ライフサイエンスコーパス: ischemic brain injury

1 ation, propagation, and resolution phases of ischemic brain injury.

2 Reactive oxygen species contribute to ischemic brain injury.

3 evidence against a role for inflammation in ischemic brain injury.

4 of biliverdin reductase (BVR) in response to ischemic brain injury.

5 cidosis is considered to be a contributor to ischemic brain injury.

6 rtant in determining the extent of anoxic or ischemic brain injury.

7 onged role for apoptosis in neonatal hypoxic ischemic brain injury.

8 ontributes to poor tissue outcome after mild ischemic brain injury.

9 and apoptosis, processes that contribute to ischemic brain injury.

10 ell death by influencing bcl-2 expression in ischemic brain injury.

11 nce suggesting that apoptosis is involved in ischemic brain injury.

12 recognized factor by which NO contributes to ischemic brain injury.

13 tion products contribute to the evolution of ischemic brain injury.

14 receptor antagonist protein (IL-1ra) reduces ischemic brain injury.

15 specifically at the secondary progression of ischemic brain injury.

16 pletion occurs with other insults, including ischemic brain injury.

17 tosides, is implicated in protection against ischemic brain injury.

18 ity represents a major cellular component of ischemic brain injury.

19 marker for the severity of perinatal hypoxic-ischemic brain injury.

20 Cerebral edema is a serious complication of ischemic brain injury.

21 effects of circulating monocytes in hypoxic-ischemic brain injury.

22 gnaling in a mouse model of neonatal hypoxic-ischemic brain injury.

23 tor (TLR) signaling after a neonatal hypoxic-ischemic brain injury.

24 signaling pathway, which plays a key role in ischemic brain injury.

25 , providing a novel therapeutic strategy for ischemic brain injury.

26 potentially important therapeutic target in ischemic brain injury.

27 ed clinical improvement often observed after ischemic brain injury.

28 r modulation of NADPH oxidase activity after ischemic brain injury.

29 imately lead to viable treatment options for ischemic brain injury.

30 examine the protective effect of MANF after ischemic brain injury.

31 that interferes with neuronal cell death and ischemic brain injury.

32 deficiency plays a critical role in hypoxic-ischemic brain injury.

33 d AP neuroprotection following traumatic and ischemic brain injury.

34 t excitotoxicity contribute significantly to ischemic brain injury.

35 ms employed by NRG-1 to protect neurons from ischemic brain injury.

36 hanism by which hyperglycemia can exacerbate ischemic brain injury.

37 latile anesthetics have been shown to reduce ischemic brain injury.

38 ain neurons, and appears to modulate hypoxic-ischemic brain injury.

39 tion may be a valuable strategy for treating ischemic brain injury.

40 o estradiol-mediated neuroprotection against ischemic brain injury.

41 which can lead to brain edema and exacerbate ischemic brain injury.

42 into clinically useful treatments to reduce ischemic brain injury.

43 Ca2+ toxicity remains the central focus of ischemic brain injury.

44 of various neurological disorders, including ischemic brain injury.

45 ces an inflammatory response and exacerbates ischemic brain injury.

46 modification are linked to the pathology of ischemic brain injury.

47 tiated oligodendrocytes in perinatal hypoxic/ischemic brain injury.

48 damage in a rodent model of neonatal hypoxic-ischemic brain injury.

49 proven neuroprotective treatment exists for ischemic brain injury after cardiac arrest.

50 Inflammation can extend ischemic brain injury and adversely affect outcome in ex

51 y, an important factor in the development of ischemic brain injury and edema formation.

52 nd histidine, is robustly neuroprotective in ischemic brain injury and has a wide clinically relevant

53 ells or brain resident cells, contributes to ischemic brain injury and hemorrhage.

54 ppresses neurovascular remodeling, increases ischemic brain injury and impairs functional recovery at

55 cerebral ischemia-reperfusion contributes to ischemic brain injury and is a potential therapeutic tar

56 eptor (A(2A)R) consistently protects against ischemic brain injury and other neural insults, but the

57 the neuroprotective effect of Bcl-xL against ischemic brain injury and provide the first evidence tha

58 ults support the functional role of MCP-1 in ischemic brain injury and reveal a distinct temporal and

59 in the genetic variability in sensitivity to ischemic brain injury and stroke outcome.

60 e involvement of MAP kinase pathway in focal ischemic brain injury and suggest that this effect might

61 ascade in BMDCs is an important modulator of ischemic brain injury and that ischemic brain and liver

62 We conclude that G-CSF ameliorates hypoxic-ischemic brain injury and that this may occur in part by

63 r role for complement-mediated cell death in ischemic brain injury and the prospect of using IVIG in

64 he mechanisms of neuronal survival following ischemic brain injury and to the development of therapeu

65 y provide insight into mechanisms of hypoxic-ischemic brain injury and, hence, recovery.

66 s of age and energy intake on the outcome of ischemic brain injury, and elucidated the underlying mec

67 Hypothermia (32-34 degrees C) can mitigate ischemic brain injury, and some evidence suggests that i

68 city, a critical factor in the initiation of ischemic brain injury, and to abrogation of the deleteri

69 Irregular, sporadic episodes of ischemic brain injury are known to occur in sickle cell

70 r improving outcome in patients with hypoxic-ischemic brain injury as a result of cardiac arrest is w

71 at potential as a therapeutic agent in focal ischemic brain injury, as exogenous beta-estradiol has p

72 BDNF also markedly protected against hypoxic-ischemic brain injury at PD7.

73 Extracellular adenosine critically modulates ischemic brain injury, at least in part through activati

74 f cerebral damage after acute global hypoxic-ischemic brain injury but, thus far, these putative neur

75 poxygenase (12/15-LOX), which contributes to ischemic brain injury, but its human and rodent isozymes

76 eceptor CD36 is a critical factor initiating ischemic brain injury, but the cell type(s) expressing C

77 inducible NO synthase (iNOS) contributes to ischemic brain injury, but the cell types expressing iNO

78 Macrophages are viewed as amplifiers of ischemic brain injury, but the origin of injury-producin

79 ic acid, is thought to contribute to hypoxic-ischemic brain injury by generating oxygen-free radicals

80 Ischemic brain injury causes local inflammation, which i

81 There were 4 deaths resulting from ischemic brain injury, chronic rejection, biliary sepsis

82 The development of new therapies for hypoxic-ischemic brain injury depends on such understanding.

83 A role of p38 MAP kinase in ischemic brain injury has been previously suggested by p

84 In ischemic brain injury, however, activation of this Ca(2+

85 donors, intracranial bleed in 24, and anoxic/ischemic brain injury in 26.

86 tudy, we demonstrated the effects of EPCs on ischemic brain injury in a mouse model of transient midd

87 d-type bone marrow cells) largely reinstates ischemic brain injury in global A(2A)R knockout mice.

88 a novel therapeutic agent for inhibition of ischemic brain injury in humans.

89 We investigated whether the reduction in ischemic brain injury in inducible nitric oxide synthase

90 d alterations in the intestinal flora reduce ischemic brain injury in mice, an effect transmissible b

91 The marked neuroprotection from ischemic brain injury in MK2(-/-) mice was not associate

92 , 3 h) produces tolerance 24 h after hypoxic-ischemic brain injury in neonatal rats.

93 Prevalence of ischemic brain injury in pediatric patients with SCD is

94 Hypoxic-ischemic brain injury in premature infants results in ce

95 (IL) 1, and profoundly exacerbated (50-90%) ischemic brain injury in rats and mice, a response that

96 inistered at 24 hrs, but not 48 hrs, worsens ischemic brain injury in rats resuscitated from asphyxia

97 Studies of ischemic brain injury in rodents have shown that adminis

98 ntaining preexisting hypertension alleviates ischemic brain injury in SHR by increasing collateral ci

99 Hypoxic-ischemic brain injury in survivors of perinatal asphyxia

100 d improves neurologic function after hypoxic ischemic brain injury in the newborn piglet.

101 Hypoxic-ischemic brain injury in the perinatal period is a major

102 represents an important component of hypoxic-ischemic brain injury in the perinatal period.

103 of a rat CART peptide is protective against ischemic brain injury in vivo.

104 es would cause damage to astrocytes after an ischemic brain injury in vivo.

105 at contributes to the tissue damage, reduced ischemic brain injury in wild-type mice, but not in CD36

106 ients on hemodialysis exhibited a pattern of ischemic brain injury (increased fractional anisotropy a

107 due to altered mental status (intoxication, ischemic brain injury), indirect lung injury (non-pulmon

108 ever at onset and in the acute setting after ischemic brain injury, intracerebral hemorrhage, and car

109 Neonatal hypoxic-ischemic brain injury is a major cause of neurological d

110 Hypoxic/ischemic brain injury is associated with accumulation of

111 While the role of BDNF in hypoxic-ischemic brain injury is not clear, evidence suggests th

112 st that VNS-induced protection against acute ischemic brain injury is not primarily mediated by chang

113 We also show that acute ischemic brain injury is regulated by mechanisms that re

114 rebral artery occlusion, or neonatal hypoxic-ischemic brain injury, Mn preferentially accumulated in

115 bitors have shown promise in several hypoxic ischemic brain injury models, and we wished to see if th

116 Hypoxic-ischemic brain injury occurring in antenatal, perinatal

117 Hypoxic-ischemic brain injury occurs frequently in infancy and c

118 ype mice before subjecting them to a hypoxic-ischemic brain injury or in APP/PS1 mice prior to the fo

119 Perinatal hypoxic-ischemic brain injury remains a major cause of cerebral

120 chemic stroke, its role in the mechanisms of ischemic brain injury remains controversial.

121 Overexpression of human IL-1ra attenuated ischemic brain injury, suggesting that IL-1 may play an

122 with severe anemia to identify unrecognized ischemic brain injury that may have permanent neurocogni

123 nting production of ROSs by NADPH oxidase in ischemic brain injury, the regulatory mechanisms of NADP

124 degrees C) attenuates the release of GLU in ischemic brain injury, this study was designed to detect

125 ssed in the periphery and brain synergize in ischemic brain injury through regulation of the MCP-1/CC

126 flammatory signaling, may also contribute to ischemic brain injury through yet unidentified mechanism

127 studied a rodent model of very early hypoxic-ischemic brain injury to investigate effects of injury o

128 confers long-lasting neuroprotection against ischemic brain injury via a previously unexplored associ

129 ion augments atherosclerosis and exacerbates ischemic brain injury via IL-1 and platelet-mediated sys

130 The salutary effect of DPH-067517 in ischemic brain injury was also observed when the first d

131 B alterations and inflammation contribute to ischemic brain injury, we examined the role of PGRN in t

132 the Rice-Vannucci model of neonatal hypoxic-ischemic brain injury, we have shown that neuronal degen

133 Chronic ischemic brain injuries were studied in 7- and 14-day-ol

134 esponse to cerebral ischemia and its role in ischemic brain injury were investigated.

135 onically hypertensive patient is at risk for ischemic brain injury when perfusion pressure is rapidly

136 rm potentiation of synaptic transmission and ischemic brain injury, whereas ASIC2a is involved in mec

137 treatment in females at risk for cardiac and ischemic brain injury, whereas progesterone appears to b

138 in S is a significant neuroprotectant during ischemic brain injury with direct effects on neurons and

139 s an important modulator of the evolution of ischemic brain injury--with hypothermia lessening and hy