ライフサイエンスコーパス: ischemic tissue

1 se analogue that exhibits enhanced uptake in ischemic tissue.

2 their incorporation into the vasculature of ischemic tissue.

3 acilitate physiological revascularization of ischemic tissue.

4 rculating CXCR4-positive progenitor cells to ischemic tissue.

5 increased numbers of BM-derived EPCs within ischemic tissue.

6 anted cell retention and survival within the ischemic tissue.

7 fying this region of potentially salvageable ischemic tissue.

8 ing 30% nonischemic lobes and reperfusion of ischemic tissue.

9 wth factor (VEGF) gene expression in hypoxic/ischemic tissue.

10 ) signaling might enhance vascularization of ischemic tissue.

11 A, which can serve as a potential target for ischemic tissue.

12 al blood vessels or erythrocytes and salvage ischemic tissue.

13 ogical modulation to promote angiogenesis in ischemic tissue.

14 sm that restores blood flow to undersupplied ischemic tissue.

15 to achieve therapeutic neovascularization of ischemic tissue.

16 tially regenerative myoblasts in chronically ischemic tissue.

17 itions of low O(2) and low pH ex vivo and in ischemic tissue.

18 involved in the homing of mobilized cells to ischemic tissue.

19 ould re-establish blood perfusion and rescue ischemic tissue.

20 issue, normally associated with infarcted or ischemic tissue.

21 strate repair, these cells must migrate into ischemic tissue.

22 ceptors (VEGFRs) overexpressed on vessels of ischemic tissue.

23 ells, thereby promoting revascularization of ischemic tissue.

24 ation can contribute to revascularization of ischemic tissues.

25 ion in vivo by augmenting EPC recruitment in ischemic tissues.

26 n be an important source of NO production in ischemic tissues.

27 reductase (Kcat) was significantly higher in ischemic tissues.

28 in mediating pathology during reperfusion of ischemic tissues.

29 nic factors stimulates neovascularization in ischemic tissues.

30 thereby contribute to neovascularization of ischemic tissues.

31 iogenic process and enhancing reperfusion of ischemic tissues.

32 py and thereby augment neovascularization of ischemic tissues.

33 as a source of VEGF in neovascularization of ischemic tissues.

34 ischemia that provides neovascularization of ischemic tissues.

35 actors known to induce neovascularization of ischemic tissues.

36 ially useful for therapeutic angiogenesis in ischemic tissues.

37 for the prevention of reperfusion injury in ischemic tissues.

38 y to adult muscle have only been reported in ischemic tissues.

39 injury that occurs following reperfusion of ischemic tissues.

40 physiologic angiogenesis and angiogenesis in ischemic tissues.

41 giogenesis and blood flow in mouse hind limb ischemic tissues.

42 physiologic angiogenesis and angiogenesis in ischemic tissues.

43 on of the regeneration process in peripheral ischemic tissues.

44 red for inflammatory cell recruitment to the ischemic tissues.

45 (hEPCs) participate in neovascularization of ischemic tissues.

46 d to increase blood flow and angiogenesis in ischemic tissues.

47 icates that for each K(+) equivalent leaving ischemic tissue, 0.8+/-0.1 Eq, on average, of Na(+) ente

48 tes impairs endogenous neovascularization of ischemic tissues; 2) the impairment in new blood vessel

49 Pathogenic Abs recognize neoantigens on the ischemic tissue, activate complement, and induce intesti

50 ries, is critical in restoring blood flow to ischemic tissue after a vascular occlusion.

51 NALE: Angiogenesis improves perfusion to the ischemic tissue after acute vascular obstruction.

52 global ischemic insult and down-regulated in ischemic tissues after focal ischemia.

53 d highly tunable delivery of VEGF protein in ischemic tissue and (ii) stable and functional angiogene

54 sized that nitrite would be reduced to NO in ischemic tissue and exert NO-dependent protective effect

55 at VEGF receptors could serve as markers for ischemic tissue and hence provide a target for imaging s

56 broblast growth factor-2 mRNA transcripts in ischemic tissue and in circulating endothelial progenito

57 hes that involve stimulating angiogenesis in ischemic tissue and inhibiting angiogenesis in neoplasti

58 a proinflammatory cytokine, is expressed in ischemic tissue and is known to modulate angiogenesis.

59 nificantly improves vascular recovery within ischemic tissue and reduces pathological neovascularizat

60 genic niches supporting revascularization of ischemic tissue and tumor growth.

61 ne accumulates to high levels in inflamed or ischemic tissues and activates A3 adenosine receptors (A

62 a key process driving blood vessel growth in ischemic tissues and an important drug target in a numbe

63 Local acidosis has been demonstrated in ischemic tissues and at inflammatory sites.

64 ated molecular pattern (DAMP), released from ischemic tissues and dying cells which, when crystalized

65 ic acid (UA) is consistently overproduced by ischemic tissues and has been shown to exert immunomodul

66 works is essential for successfully treating ischemic tissues and maintaining function of engineered

67 active oxygen species (ROS) are increased in ischemic tissues and necessary for revascularization; ho

68 in enhancing hEPC function and blood flow to ischemic tissues and show that Wnt1 enhances the prolife

69 s tPA activity and neuroserpin expression in ischemic tissue, and genetic deficiency of tPA or either

70 y could be used to reestablish blood flow in ischemic tissues, and this may be enhanced by coordinate

71 blood flow was associated with increases in ischemic tissue angiogenesis activity and cell prolifera

72 to achieve improved collateral formation in ischemic tissues are showing some promise in the early s

73 nd decreased levels of NO2-/NO3- and cGMP in ischemic tissues as compared with wild-type mice, and it

74 Recruitment of inflammatory cells into ischemic tissues as well as numbers of inflammatory cell

75 ular endothelial growth factor (VEGF) in the ischemic tissues, as assessed by Northern blot, Western

76 y was not detected in shams or in previously ischemic tissue at 15 minutes of reperfusion; it was det

77 Significant amounts of glutamine remain in ischemic tissue at prolonged times after focal ischemia,

78 xia-inducible factor 1alpha stabilization in ischemic tissues because of increased prolyl hydroxylase

79 of such channels by RBC-PAs may help rescue ischemic tissue before bulk dissolution of potentially o

80 ompletely abolished sodium nitrite-dependent ischemic tissue blood flow and angiogenic activity consi

81 r survival and growth in a distantly located ischemic tissue by a remote signaling mechanism.

82 d that nitroglycerin improves O2 delivery to ischemic tissue by altering erythrocyte rheology and O2

83 Estradiol preserves the integrity of ischemic tissue by augmenting the mobilization and incor

84 vascular endothelial growth factor (VEGF) in ischemic tissues (by Northern blot, Western blot, and im

85 -based quantification of water uptake in the ischemic tissue can identify patients with stroke onset

86 e oxygen species (ROS) during reperfusion of ischemic tissues can trigger the opening of the mitochon

87 Reperfusion of ischemic tissue causes an immediate increase in DNA dama

88 more potent at acidic pH 6.9 associated with ischemic tissue compared to pH 7.6, a value close to the

89 Collagen type I synthesis was upregulated in ischemic tissue compared with non-ischemic matched pairs

90 We found that MPO is widely distributed in ischemic tissues, correlates positively with infarct siz

91 ogical emergency since it is associated with ischemic tissue damage and erectile disability.

92 oxygen-carrying agents for the prevention of ischemic tissue damage and hypovolemic (low blood volume

93 for Egr-1 activation in the pathogenesis of ischemic tissue damage.

94 trauma and hemorrhage, reperfusion magnifies ischemic tissue damage.

95 reduced number of infiltrating cells in the ischemic tissue despite the massive expression of CXCL12

96 applications such as tissue engineering and ischemic tissue disorders.

97 Reperfusion of ischemic tissues elicits an acute inflammatory response

98 ectin/ligand pairs reciprocally expressed on ischemic tissue endothelium and BMD-EPC act as double-lo

99 can act both locally and remotely to induce ischemic tissue endothelium and BMD-EPC to express both

100 Algorithms to predict ischemic tissue fate based on acute stroke MRI typically

101 Accurate and quantitative prediction of ischemic tissue fate could improve decision-making in th

102 thelial progenitor cells (EPCs) in repair of ischemic tissue has been the subject of intense scrutiny

103 ter understand systemic interactions between ischemic tissue, immunity, and hematopoiesis, as turnove

104 in selective in vivo expression of SDF-1 in ischemic tissue in direct proportion to reduced oxygen t

105 re thought to enhance vascular remodeling in ischemic tissue in part through paracrine effects.

106 othesis that digoxin reduces HIF-1 levels in ischemic tissue in vivo and suppresses neovascularizatio

107 nsfer significantly improved angiogenesis in ischemic tissue in XBP1ecko mice.

108 als to other cell-based implants, as well as ischemic tissues in general, is envisioned.

109 or (VEGF) couples hypoxia to angiogenesis in ischemic tissues, including brain.

110 ly expressed on the activated endothelium in ischemic tissues, including E-selectin.

111 By Western blotting, nestin within ischemic tissue increased slightly as early as 6 h, peak

112 ammation in which xanthine oxidase (XO) from ischemic tissues increases vascular superoxide anion (O2

113 The dihydroethidium staining of ischemic tissues indicates that O2*- is mainly produced

114 Thus, ecSOD in BM and ischemic tissues induced by hindlimb ischemia may repres

115 Reperfusion of ischemic tissue induces an acute inflammatory response t

116 Reperfusion of ischemic tissue induces significant tissue damage in mul

117 nisms behind adenosine triphosphate-mediated ischemic tissue injury and evaluate the role of extracel

118 They lessen ischemic tissue injury by serving as endogenous bypass v

119 Ischemic tissue injury contributes to significant morbid

120 a key role in modulating local responses to ischemic tissue injury in the kidney and potentially oth

121 Because ischemic tissue injury provides a potential source for N

122 is a major factor underlying differences in ischemic tissue injury, and generated a congenic strain

123 in BVR expression with display of indices of ischemic tissue injury.

124 initiate intravascular occlusion leading to ischemic tissue injury.

125 x formation is a novel target for preventing ischemic tissue injury.

126 onists may enhance AMPK activation and limit ischemic tissue injury.

127 Impaired angiogenesis in ischemic tissue is a hallmark of diabetes.

128 in cellular models show that reperfusion of ischemic tissue is associated with a burst of reactive o

129 Myocardial damage due to reperfusion of ischemic tissue is caused primarily by infiltrating neut

130 Neutrophil survival in ischemic tissue is required to attract monocytes that co

131 of endothelial progenitor cells (EPC) to the ischemic tissues is a key event in neovascularization an

132 is but fails to induce neovascularization in ischemic tissue lesions in mice lacking endothelial nitr

133 show a cardinal role for CD73 in suppressing ischemic tissue leukosequestration.

134 tion of L-histidine and thioperamide reduces ischemic tissue loss, in part by inhibition of apoptotic

135 with rest pain, and 1% were associated with ischemic tissue loss.

136 maintain energy homeostasis in low-oxygen or ischemic-tissue microenvironments.

137 t can suppress vessel activation and protect ischemic tissue might ultimately find a niche in the pre

138 plays an important role in the prevention of ischemic tissue necrosis.

139 Sodium nitrite therapy also increased ischemic tissue nitrite and NO metabolites compared to n

140 Nitrite significantly increased ischemic tissue NO bioavailability along with concomitan

141 though effects of reperfusion were rapid, in ischemic tissue not reperfused, low levels of C/EBP were

142 in expression is acutely up-regulated in the ischemic tissue of experimental wounds.

143 h increased recovery of oxygen levels in the ischemic tissue of thrombospondin-1-null mice as measure

144 For the ischemic tissues of the scleroderma hand the prerequisit

145 Blockade of SDF-1 in ischemic tissue or CXCR4 on circulating cells prevents p

146 her the goal is to induce vascular growth in ischemic tissue or scale up tissue-engineered constructs

147 ng the TMLR channel remnants than in control ischemic tissue (p < 0.001).

148 At day 28 after treatment, ischemic tissue perfusion was improved in the SDF-1 grou

149 tribution of young WT-BM cell to adult p75KO ischemic tissue recovery.

150 n the ischemic brain may play a role in post-ischemic tissue remodeling by enhancing angiogenesis and

151 plays a critical role in the early phase of ischemic tissue remodeling.

152 estigated the mechanisms of CD34Exo-mediated ischemic tissue repair and therapeutic angiogenesis by s

153 echanism by which cell-free CD34Exo mediates ischemic tissue repair via beneficial angiogenesis.

154 ance of bone marrow-derived EPC phenotype in ischemic tissue repair.

155 late regenerative processes underlying post-ischemic tissue repair.

156 ay a critical role in BM PC mobilization and ischemic tissue repair.

157 on of blood flow is mandatory for salvage of ischemic tissues, reperfusion can paradoxically place ti

158 Reperfusion injury of ischemic tissue represents an acute inflammatory respons

159 Ischemic tissues require mechanisms to alert the immune

160 Reperfusion of ischemic tissue results in the generation of reactive ox

161 nthases, NO formation from nitrite occurs in ischemic tissues, such as the heart.

162 ible nitric-oxide synthase expression in the ischemic tissue, suggesting a cytokine-like plasminogen-

163 ons but did not significantly integrate into ischemic tissue, suggesting that transient ALDH(hi) cell

164 revascularization and restoring function of ischemic tissue suggests its therapeutic potential in is

165 that blocking TSP1-CD47 signaling increases ischemic tissue survival in random cutaneous porcine fla

166 onance imaging: it can predict the volume of ischemic tissue that will progress to infarction and det

167 l for augmenting collateral vessel growth to ischemic tissues (therapeutic angiogenesis) and for deli

168 crucial first minutes of the reperfusion of ischemic tissue, thereby decreasing ROS production, oxid

169 MCs significantly attenuated angiogenesis in ischemic tissues, therefore retarded the foot blood perf

170 Identifying ischemic tissue to direct tissue sampling towards ischem

171 tified a relationship between recruitment of ischemic tissue to the final infarct and hyperglycemia,

172 l a unique function of Nrf2 in reprogramming ischemic tissue toward neurovascular repair via Sema6A r

173 enosine that accumulates to > 1 mM levels in ischemic tissues, triggers mast cell degranulation.

174 g the formation of new collateral vessels in ischemic tissues using angiogenic growth factors (therap

175 Nitrite therapy significantly increased ischemic tissue vascular endothelial growth factor (VEGF

176 owever, effects of nitrite anion therapy for ischemic tissue vascular remodeling during diabetes rema

177 that nitrite therapy effectively stimulates ischemic tissue vascular remodeling in the setting of me

178 Macrophage VEGF-A production, ischemic tissue VEGF-A levels, and flow recovery to hind

179 % of baseline, and endogenous VEGF levels in ischemic tissue were increased.

180 ies, may help protect against such injury of ischemic tissue when reperfused at the return of spontan

181 a significant increase in ecSOD activity in ischemic tissues where ecSOD protein is highly expressed

182 Adenosine is formed in injured/ischemic tissues, where it suppresses the actions of ess

183 r FTY720, an S1P1/3 agonist, to inflamed and ischemic tissues, which resulted in a reduction in proin

184 density in WT and no change in the MMP-9-/- ischemic tissues, which translated into increased (39%)

185 This should maximize neuroprotection in ischemic tissue while minimizing on-target side effects

186 aximizes the projection of a desired tissue (ischemic tissue) while it minimizes the projection of un

187 easing the number of vessels that supply the ischemic tissue with blood.

188 BM-derived EPCs were recruited to ischemic tissue within 72 hours, and the extent of recru

189 ing interstitial adenosine concentrations in ischemic tissue-would improve long-term survival after p