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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

35 Post-ischemic contractile dysfunction is a contributor t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Post-ischemic inflammation was examined by expression of

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

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

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

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

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

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

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

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

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

77 which complement subcomponents contribute to post-ischemic injury.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 Post-ischemic neurodegeneration may be accelerated by a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 Post-ischemic TubA treatment robustly improved functiona

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

131 424 plays an important physiological role in post-ischemic vascular remodeling and angiogenesis.

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