ライフサイエンスコーパス: ischemic insult

1 s (32 mm(3), 40-120 mum microemboli) (double ischemic insults).

2 educing complement-mediated damage following ischemic insult.

3 protecting cells from subsequent hypoxic or ischemic insult.

4 eurons in the rat hippocampus from forebrain ischemic insult.

5 n is known to protect the myocardium from an ischemic insult.

6 ferentiate and repair muscle injury after an ischemic insult.

7 tricular zone by 31% 1 day following hypoxic-ischemic insult.

8 restoration of epithelial integrity after an ischemic insult.

9 eonatal brain is highly sensitive to hypoxic-ischemic insult.

10 regeneration, and functional recovery after ischemic insult.

11 show significant modulation up to 12 h after ischemic insult.

12 and improves contraction force after severe ischemic insult.

13 eclaim and preserve liver tissues after warm ischemic insult.

14 he survival and recovery of neurons after an ischemic insult.

15 crease tissue inflammation in response to an ischemic insult.

16 s protective when given up to 14 h after the ischemic insult.

17 allow the injured graft to recover from its ischemic insult.

18 tes importantly to neuronal cell death after ischemic insult.

19 imuli before induction of a controlled, mild ischemic insult.

20 dium was proportional to the severity of the ischemic insult.

21 rotect against a subsequent, more prolonged, ischemic insult.

22 imate brain cell death at a time remote from ischemic insult.

23 kground strains using two different types of ischemic insult.

24 nsive mucosal loss, consistent with an acute ischemic insult.

25 ned elevated during the first week after the ischemic insult.

26 omy or the type of model used to produce the ischemic insult.

27 rt-term cardioprotection against a prolonged ischemic insult.

28 role of diffusion and perfusion imaging for ischemic insult.

29 s than IPC at protecting against a 90-minute ischemic insult.

30 gnificantly contributes to the outcome after ischemic insult.

31 e cells was transiently suppressed after the ischemic insult.

32 c preservation or when subjected to a direct ischemic insult.

33 ers/products are upregulated early after the ischemic insult.

34 ical infarct volumes measured 24 h after the ischemic insult.

35 osis was evident 24 h after the hyperthermic ischemic insult.

36 nuate acidosis during a subsequent prolonged ischemic insult.

37 ization of the retinal vasculature following ischemic insult.

38 acent to the CA1 layer as early as 2 d after ischemic insult.

39 e primary mediators of neuronal damage after ischemic insult.

40 ated heparanase were confirmed in lungs with ischemic insult.

41 rgoes both cold and warm ischemia and global ischemic insult.

42 e, B-Myb and C-Myb expression increases with ischemic insult.

43 increases the onset of seizures following an ischemic insult.

44 ikely to stabilize cellular structure during ischemic insult.

45 Ca) agonist, NS1619, protects the heart from ischemic insult.

46 st that is putatively cytoprotective against ischemic insult.

47 for treating fatty livers at the time of an ischemic insult.

48 contribute to neural damage following focal ischemic insult.

49 re vulnerable to neuronal death following an ischemic insult.

50 and neurobehavioral deficits after a hypoxic-ischemic insult.

51 nction and cellular injury in the face of an ischemic insult.

52 ant to ischemic injury following a sublethal ischemic insult.

53 arct area, even when delivered 1 h after the ischemic insult.

54 the brain resistant to a subsequent damaging ischemic insult.

55 citoxicity is a major focus of treatment for ischemic insults.

56 confer neuroprotection in response to brief ischemic insults.

57 helps promote neuronal survival from hypoxic-ischemic insults.

58 have inherent differential sensitivities to ischemic insults.

59 various tissues against subsequent sustained ischemic insults.

60 ission may be a protective mechanism against ischemic insults.

61 ective neuronal death after transient global ischemic insults.

62 dergo apoptosis after either global or focal ischemic insults.

63 esis of cerebral infarction induced by focal ischemic insults.

64 in human diseases associated with immune or ischemic insults.

65 llary perfusion and sensitized the retina to ischemic insults.

66 upling of NMDAR to an ion channel TRPM2 upon ischemic insults.

67 scaffold to initiate AMPK activation during ischemic insults.

68 titis, indicating that it can protect beyond ischemic insults.

69 ronal death in response to subsequent severe ischemic insults.

70 enerative diseases, as well as traumatic and ischemic insults.

71 pective regions, in pigs subjected to double ischemic insults.

72 e of SIRT1 in the tolerance of aged heart to ischemic insults.

73 s during brain development and after hypoxic-ischemic insults.

74 metabolism, and an increased sensitivity to ischemic insults.

75 sites and protects neurons against cerebral ischemic insults.

76 t loss of cerebral blood flow such as during ischemic insults.

77 ubstantial amounts of myocardium early after ischemic insults.

78 inst free radical-mediated, excitotoxic, and ischemic insults.

79 europrotective action extends beyond hypoxic-ischemic insults.

80 , increased during reperfusion after a short ischemic insult (15 min of occlusion), from which the an

81 ect the heart against a subsequent prolonged ischemic insult, a phenomenon known as ischemic precondi

82 ieved by priming the brain with a sub-lethal ischemic insult, a phenomenon known as ischemic precondi

83 thermore, they showed improved resilience to ischemic insult, a promising finding in the context of p

84 Although ischemic insults activate REST in selectively vulnerable

85 brain enters the tissue within minutes of an ischemic insult along perivascular flow channels.

86 eristic of cytotoxic edema, a consequence of ischemic insult and a precursor to fixed structural WM i

87 These grafts are subjected to a greater ischemic insult and are arguably at higher risk of poor

88 arkin and ATG5 levels are related to hypoxic-ischemic insult and are reliable also at birth.

89 hat should be limited to the acute phases of ischemic insult and avoided for long-term treatment afte

90 is up-regulated in brain following a global ischemic insult and down-regulated in ischemic tissues a

91 uce infarct size (IS) induced by a 90-minute ischemic insult and examined the interaction between NHE

92 with IL-18-neutralizing antiserum before the ischemic insult and found a similar degree of protection

93 n delayed neurodegeneration after a cerebral ischemic insult and highlights the significant potential

94 e was significantly increased 18 h after the ischemic insult and remained increased through 72 h.

95 IR involves 2 injuries, an initial ischemic insult and subsequent inflammatory amplificatio

96 C activation is required for protection from ischemic insult and suggest that small molecules that mi

97 show that sumo-2/3-ylation occurs during the ischemic insult and that preconditioning does not change

98 ortant link between the severity of an acute ischemic insult and the circulating levels of BNP.

99 g grafts with damaged or preserved eGC using ischemic insult and transplanted the grafts into recipie

100 hat has been shown to sensitize the heart to ischemic insult and ventricular dysfunction.

101 ndrocytes might be major targets for chronic ischemic insults and activated microglia/macrophages are

102 minutes reperfusion) prior to the prolonged ischemic insult, and intermittent clamping (cycles of 15

103 Younger age, greater injury severity, early ischemic insults, and the use of etomidate and metabolic

104 However, severity of the ischemic insult appears to limit the therapeutic efficac

105 ng to cyclin D/Cdk4/pRb activation following ischemic insult are presently not clear.

106 spholipases that usually occurs following an ischemic insult as evidenced by its attenuation of phosp

107 eads to significantly decreased tolerance to ischemic insult, as demonstrated by impaired postischemi

108 ents in coma or shock or during an anoxic or ischemic insult, as this toxic gas dramatically reduces

109 cent developments have focused upon reducing ischemic insult, as well as decreasing reliance upon the

110 effector protein early during the subsequent ischemic insult, before loss of adenosine triphosphate o

111 th evoked by DNA damage, hypoxia, and global ischemic insult both in vitro and in vivo.

112 d and damages axons that survive the initial ischemic insult but go on to experience a delayed axonal

113 ced neuronal loss by approximately 50% under ischemic insult, but ablation of Cx36 offered no protect

114 reased tissue damage for weeks following the ischemic insult, but there are no approved therapies tha

115 ature asphyxiation suffer an additional warm ischemic insult, but this does not negatively impact tra

116 ot significantly decreased at 18 h after the ischemic insult, but was significantly reduced after 36

117 E2F4 plays a protective role in neurons from ischemic insult by forming repressive complexes that pre

118 Following an ischemic insult, CA1 vessels had more extensive blood-br

119 Secondary ischemic insults caused by systemic factors after severe

120 Myocardial ischemic insult causes depression of fatty-acid beta-oxi

121 After mild, but not severe, ischemic insults, cerebral infarction develops slowly an

122 70% after induction of either excitotoxic or ischemic insult conditions.

123 ce exhibited enhanced vulnerability to brief ischemic insults, consistent with a role for Cx32 gap ju

124 te therapy were evident within 3 days of the ischemic insult demonstrating the potency and efficacy o

125 elate closely with neuronal survival against ischemic insults, depending on the CNS region, protectiv

126 ull mice were markedly protected against the ischemic insult, displaying a reduced infarct size and p

127 nsistent with a model in which after a short ischemic insult, DNA repair proteins such as DNA-PK are

128 However, for prolonged ischemic insults exceeding 75 minutes, intermittent clam

129 defining the extent and location of maximum ischemic insult following RVO compared to FFA, hence rep

130 the acute response of neurons to hypoxic or ischemic insults, for which the mammalian brain is not a

131 nse with LPS converts a subthreshold hypoxic-ischemic insult from no discernable neuronal injury to s

132 Preconditioning the heart before an ischemic insult has been shown to protect against contra

133 imb ischemia administered before a prolonged ischemic insult has systemic protective effects against

134 e intrinsic sensitivity of tissues in SCD to ischemic insults has never been addressed.

135 with protection of the brain against hypoxic-ischemic insult (HI).

136 nt myocardial cytoprotection following acute ischemic insult; however, its sustained activation parad

137 y (p = .02), had a higher frequency of early ischemic insults (hypotension, hypoxia, severe anemia) (

138 osure to ischemia protected against a second ischemic insult imposed 8 or 15 days later.

139 ratories performed a standard focal cerebral ischemic insult in five animal models that included equa

140 evant, because the compound protects against ischemic insult in native A1AR-expressing cardiomyoblast

141 Hypoxic-ischemic insult in newborns results in progressive neuro

142 scular proliferation in the eye, reduced the ischemic insult in OIR (IC(50), 2.6 pg/eye).

143 DA) has been proposed as a model for hypoxic-ischemic insult in the immature brain.

144 , was expressed in brain, activated after an ischemic insult in vivo and in vitro, and contributed to

145 ulated in vitro following hypoxia and global ischemic insult in vivo Finally, we show that shRNA targ

146 haracterize the role of the APC-EPCR axis in ischemic insults in aging.

147 Relevant to recurrent hypoxic-ischemic insults in developing white matter, we examined

148 und protection against glutamate-NO-mediated ischemic insults in vitro and major decreases in infarct

149 oronary artery occlusion-reperfusion (single ischemic insult) in 16 pigs and coronary embolization in

150 resistance to a subsequent, otherwise lethal ischemic insult, in a process termed ischemic preconditi

151 Ischemic insult increased COX-2 expression in endothelia

152 The results presented here show that the ischemic insult increases total and nuclear AhR levels a

153 l excitability and ischemic infarct, whereas ischemic insults induce the release of endogenous biliru

154 The onset of the ischemic insult induced activation of the NF-kappaB path

155 We found that the ischemic insult induces shedding of LRP's ectodomain fro

156 In response to ischemic insult, injured tissues secrete several chemo-c

157 s, presumably as an extension of the initial ischemic insult into areas of vital, noninjured tissue.

158 Increased cell survival after an ischemic insult is critical and depends on several cellu

159 A prominent characteristic of ischemic insults is endoplasmic reticulum (ER) stress as

160 serve, which reduces the ability to tolerate ischemic insults, is a risk for periprocedural MI and th

161 olerance is a phenomenon whereby a sublethal ischemic insult [ischemic preconditioning (IPC)] provide

162 However, ischemic insult leads to a pathogenic level of IgM bindi

163 ighly effective in protecting old liver from ischemic insults, mainly owing to its ability to induce

164 indicate that neuroprotection against acute ischemic insults may require a combination therapy appro

165 nonselective ET-R antagonist given after the ischemic insult, mitigated the decline in GFR at 2 month

166 e of canagliflozin administered shortly into ischemic insult mitigates AKI and attenuates harmful pro

167 etween pairs of samples before and after the ischemic insult of cardiopulmonary bypass.

168 preconditioning were both protective against ischemic insults of 75 and 120 minutes compared with con

169 ent of cardiac viability following transient ischemic insult or myocardial infarction.

170 knockdown did not protect against subsequent ischemic insults or antisense knockdown.

171 Kidney injury, whether due to ischemic insults or chemotherapeutic agents, is exacerba

172 Inflammatory cytokines, brain injury and ischemic insult, or exposure to psychological acute stre

173 A previous exposure to a non-harmful ischemic insult (preconditioning) protects the brain aga

174 erazine, a compound that protects cells from ischemic insults, prevented necrosis of H9c2 cells throu

175 ceptor stimulation, 24 to 48 hours before an ischemic insult, produces a delayed cardioprotective eff

176 Here we show that ischemic insults promote REST binding and epigenetic rem

177 In ischemic preconditioning, a sublethal ischemic insult protects neurons from subsequent ischemi

178 lurane or sevoflurane administered after the ischemic insult reduced brain infarct percentage and neu

179 tions including protection of tissue against ischemic insult, regulation of vascular tone, and modula

180 nerability of CA3 and CA1 to excitotoxic and ischemic insults, respectively.

181 ocytes are known to be highly susceptible to ischemic insults, responding to injury with increased ce

182 The ischemic insult resulted in a greater than 50% decline i

183 With the pericardium open, the same ischemic insult resulted in both LV and RV dilatation, w

184 l features consistent with perinatal hypoxic-ischemic insult(s), warrant the specific designation of

185 iately before or immediately after a hypoxic-ischemic insult substantially blocks tissue damage in a

186 nt with this, brain-mapping studies after an ischemic insult suggest re-emergence of childhood organi

187 g mice and humans, and the protection beyond ischemic insults suggest that the platelet-dependent axi

188 recovery, as well as cell survival after an ischemic insult, suggesting that active I-1 may represen

189 angiopoietin 2 protected the kidneys from an ischemic insult, suggesting that the previously reported

190 lial cells (PTECs) are highly susceptible to ischemic insults that frequently cause acute kidney inju

191 o protect the heart against a more prolonged ischemic insult, the result of which is a marked reducti

192 e results demonstrate that after a transient ischemic insult, the subcellular responses to the accumu

193 During the ischemic insult there were intergroup differences in the

194 Despite the reduction in secondary ischemic insults, there was no difference in neurologic

195 here c-fos mRNA increased in response to the ischemic insult; these elevations were not observed for

196 stimulates revascularization in response to ischemic insult through its ability to activate Akt-eNOS

197 elevated the resistance of the aged heart to ischemic insults through stabilizing EPCR.

198 clamp-and-go technique results in a massive ischemic insult to several major organ systems.

199 unologic process, which is accelerated by an ischemic insult to the allograft.

200 balance and neuronal cell death following an ischemic insult to the brain.

201 Endotoxin causes an ischemic insult to the gallbladder similar to that seen

202 T/HS cause ischemic insult to the gut, resulting in the release of

203 Thus, Rieckmann et al. showed that an acute ischemic insult to the heart, which induces sterile infl

204 epiphenomenon and a manifestation of greater ischemic insult to the myocardium.

205 inistration of this analog up to 1h after an ischemic insult to the rat brain had a potent neuroprote

206 mia was also protective against a subsequent ischemic insult to the same kidney, revealing that syste

207 nt excitotoxicity in vitro, and mild hypoxic/ischemic insult to these mice in vivo results in signifi

208 that could produce recurrent and cumulative ischemic insults to multiple organs, such as the brain.

209 ch may allow distinction of acute vs. remote ischemic insults to the myocardium.

210 After an ischemic insult, total renal blood flow returns toward n

211 Injury-ischemic insults trigger AKT growth signaling that activ

212 ious cycle of stroke injury in which initial ischemic insults trigger the release of endogenous bilir

213 The response of the retina to ischemic insult typically leads to aberrant retinal neov

214 We delivered a brief in vivo preconditioning ischemic insult (unilateral common carotid artery ligati

215 uingly, in the long term (4 months after the ischemic insult), Vhl-deficient kidneys displayed a hete

216 in response to various acute stimuli such as ischemic insult, visceral pain and electroconvulsive sho

217 If the duration of ischemic insult was increased to 90 min, the therapeutic

218 accentuated LV dysfunction caused by double ischemic insults was linked to expansion of the MVO zone

219 Remarkably, within weeks after the initial ischemic insult, we observed functional cardiac recovery

220 anism of the muscle stem cell in response to ischemic insults, we explored cellular interactions betw

221 e vulnerability of these circuits to hypoxic-ischemic insults, we hypothesize that quantitative SSEP

222 te that M40401 protects cerebral tissue from ischemic insult when administered before MCAO, probably

223 marked neuroprotective effects against focal ischemic insults when it was given up to 6 hr after isch

224 ent that can be administered after a hypoxic-ischemic insult, which provides robust, nearly complete

225 such as the lower limb, to a similar priming ischemic insult would result in protection of the brain

226 paired in aging that sensitizes the heart to ischemic insults, young C57BL/6 mice (age 3-4 mo), middl