ライフサイエンスコーパス: post-ischemic

1 The compound effectively reduces delayed post-ischemic (5 min bilateral carotid occlusion) hippoc

2 ia, whereas preconditioning had no effect on post-ischemic activation of ERK1/2.

3 f Rac1 AS-ODNs also significantly attenuated post-ischemic activation of JNK, downstream of MLK3, and

4 Post-ischemic activation of NMDA receptors (NMDARs) has

5 In conclusion, testosterone inhibits the post-ischemic activation of NOSs and Akt and the ratio o

6 The post-ischemic activation patterns of MAPKs may explain t

7 hly formed clot, and evaluate the effects of post-ischemic administration of simvastatin on stroke ou

8 at reducing infarct volume after intravenous post-ischemic administration.

9 Post-ischemic angiogenesis occurred in P-treated as well

10 Finally, the role of IMZ in post-ischemic angiogenesis was examined in a chronic hyp

11 t against cerebral I/R injury by suppressing post-ischemic apoptosis, whereas heavy ethanol consumpti

12 vate restored the morphological integrity of post-ischemic astrocytes and prevented gliosis.

13 Pyruvate prevented the cell death of post-ischemic astrocytes by inhibiting the leakage of la

14 and thus restores the cellular ATP levels in post-ischemic astrocytes.

15 s, would prevent sound-triggered seizures in post-ischemic audiogenic seizure-prone rats.

16 Rather, massive hemorrhages and post-ischemic BBB disruption were observed, unrelated to

17 The levels of post-ischemic bcl-2 mRNA and protein were increased excl

18 Compared with placebo, UDCA improved peak post-ischemic blood flow in the arm (+18%, p = 0.038), a

19 %, p = 0.038), and a trend for improved peak post-ischemic blood flow in the leg was found (+17%, p =

20 wild-type mice, iNOS mRNA expression in the post-ischemic brain begun between 24 and 48 hr peaked at

21 correlated with higher phagocytic indices in post-ischemic brain immune cells.

22 However, the role of heparanase in the post-ischemic brain is not well defined.

23 ting that cell surface CD36 expressed in the post-ischemic brain originates from the periphery.

24 n response to osmotic stress and ameliorates post-ischemic brain swelling through a simultaneous inhi

25 Cerebral T cell accumulation in the post-ischemic brain was driven by increased local T cell

26 AG is medicated by inhibition of iNOS in the post-ischemic brain.

27 based on modulation of NO production in the post-ischemic brain.

28 mulation-evading the systemic therapy-in the post-ischemic brain.

29 ersus the full agonist diazepam to attenuate post-ischemic CA1 damage.

30 Excitatory postsynaptic currents in post-ischemic CA1 exhibit an enhanced Ca(2+)-dependent c

31 se-3 and blocked the increase in p75(NTR) in post-ischemic CA1 neurons but did not prevent ischemia-i

32 effects, including the potential to improve post-ischemic cardiac function and hemodynamics, decreas

33 This resulted in beneficial effects on post-ischemic cardiac function, with the impaired contra

34 Whereas HO-1 deficiency exacerbates post-ischemic cardiac inflammation in mice, hHO-1 gene t

35 atherogenesis, vascular aneurysm and impairs post-ischemic cardiac remodeling through concerted roles

36 es to the ischemic myocardium and to adverse post-ischemic cardiac remodeling.

37 pression may determine the outcome as either post-ischemic cell death or tolerance.

38 ecause it targets a fundamental mechanism of post-ischemic cell death: intramitochondrial Ca(2+) over

39 photothrombosis to the motor cortex of mice, post-ischemic cerebral blood flow was measured using mul

40 ain barrier (BBB) function may contribute to post-ischemic cerebral injury by yet unknown mechanisms.

41 cient mice that was concomitant with reduced post-ischemic cerebral thrombo-inflammation (intracerebr

42 critical braking mechanism against excessive post-ischemic CF activation and proliferation through re

43 critical braking mechanism against excessive post-ischemic CF activation and proliferation through re

44 beta agonist treatments every 48 hr improved post-ischemic cognition.

45 Post-ischemic contractile dysfunction is a contributor t

46 novel cardioprotective intervention to limit post-ischemic contractile dysfunction.

47 s measured in vitro and in vivo toxicity and post-ischemic cytoprotective effects of a cysteine prote

48 of an superoxide dismutase mimetic corrected post-ischemic defects in neovascularization, oxygen deli

49 from cerebral ischemia is by preventing the post-ischemic elevation of Dkk1, a neurodegenerative fac

50 Both red wine and ethanol suppressed post-ischemic expression of adhesion molecules and micro

51 lin-1 was not altered in the ethanol groups, post-ischemic expression of Bcl-2 was significantly grea

52 Moreover, although post-ischemic expression of Beclin-1 was not altered in

53 nes/chemokines, and significantly alleviated post-ischemic expression of inflammatory mediators.

54 Post-ischemic expression of LC3B and LC3B-positive neuro

55 eatment bypassed AK1 deficiency and restored post-ischemic flow to wild-type levels, achieving phenot

56 c curve C-statistic of 0.94 to differentiate post-ischemic from remote territory.

57 ficantly enhanced infarct size reduction and post-ischemic functional recovery (P:<0.05 versus IPC).

58 would improve cardiac energy production and post-ischemic functional recovery in neonatal rabbit hea

59 Perfusion with carnosine promoted post-ischemic functional recovery in WT but not in AR-nu

60 g effects of APC in contributing to enhanced post-ischemic functional recovery were determined and co

61 reconditioned hearts correlated tightly with post-ischemic functional recovery.

62 ing infarct size and significantly enhancing post-ischemic functional recovery.

63 rall ATP production and an improved in vitro post-ischemic functional recovery.

64 gered impairment of complex II occurs in the post-ischemic heart and should be useful to identify dis

65 a specific mechanism for DJ-1's role in the post-ischemic heart, these data break new ground for pot

66 zones and non-ischemic remote regions of the post-ischemic heart.

67 n of the 70-kDa flavin protein occurs in the post-ischemic heart.

68 lectrical and contractile dysfunction in the post-ischemic heart.

69 educed energetic signal communication in the post-ischemic heart.

70 In post-ischemic hearts, procaspase-1 overexpression was as

71 dial insulin signaling in protection against post-ischemic HF.

72 E2-treatment improves cognition and reduces post-ischemic hippocampal injury by means of ER-beta act

73 Pre- and post-ischemic HSP-25 levels were much higher in the prec

74 Behavioral groups had inadvertent post-ischemic hypothermia that decreased CA1 death and l

75 that microglial CD36 is a key determinant of post-ischemic IL-1B production by regulating caspase-1 a

76 The role of TnC for ischemic brain injury, post-ischemic immune responses and stroke recovery has s

77 The post ischemic increase in T2 of the control group was si

78 synergistic actions dramatically prevent the post-ischemic induction of caspase activity associated w

79 gated the regulatory mechanisms that lead to post-ischemic induction of p75(NTR).

80 lls (by 54 +/- 6%; p<0.05) and decreased the post-ischemic infarct volume in rats (by 30 +/- 5%; p<0.

81 uman heme oxygenase-1 (hHO-1) in attenuating post-ischemic inflammation in a murine and a porcine isc

82 Mechanistically, PKM2 regulates post-ischemic inflammation in peripheral neutrophils by

83 reported in rodents, its role in attenuating post-ischemic inflammation is unclear.

84 es also provide evidence that suppression of post-ischemic inflammation may play a critical role in e

85 Post-ischemic inflammation was examined by expression of

86 on with Ccr2(-/-) bone marrow dampened renal post-ischemic inflammation, reduced aortic Ccl2 and infl

87 plays an essential role in the regulation of post-ischemic inflammation, which is detrimental to reco

88 We determined the influence of LAC on post-ischemic inflammation.

89 brain against its I/R injury by suppressing post-ischemic inflammation.

90 effect independent of hemodynamic factors or post-ischemic inflammation.

91 f a STEP-derived peptide mimetic reduces the post-ischemic inflammatory response and attenuates brain

92 ated pathologies such as atherosclerosis and post-ischemic inflammatory responses.

93 or descending occlusion and reperfusion, the post-ischemic influx of CD45(+) leukocytes, Ly-6G(+) neu

94 rsely, in our porcine model of ischemia, the post-ischemic influx of myeloperoxidase-positive neutrop

95 work will examine the utility in preventing post-ischemic injury during renal transplantation, where

96 We conclude that post-ischemic injury led to transient up-regulation of g

97 The first phase coincided with post-ischemic injury over 2 days post-transplantation an

98 iR21/HIF-alpha signaling in MZB cells during post-ischemic injury.

99 which complement subcomponents contribute to post-ischemic injury.

100 uel substrate to protect rat astrocytes from post-ischemic injury.

101 the amygdala and the frontal cortex at three post-ischemic intervals: 4, 24, and 72 h (Experiment 1).

102 rine proteases could be beneficial to reduce post-ischemic intestinal inflammation.

103 In summary, post-ischemic JNK and p38 (but not ERK1/2) activation wa

104 -srIkB treatment also significantly affected post-ischemic kidney immune cell populations, lowering n

105 CCR2 mediated myeloid cell homing to the post-ischemic kidney in a cell-individual manner.

106 fucose dose, complement activation and acute post-ischemic kidney injury are prevented, with addition

107 ery of Exo-srIkB decreased NF-kB activity in post-ischemic kidneys and reduced apoptosis.

108 Intravital imaging of post-ischemic kidneys revealed reduced vascular leak wit

109 Post-ischemic kidneys showed decreased gene expression o

110 Global gene expression profiling of post-ischemic kidneys showed that alphavbeta5 inhibition

111 icroglial morphology in 3D we found that the post-ischemic loss of microglial cell territory, branchi

112 function reduced histological injury of the post-ischemic lung and reduced mortality from 55 to 9%.

113 eutrophil gelatinase-associated lipocalin in post-ischemic mice than in the Exo-Naive treatment group

114 We observed a strong divergence of post-ischemic microglia, monocyte-derived macrophages an

115 Early astroglial response to post-ischemic microvascular hypoperfusion may contribute

116 ore, treatment with REST siRNA prevented the post-ischemic miR-29c down-regulation and DNMT3a inducti

117 c and subjected to transient focal ischemia, post-ischemic miR-29c levels were restored and the infar

118 ore was to determine whether a difference in post-ischemic mitochondrial function may play a role in

119 the 70 kDa FAD-binding protein occur in the post-ischemic myocardium and are thought to be mediated

120 protein S-glutathionylation was enhanced in post-ischemic myocardium at the NQR 51-kDa subunit, but

121 ition reduces macrophage infiltration to the post-ischemic myocardium in vivo.

122 a were partially or completely eliminated in post-ischemic myocardium obtained from in vivo regional

123 e electron transfer activity (ETA) of SQR in post-ischemic myocardium was significantly decreased by

124 ve modification of the 70-kDa protein in the post-ischemic myocardium, we used the identified S-gluta

125 recruitment and macrophage activation in the post-ischemic myocardium.

126 otein tyrosine nitration was detected in the post-ischemic myocardium.

127 ddress the role of endogenous H2O2 in ECs in post-ischemic neovascularization in vivo.

128 -dysfunctional ATP7Amut mice showed impaired post-ischemic neovascularization.

129 Post-ischemic neurodegeneration may be accelerated by a

130 Whether 3K3A-APC can influence post-ischemic neurogenesis and improve neurological outc

131 identify a unique role of STEP in regulating post-ischemic neuroinflammation and further emphasizes t

132 -2) and the c-Jun N-terminal kinase (JNK) in post-ischemic neuronal damage was assessed in a model of

133 ation prevents GluR2 suppression and rescues post-ischemic neurons from ischemia-induced cell death i

134 of Akt, phosphorylated Akt was not active in post-ischemic neurons, as assessed by kinase assays and

135 Furthermore, red wine significantly reduced post-ischemic neutrophil infiltration.

136 yl rats were treated identically except that post-ischemic oxygenation was maintained for 6 h and cer

137 The primary endpoint was post-ischemic peak peripheral arm blood flow as assessed

138 administered intravenously in the immediate post-ischemic period following a 2-h period of transient

139 nsion of the brain damage that occurs in the post-ischemic period.

140 omitantly improves cortical perfusion in the post-ischemic period.

141 r neuroprotection, at least during the early post-ischemic period.

142 The present study examined the effect of post-ischemic pharmacological inhibition of PARP in a ra

143 ced by ischemic preconditioning, whereas the post-ischemic phosphorylation of MEK1/2, the upstream ac

144 A decrease in post-ischemic proton production and endoplasmic reticulu

145 etics suppressed sound-triggered seizures in post-ischemic rats tested 2 days to 4 weeks after the is

146 Mannitol 2 g/kg had no effect in 6/6 post-ischemic rats, indicating that the effect was not d

147 ced intracellular acidification and enhanced post- ischemic recovery of phosphocreatine levels, both

148 AR inhibitors sorbinil or tolrestat reduced post-ischemic recovery in the rat hearts subjected to gl

149 Intermittent ISO treatment improved post-ischemic recovery of LVDP (58.5+/-4.8% vs. 22.0+/-6

150 The post-ischemic recovery of LVDP in the untreated control

151 he abnormal metabolic phenotype and impaired post-ischemic recovery of the diabetic heart.

152 ed with EPO exhibited significantly improved post-ischemic recovery to 57 +/- 7%.

153 ir but is also implicated in pathogenesis of post-ischemic remodeling in several organs in human.

154 ivation of HIF1a contributes to the impaired post-ischemic remodeling observed following myocardial i

155 Post-ischemic reperfusion injury (PIRI) triggers an inte

156 e autocoid adenosine mitigates the extent of post-ischemic reperfusion injury in animal models.

157 iolation, which is increased 3.6-fold during post-ischemic reperfusion.

158 nase B, and myoglobin are S-thiolated during post-ischemic reperfusion.

159 The mechanisms of post-ischemic retinal atrophy and cerebral atrophy with

160 d the role of newly formed astrocytes in the post-ischemic scenario remain subjects of debate.

161 Thus, the post-ischemic state is associated with decreased levels

162 EVs (ODEs) in 58 patients 5, 15, and 30 days post-ischemic stroke and 46 controls matched for cardiov

163 DESIGN, SETTING, AND PARTICIPANTS: The Post-Ischemic Stroke Cardiovascular Exercise Study (PISC

164 derate dietary protein restriction initiated post-ischemic stroke induces neurological recovery, brai

165 ention of long-term neurological dysfunction post-ischemic stroke.

166 Such enhanced post-ischemic synchrony was found to be driven by increa

167 tes in the ischemic brain may play a role in post-ischemic tissue remodeling by enhancing angiogenesi

168 o the late regenerative processes underlying post-ischemic tissue repair.

169 is association suggests that sepsis disturbs post-ischemic tissue survival and brain remodeling.

170 mic treatment, intra-ischemic treatment, and post-ischemic treatment (Sham n=32, HI n=82, HI+H(2)n=86

171 tanide-treated group (P<0.05) but not in the post-ischemic treatment group (P>0.05).

172 c potential and optimal dosing paradigm of a post-ischemic treatment with a statin.

173 We found that post-ischemic treatment with the EP1 antagonist, SC-5108

174 Post-ischemic TubA treatment robustly improved functiona

175 IL-22 deficiency or IL-22 blockade impaired post-ischemic tubular recovery after AKI in mice.

176 424 plays an important physiological role in post-ischemic vascular remodeling and angiogenesis.

177 results indicate that both models instigated post-ischemic vascular structural changes.

178 receptor knockout mice exhibited aggravated post-ischemic ventricular remodeling and dysfunction com