ライフサイエンスコーパス: penumbra

1 f recruited neurons and a surrounding 'ictal penumbra'.

2 mbral pattern (large core or small or absent penumbra).

3 abnormalities serves as an indicator of the penumbra.

4 ked beta-catenin degradation in the ischemic penumbra.

5 ng and neuronal excitotoxicity in the injury penumbra.

6 a defect that is reversed by reexpression of Penumbra.

7 r in the delayed cell losses of the ischemic penumbra.

8 ion and apoptotic cell death in the ischemic penumbra.

9 rization and cell death, particularly in the penumbra.

10 ution of irreversible damage in the ischemic penumbra.

11 the temporal and spatial progression of the penumbra.

12 in diabetic rats in both ischemic focus and penumbra.

13 n may represent resolution of the reversible penumbra.

14 a 67.9% (p<0.05) increase in APP mRNA in the penumbra.

15 xia that mimics many features of an ischemic penumbra.

16 chemic region, and to a lesser extent in the penumbra.

17 ate and GABA observed in the focal ischaemic penumbra.

18 bition of glutamate release in the ischaemic penumbra.

19 rstanding the pathophysiology of an ischemic penumbra.

20 and their continued accumulation within the penumbra.

21 proposed as a metabolic marker of ischaemic penumbra.

22 core seizure territory from the surrounding penumbra.

23 an10, Tspan14, Tspan15, Tspan17, and Tspan33/Penumbra.

24 el that included the volume of non-infarcted penumbra.

25 damage to the surrounding area known as the penumbra.

26 rated peak NP accumulation within the injury penumbra 1 h post-injury.

27 eas temperature was highest in the potential penumbra (37.7 versus 37.3 degrees C in lesion core, P <

28 vely) was much smaller than that of salvaged penumbra (59.3 and 93 ml, respectively), it was substant

29 k of a simple in vitro model of the ischemic penumbra, a clinically relevant region of stroke-afflict

30 he ischemic core and diffuse to the ischemic penumbra, activating microglia and promoting proinflamma

31 astrocyte signalling through the 'mechanical penumbra' affects the activity of neural circuits distan

32 inistered during periods of the inflammatory penumbra after active lesion formation, and was shown to

33 Thus, increasing the energy imbalance in the penumbra after multiple SDs may hasten the deterioration

34 , California) (40%) and the Penumbra System (Penumbra, Alameda, California) (9%), represented a large

35 Hence, strategies to keep the penumbra alive until reperfusion occurs are needed.

36 ral O2 pressure and by such may maintain the penumbra alive until reperfusion.

37 ng reduction of the GAG chains in the lesion penumbra and allowed axons to regenerate around the core

38 ade of collateral circulation, the ischaemic penumbra and clinical functional outcome.

39 whole-brain coverage to measure the ischemic penumbra and core and to compare its performance to that

40 volume at CT perfusion was compared with the penumbra and core reference values at magnetic resonance

41 in ischemic volume delineated by the optimal penumbra and core threshold was determined as the brain

42 Results CT perfusion at penumbra and core thresholds resulted in the least volum

43 esonance (MR) imaging to derive CT perfusion penumbra and core thresholds.

44 iently increased at 5 h in both the ischemic penumbra and core, and the total protein level of beta-c

45 re measured in contralateral (non-ischemic), penumbra and densely ischemic brain regions.

46 An overlap between non-infarcted penumbra and functional magnetic resonance imaging clust

47 TBI penumbra and hippocampus had higher cellular proliferati

48 of different perfusion CT thresholds for the penumbra and infarct core with each postprocessing metho

49 as shown that there is marked variability in penumbra and infarct prediction among various deconvolut

50 ith significant fewer apoptotic cells in the penumbra and less BBB disruption; PHD3-/- mice had impai

51 c rats enhanced angiogenesis in the ischemic penumbra and significantly improved neurological recover

52 induced by IS accurately mimics the in vivo penumbra and thus whether our model system is suitable f

53 target of acute stroke therapy, the ischemic penumbra, and clinically available imaging modalities su

54 is this boundary zone that comprises the new penumbra, and future investigations should dissect where

55 esonance imaging responses and non-infarcted penumbra, and tested the hypothesis that the former do t

56 f LRP in neurons within the area of ischemic penumbra, and this effect was attenuated in mice treated

57 identify a small ischemic core and ischemic penumbra, and this information will contribute increasin

58 nge between these thresholds was termed the "penumbra," and restitution of flow above the functional

59 Moreover, the ischemic penumbra APN levels increased and peaked in T1DM-2W mice

60 perfusion 'mismatch' being representative of penumbra appears to be an oversimplification.

61 reduced VT recurrence and increased unipolar penumbra area predicted cardiac death.

62 concentrations of reactive aldehydes in the penumbra area, we investigated if the hydrazine function

63 low voltage areas, unipolar low voltage and penumbra areas) and morphology characteristics (presence

64 However, although the non-infarcted penumbra as a whole was affected by selective neuronal l

65 motor and somatosensory areas of the injury penumbra as compared to the parietal association and vis

66 e than 2 seconds most accurately defined the penumbra (AUC = 0.86, P = .046, mean volume difference b

67 teral cerebral blood flow (CBF) to ischaemic penumbra because it can cause vasoconstriction.

68 emerged that focus not only on the ischemic penumbra but also on the infarct core.

69 ed preferentially in neurons in the ischemic penumbra but not in the ischemic core or in brain region

70 the tissue putrescine level was found in the penumbra but there was no difference in the putrescine l

71 ulated angiogenesis in the striatal ischemic penumbra, but not the dentate gyrus.

72 reased apoptotic cell counts in the ischemic penumbra by more than 50%.

73 of irreversible infarction as well as of the penumbra by the MRI modalities.

74 tion of erythropoiesis, we identified murine Penumbra cDNA from a multipotent hematopoietic cell line

75 wing image coregistration, the non-infarcted penumbra comprised all acutely ischaemic voxels (identif

76 Human and murine Penumbras contain 283 amino acids and are 97% identical.

77 rvation of these glial cells in the ischemic penumbra corresponded with a markedly reduced area of in

78 Selective neuronal loss (SNL) in the rescued penumbra could account for suboptimal clinical recovery

79 The "salvaged penumbra" defined by the area of mismatch between the fi

80 To study the effects of Penumbra deletions, we created a knockout mouse model by

81 severe, cerebral blood flow in the ischemic penumbra during reperfusion was reduced, and NMDA neurot

82 ggest that stroke victims with a significant penumbra estimated by the diffusion/perfusion mismatch o

83 to improve cerebal blood flow to reduce the penumbra following stroke.

84 Subsequently, we identified the human PENUMBRA from a bone marrow cDNA library.

85 CT perfusion allowed differentiation of the penumbra from the ischemic core in patients with acute i

86 The human PENUMBRA gene is mapped to chromosome 7q32, a hot spot f

87 These findings indicate that Penumbra has a positive function in erythropoiesis and i

88 ing depolarizations in an electrophysiologic penumbra (i.e. isoelectric cortex with no spontaneous ac

89 ntracerebally transplanted into the ischemic penumbra immediately (within 1 h) after stroke surgery.

90 The existence of a penumbra implies that therapeutic salvage is theoretical

91 ies that selectively target the inflammatory penumbra in experimental autoimmune encephalomyelitis le

92 ies, continues to be advanced by imaging the penumbra in novel ways.

93 Given the key role of the ischaemic penumbra in stroke pathophysiology, we hypothesised that

94 ut potentially salvageable tissue (i.e., the penumbra) in stroke patients can be achieved.

95 l role of PGs, and particularly those in the penumbra, in causing regeneration failure in the adult s

96 The ischemic penumbra includes not only the region of diffusion/perfu

97 osis/autophagy characteristic of the in vivo penumbra, including: (1) short-term elevation of [ATP] f

98 lude that our in vitro model of the ischemic penumbra induces autophagy and apoptosis in cultured neu

99 fts and cause progressive recruitment of the penumbra into the core infarct.

100 ause vasoconstriction and recruitment of the penumbra into the ischemic core in the critical first ho

101 levation in diffusion lesion core, potential penumbra, ipsilateral and contralateral normal brain and

102 Penumbra is a new member of the tetraspanin superfamily

103 keeping with the hypothesis that the rescued penumbra is affected by SNL.

104 The penumbra is an area of brain tissue that is damaged but

105 However, whether the non-infarcted penumbra is capable of neuronal activation, and how sele

106 at 1-3 months after stroke the non-infarcted penumbra is capable of neuronal activation, consistent w

107 Imaging the penumbra is essential, not only to identify patients who

108 Penumbra is targeted to the cell surface and forms disul

109 The defining feature of the 'ictal penumbra' is the contrast between the large amplitude EE

110 produce a square-shaped lesion surrounding a penumbra-like "area at risk" in middle cerebral artery t

111 uorescent protein-expressing neurons in this penumbra-like area at risk revealed that SDs were tempor

112 However, the rescued penumbra may be affected by selective neuronal loss, as

113 that increase in BVR expression in ischemic penumbra may present a cellular defense mechanism agains

114 Penumbra(-/-) mice develop massive splenomegaly, basophi

115 X, was established from the bone marrow of a Penumbra(-/-) mouse.

116 Bland-Altman plots indicated that these penumbra-nulled IR images provided more accurate predict

117 btained from tp3 T2-weighted images and the "penumbra" obtained from the tp1 perfusion-weighted image

118 cumulation of Abeta deposits decrease in the penumbra of CCI months after TBI.

119 amples were harvested from ischemic core and penumbra of cortices at one hour and twenty-four hours f

120 accumulates within neuronal processes in the penumbra of hypoxic damage in adult brain, and within ne

121 lation of PrP(C) in neuronal soma within the penumbra of ischemic lesions.

122 e or male human iESCs were injected into the penumbra of ischemic myocardial tissue of female mice or

123 with local metabolic stress, similar to the penumbra of ischemic/hypoxic states.

124 To assess whether quantifying this penumbra of lung at risk would predict FEV1 decline.

125 in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also dist

126 n with promoted angiogenesis in the ischemic penumbra of rat brains after treadmill exercise.

127 xercise-induced angiogenesis in the ischemic penumbra of rat brains, and whether caveolin-1 changes c

128 nes were then transplanted into the striatal penumbra of rats, 1 h following middle cerebral artery o

129 e, Bif-1 expression was downregulated in the penumbra of wild-type mice.

130 ularly in the inner infarct border zone (the penumbra), of the bid-deficient brains.

131 ute anterior circulation stroke, presence of penumbra on computed tomography perfusion performed with

132 f they had a small ischemic core and a large penumbra on their baseline CT perfusion.

133 ificantly reduced in the whole non-infarcted penumbra (P < 0.01) but not within the functional magnet

134 ct growth (P = .004) and had higher salvaged penumbra (P = .009) volumes than patients without reperf

135 of maximal injury at 48 h postinjury (injury penumbra) (p<0.001).

136 lesion core (42 versus 26 units in potential penumbra, P < 0.05), whereas temperature was highest in

137 mic core, which gradually expands toward the penumbra, partly as the result of a neuroinflammatory re

138 fusion-weighted imaging lesion) and presumed penumbra (perfusion-diffusion mismatch [threshold = T(ma

139 In the focal ischaemic penumbra, peri-infarct depolarizations have prolonged di

140 The main therapeutic target is the ischemic penumbra, potentially salvageable brain tissue that dies

141 e present at elevated levels in the ischemic penumbra region after middle cerebral artery occlusion.

142 eath but not typical apoptosis occurs in the penumbra region and non-ischemic thalamus after cerebral

143 placed into the previously defined ischemic penumbra region and perfused with a salicylate/CSF solut

144 of free radical adduct formation within the penumbra region during cerebral ischemia/reperfusion may

145 radical adduct formation was observed in the penumbra region during ischemia/reperfusion.

146 ositive cells in the thalamus and the cortex penumbra region represented a hybrid death, featured by

147 c and apoptosis-inducing factor (AIF) in the penumbra region were reduced by NBP.

148 n that tissue putrescine is increased in the penumbra region, an area of incomplete ischemia that is

149 le for monitoring metabolic responses in the penumbra region.

150 p<0.05) including the most affected ischemic penumbra regions (e.g. hippocampus, pallium).

151 rmation was observed in densely ischemic and penumbra regions.

152 -induced injury to synaptic circuitry in the penumbra remain unknown.

153 the therapeutic aim to salvage the ischemic penumbra remains a formidable challenge.

154 k ahead as we move into the fourth decade of penumbra research?

155 of 52.9% and 57.0% (p<0.05) in the core and penumbra, respectively.

156 The primary endpoint was percentage of penumbra salvaged (CT perfusion-defined penumbra volume

157 In the penumbra, six genes related to axongenesis (Erbb2); grow

158 A key finding was that in the penumbra, spike stereotypy was maintained even during th

159 As expected, salvaged penumbra strongly positively influenced early neurologic

160 Care, Medtronic/Covidien/EV3, Medac/Lamepro, Penumbra, Stryker, and Top Medical.

161 The original concept of the ischaemic penumbra suggested imaging of regional cerebral blood fl

162 rily associated with neurons in the ischemic penumbra, suggesting an important role for PPARgamma in

163 erfusion; however, recent examination of the penumbra suggests a central role for NADPH-oxidase (Nox)

164 newborn neurons are present in the ischemic penumbra surrounding cerebral cortical infarcts, where t

165 spreading depolarizations (SDs) occur in the penumbra surrounding ischemic core.

166 selected to null signal from the peripheral penumbra surrounding the ablation zone (r = 0.939, P < .

167 al, Mountain View, California) (40%) and the Penumbra System (Penumbra, Alameda, California) (9%), re

168 h the MERCI Retriever and 0% to 11% with the Penumbra System) or asymptomatic (13 studies; 28% to 43%

169 o mechanical embolectomy (Merci Retriever or Penumbra System) or receive standard care.

170 the MERCI Retriever and 83% to 100% with the Penumbra System).

171 magnitude of the changes was greater in the penumbra than in the normal cortex.

172 on depolarizing waves (PIDs) in the ischemic penumbra, the territory of salvage.

173 lectively dilates arterioles in the ischemic penumbra, thereby increasing collateral blood flow and s

174 n tips dieback from the lesion core into the penumbra they closely associate with NG2+ cells.

175 an be repeatedly investigated to demonstrate penumbra tissue, which can benefit from therapeutic inte

176 ential in the transfer of the concept of the penumbra to clinical stroke and thereby had a great impa

177 e, we utilized a novel in vitro model of the penumbra to examine the free radical profile of ischemic

178 l and ischemic brain, but the ability of the penumbra to recover from the insult is compromised.

179 became upregulated in vessels of the stroke penumbra using a mouse model of reversible middle cerebr

180 e of penumbra salvaged (CT perfusion-defined penumbra volume at baseline minus CT infarct volume at 2

181 The concept of the ischemic penumbra was formulated on the basis of animal experimen

182 4 double-positive cells towards the ischemic penumbra was increased in the exercise group.

183 maging activation clusters and non-infarcted penumbra was mapped, and binding potential values then c

184 Cell death in the thalamus and the cortex penumbra were attenuated by delayed administration of th

185 ted tissue, and the eventually non-infarcted penumbra, were determined by performing voxel-wise analy

186 ion size and neuronal damage in the ischemic penumbra when administered six hours post middle cerebra

187 o gives valuable information on the ischemic penumbra which are very important in early diagnosis and

188 central umbra is surrounded by a filamentary penumbra, whose complicated fine structure has only rece

189 ies demonstrate that imaging of the ischemic penumbra with diffusion/perfusion magnetic resonance ima

190 nt of a more severe perfusion deficit in the penumbra within 4 h of MCAO supports the hypothesis that

191 rons surrounding the ischemic core (ischemic penumbra) within 6 hours of occlusion of the middle cere

192 rations should benefit damaged tissue in the penumbra zones and in remote brain regions.