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 ferentiate and repair muscle injury after an ischemic insult.

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

4 restoration of epithelial integrity after an ischemic insult.

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

6 regeneration, and functional recovery after ischemic insult.

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

8 eclaim and preserve liver tissues after warm ischemic insult.

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

10 ization of the retinal vasculature following ischemic insult.

11 crease tissue inflammation in response to an ischemic insult.

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

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

14 tes importantly to neuronal cell death after ischemic insult.

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

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

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

18 kground strains using two different types of ischemic insult.

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

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

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

22 rt-term cardioprotection against a prolonged ischemic insult.

23 role of diffusion and perfusion imaging for ischemic insult.

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

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

26 gnificantly contributes to the outcome after ischemic insult.

27 e cells was transiently suppressed after the ischemic insult.

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

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

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

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

32 nuate acidosis during a subsequent prolonged ischemic insult.

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

34 e primary mediators of neuronal damage after ischemic insult.

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

36 increases the onset of seizures following an ischemic insult.

37 ikely to stabilize cellular structure during ischemic insult.

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

39 st that is putatively cytoprotective against ischemic insult.

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

41 contribute to neural damage following focal ischemic insult.

42 and improves contraction force after severe ischemic insult.

43 re vulnerable to neuronal death following an ischemic insult.

44 and neurobehavioral deficits after a hypoxic-ischemic insult.

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

46 ant to ischemic injury following a sublethal ischemic insult.

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

48 the brain resistant to a subsequent damaging ischemic insult.

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

50 protecting cells from subsequent hypoxic or ischemic insult.

51 eurons in the rat hippocampus from forebrain ischemic insult.

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

53 metabolism, and an increased sensitivity to ischemic insults.

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

55 confer neuroprotection in response to brief ischemic insults.

56 helps promote neuronal survival from hypoxic-ischemic insults.

57 have inherent differential sensitivities to ischemic insults.

58 scaffold to initiate AMPK activation during ischemic insults.

59 various tissues against subsequent sustained ischemic insults.

60 ission may be a protective mechanism against ischemic insults.

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

62 ective neuronal death after transient global ischemic insults.

63 dergo apoptosis after either global or focal ischemic insults.

64 esis of cerebral infarction induced by focal ischemic insults.

65 ronal death in response to subsequent severe ischemic insults.

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

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

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

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

70 sites and protects neurons against cerebral ischemic insults.

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

72 ubstantial amounts of myocardium early after ischemic insults.

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

74 europrotective action extends beyond hypoxic-ischemic insults.

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

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

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

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

79 Although ischemic insults activate REST in selectively vulnerable

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 Secondary ischemic insults caused by systemic factors after severe

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

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

110 70% after induction of either excitotoxic or ischemic insult conditions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Hypoxic-ischemic insult in newborns results in progressive neuro

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

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

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

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

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

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

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

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

135 Ischemic insult increased COX-2 expression in endothelia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 During the ischemic insult there were intergroup differences in the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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