarming caused a decline in steady-state myocyte short

86 Hyperkalemic cardioplegia and rewarming caused a significant reduction in myocyte velo

87 Rewarming caused retraction of pseudopods on taxol-treat

88 ming protocol using continuous arteriovenous rewarming (CAVR) or to a standard rewarming (SR) control

89 es during cardiopulmonary bypass just before rewarming commenced (hypotensive, hypothermic), after re

90 ng was reduced after cardioplegic arrest and rewarming compared with normothermic control (37 +/- 3 v

91 We aimed to determine whether hypothermia-rewarming completed prior to reperfusion, also prevents

92 machine-assisted slow controlled oxygenated rewarming (COR) for 90 minutes before engrafting.

93 study aims to compare controlled oxygenated rewarming (COR) with continuous upfront normothermic per

94 n phase) and 1 hour of controlled oxygenated rewarming (COR), using a perfusion fluid containing an h

95 radual rewarming using controlled oxygenated rewarming (COR).

96 For instance, in dielectric rewarming CPA is the target for heating, while in nanowa

97 ance) for capillary morphologic features and rewarming curve characteristics.

98 kin temperature, and for the areas under the rewarming curves (0.684).

99 atures were measured and baseline images and rewarming curves were analyzed.

100 Area measurements and rewarming distinguished true temperature sensitivity fro

101 perature management time (initiation through rewarming) divided by calculated total ischemia time (ap

102 Hypothermia for 48 h with slow rewarming does not reduce mortality of improve global fu

103 nd glucose at the start of NMP compared with rewarming durations of 30 min (COR-30) and 60 min (COR-6

104 We examined brain cooling and rewarming during pH-stat and alpha-stat cardiopulmonary

105 age due to prolonged cold ischemia times and rewarming during the long benching procedure.

106 Rewarming eliminated open canalicular system dilation an

107 fants had electrographic seizures during the rewarming epoch compared with the preceding epoch (group

108 ography readers blinded to treatment arm and rewarming epoch.

109 ed in the 12 hours prior and 12 hours during rewarming for evidence of electrographic seizure activit

110 g hypothermia (FPR 3; 95% CI, 1-7) and after rewarming (FPR 0; 95% CI, 0-18) were reliable predictors

111 Complement activation occurs during rewarming from mild therapeutic hypothermia after cardia

112 commenced (hypotensive, hypothermic), after rewarming (hypotensive, normothermic) just before discon

113 3.5 degrees C for 72 hours, followed by slow rewarming (hypothermia group).

114 (3) preconditioning/cardioplegic arrest and rewarming, hypoxia (20 minutes) and reoxygenation (20 mi

115 herapeutic hypothermia for 48-72 h with slow rewarming improved mortality in children after brain inj

116 cultures followed by cardioplegic arrest and rewarming improved myocyte function compared with cardio

117 This study tested vitrification and rewarming in 0.5-3 L volumes using cryoprotective agents

118 ive temperature 36.0 degrees C, using active rewarming in 92% and 1-hour presurgical antibiotic admin

119 inuous venovenous hemofiltration circuit for rewarming in a juvenile goat model after induction of mo

120 rain histology were evaluated 60 hours after rewarming in all dogs.

121 of electroencephalography monitoring during rewarming in infants at risk.

122 y blood flow was similar and unchanged after rewarming in the three experimental groups.

123 hours; (2) simulated cardioplegic arrest and rewarming, incubated in crystalloid cardioplegic solutio

124 ion of 2-MAC and DFO significantly inhibited rewarming-induced apoptotic cell death (plus 2-MAC: 3+/-

125 ers protection against both cold storage and rewarming-induced necrosis and apoptosis.

126 occurrence of electrographic seizures during rewarming initiated at 72 or 120 hours compared with the

127 The resultant rewarming injury could be alleviated by gradual rewarmin

128 sults in the best protective effect on renal rewarming injury during subsequent NMP.

129 y provide the best protective effect against rewarming injury.

130 However, rewarming is associated with significant apoptosis in th

131 Ultrasonic rewarming is currently under development, but its effect

132 Ultrasonic rewarming is faster than the gold-standard (120+/-5 s),

133 too slow or cracking from thermal stress if rewarming is not uniform.

134 ept that human organ scale vitrification and rewarming is physically possible, thereby enabling human

135 similarly fail due to ice crystallization if rewarming is too slow or cracking from thermal stress if

136 The optimal rate of rewarming is unknown.

137 We measure post-rewarming liver spheroid viability and viable cell numbe

138 At most sites examined in PPCr, rewarming M1 resulted in a reestablishment of the baseli

139 sodes is unknown, but one suggestion is that rewarming may be related to replacement of gene products

140 uced by short-term hypothermic perfusion and rewarming, may protect hearts against ischaemic/reperfus

141 ollowing targeted temperature management and rewarming (median 34 hr from ICU admission).

142 Rapid volumetric rewarming methods are needed to enable the effective cry

143 Optimal duration of, and rewarming methods from, resuscitative hypothermia need c

144 nt differences in viable cell number between rewarming methods.

145 The present study has used the chilling-rewarming model, together with microtubule stabilizing (

146 After rewarming, myocardial function was restored.

147 rees C x 2 hours followed by reperfusion and rewarming (n = 62); and (3) PCO/cardioplegia: 5 minutes

148 ees C x 2 hours) followed by reperfusion and rewarming (n = 8); and (2) PCO/cardioplegia: institution

149 ) or 24 hours (n = 179), followed by gradual rewarming of 0.5 degrees C per hour until reaching 37 de

150 restoration after submaximal stimulation or rewarming of chilled platelets.

151 However, rewarming of vitrified organs can similarly fail due to

152 ep hypothermic circulatory arrest (DHCA) and rewarming on CPB.

153 effects during cooling and the effects after rewarming on drug metabolism and response.

154 cooling to 32-33 degrees C followed by slow rewarming or controlled normothermia.

155 ular cells whether apoptosis is specific for rewarming or it also occurs during cold storage and whet

156 ing different periods of cold ischemia (CI), rewarming, or reperfusion, and (ii) effects of inhibitio

157 hypothermia at 33 C, followed by controlled rewarming, or targeted normothermia with early treatment

158 ": during induction, maintenance of cooling, rewarming, or within 15 hrs after normothermia in 57% (2

159 mic) rats at the end of both hypothermia and rewarming (p <.05), demonstrating that hypothermia reduc

160 ersity of Wisconsin solution after four-hour rewarming (P<0.05).

161 Activity also increased within 30 min of rewarming, peaking at 120 min.

162 sion volume, those animals undergoing a slow rewarming period (120 mins) demonstrated significantly (

163 al membrane was inhibited during the initial rewarming period after cold exposure.

164 ary hypoxia and stress the importance of the rewarming period in this therapeutic intervention.

165 In addition, the importance of the rewarming period on histopathologic outcome was investig

166 During the rewarming period, however, reductions in SjvO2 to < 50%

167 01) and with lower average rSO(2) during the rewarming phase (72+/-12% versus 83+/-9%, P=.003) and du

168 mpared with group C and group HTS during the rewarming phase (P < .05).

169 netics of dopamine are maintained during the rewarming phase at moderate hypothermia.

170 seven received initiation of LLV during the rewarming phase of CPB (treatment).

171 The rewarming phase was passive.

172 Thus, like continuous CPR, ECMO rewarming plays a crucial role in "the chain of survival

173 Rewarming pre-reperfusion prevented ICP elevation ( ICP

174 rels (GSs) associated with their hibernation-rewarming process.

175 xclusively fuels deep torpor and most of the rewarming process.

176 y artery catheter were randomized to a rapid rewarming protocol using continuous arteriovenous rewarm

177 To design effective EM rewarming protocols for cryopreserved biomaterials, unde

178 et temperature, duration of hypothermia, and rewarming protocols were extracted.

179 studies are needed to determine the optimal rewarming rate and strategy.

180 This study aimed to establish which rewarming rate during COR results in the best protective

181 This study suggests that a rewarming rate of 1.10%/min during COR-120 could result

182 Mean rewarming rates are used to establish the exposure time

183 solution was used during the paired RCCs and rewarming, RCC2/RCC1 x 100 was increased to 96 and 95% i

184 During rewarming, regional brain temperatures and neocortical t

185 infants with electrographic seizures during rewarming (relative risk [95% CI], 1.7 [1.25-2.37]) afte

186 econditioning during cardioplegic arrest and rewarming remain unclear.

187 Although active rewarming remains an accepted and valid process measure,

188 Passive rewarming resulted in a temperature of 37.8 +/- 0.5 degr

189 Rewarming resulted in restoration of disc shape, pseudop

190 Increased durations of CI preceding rewarming resulted in significantly higher activity (P <

191 Rewarming reverses chromatin compaction and releases the

192 pothermia during torpor followed by periodic rewarming (REW) during interbout arousal (IBA), proapopt

193 iod of cardioplegia-ischemia was followed by rewarming, separation from CPB, and 2 hours of post-CPB

194 After rewarming, significant cytoprotection was also observed

195 eriovenous rewarming (CAVR) or to a standard rewarming (SR) control group.

196 ing induced hypothermia (T1), directly after rewarming (T2), and another 24 hrs later (T3).

197 , and five were assigned to the experimental rewarming technique of a modified continuous venovenous

198 However, rewarming techniques that are rapid and scalable (both i

199 Rewarming the cells caused even greater bleb formation a

200 ld be restored to ~95% by simply cooling and rewarming the device.

201 ation toward baseline although at the end of rewarming the metabolic recovery was complete in both gr

202 Rewarming the protoplasts to 29 degrees C reestablished

203 3.5 degrees C for 72 hours, followed by slow rewarming (the hypothermia group).

204 During the first 10 minutes of rewarming, the cerebral microvascular diameter was signi

205 Upon rewarming, the jugular bulb oxygenation remained constan

206 Upon rewarming, the mean flow velocity in the middle cerebral

207 We thus urge caution when using hypothermia-rewarming therapeutically in TSCI.

208 by reducing cord inflammation, though after rewarming these benefits are lost due to increases in co

209 ime was 223.8 and 175.7 min (P=0.07) and the rewarming time was 60.3 and 30.3 min (P=0.03) in the LKT

210 Mean console, warm ischemia, and rewarming times were 130.8 minutes, 2.3 minutes and 42.9

211 bules (MTs) by cold treatment and subsequent rewarming to 29 degrees C.

212 After rewarming to 36.5 degrees C, neurologic examination show

213 ere hypothermia at T(b)= 25 degrees C and on rewarming to 37 degrees C.

214 l cooling, the importance of slow controlled rewarming to avoid rebound brain edema, and the high ris

215 hypothermia for 24 hours followed by passive rewarming to normothermia.

216 f extracorporeal membrane oxygenation (ECMO) rewarming to restore DO(2) and organ blood flow after pr

217 Rewarming took a median of 21.5 hours (16-35 hr) and was

218 ld stored for 6 h with subsequent controlled rewarming up to 35 C for 2 h (COR), or directly subjecte

219 ld stored for 6 h with subsequent controlled rewarming up to 35 degrees C for 2 h (COR), or directly

220 arming injury could be alleviated by gradual rewarming using controlled oxygenated rewarming (COR).

221 ment, but its effect on cells and their post-rewarming viability has not yet been established.

222 conditions and methods for vitrification and rewarming (VR).

223 nd a newly developed 120 kW RF coil, uniform rewarming was achieved in up to 2 L volumes of M22 at ~8

224 r 45 mins of reperfusion after which passive rewarming was allowed.

225 Compared with pre-cooling baseline, rewarming was associated with significantly worse cord p

226 A significant increase after rewarming was demonstrated on high-mobility group box-1

227 SjvO2 during rewarming was dependent on mean arterial pressure, with

228 ixty-minute hypothermia to 33 C, followed by rewarming was induced prior to reperfusion in one group,

229 oup (p=0.051) to a median of 2.2 mg/L during rewarming was observed and was not explained by dosing d

230 When the rewarming was performed either in Na(+)- and Ca(2+)-free

231 The whole body lactate during early rewarming was significantly less with the pH stat strate

232 ere <20%, a repeat short exercise test after rewarming was useful in patients with myotonia congenita

233 atios (95% CIs) for seizure frequency during rewarming were 2.7 (1.0-7.5) for group A and 3.2 (0.9-11

234 The hypothesis was that seizures during rewarming were associated with higher odds of abnormal n

235 ctile processes with cardioplegic arrest and rewarming were examined in a final series of experiments

236 ehydrogenase [LDH] release) before and after rewarming were studied.

237 the cytoplasm after hypothermia followed by rewarming, whereas Na-K-ATPase retained its basolateral

238 urs increased endothelial permeability after rewarming, which appears to depend on the duration of co

239 the survivors were directly extubated after rewarming while two were once more sedated due to pneumo

240 latory arrest at 15 degrees C, and 40-minute rewarming with alpha-stat (group alpha) or pH-stat (grou

241 Rewarming with ECMO restored MAP, CO, DO(2), and blood f

242 Rewarming with ECMO restores blood flow to the heart and

243 Here, we compare ultrasonic rewarming with the gold-standard [Formula: see text]C wa

244 How to achieve optimized hypothermia and rewarming without delayed brain herniation remains a cha