ライフサイエンスコーパス: ischemic tissue

1 to recovery of perfusion and preservation of ischemic tissue.

2 issue, normally associated with infarcted or ischemic tissue.

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

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

5 ells, thereby promoting revascularization of ischemic tissue.

6 y in the physiological response occurring in ischemic tissue.

7 se analogue that exhibits enhanced uptake in ischemic tissue.

8 their incorporation into the vasculature of ischemic tissue.

9 acilitate physiological revascularization of ischemic tissue.

10 rculating CXCR4-positive progenitor cells to ischemic tissue.

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

12 anted cell retention and survival within the ischemic tissue.

13 fying this region of potentially salvageable ischemic tissue.

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

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

16 ) signaling might enhance vascularization of ischemic tissue.

17 ish between infracted tissue and recoverable ischemic tissue.

18 otocin-injected) and type 2 (db/db) diabetic ischemic tissue.

19 blood vessel development to rescue diabetic ischemic tissue.

20 al blood vessels or erythrocytes and salvage ischemic tissue.

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

22 C5aR1-mediated neutrophil recruitment to the ischemic tissue.

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

24 ogical modulation to promote angiogenesis in ischemic tissue.

25 sm that restores blood flow to undersupplied ischemic tissue.

26 to achieve therapeutic neovascularization of ischemic tissue.

27 tially regenerative myoblasts in chronically ischemic tissue.

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

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

30 ation can contribute to revascularization of ischemic tissues.

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

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

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

34 in mediating pathology during reperfusion of ischemic tissues.

35 nic factors stimulates neovascularization in ischemic tissues.

36 thereby contribute to neovascularization of ischemic tissues.

37 iogenic process and enhancing reperfusion of ischemic tissues.

38 py and thereby augment neovascularization of ischemic tissues.

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

40 ischemia that provides neovascularization of ischemic tissues.

41 actors known to induce neovascularization of ischemic tissues.

42 ially useful for therapeutic angiogenesis in ischemic tissues.

43 for the prevention of reperfusion injury in ischemic tissues.

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

45 injury that occurs following reperfusion of ischemic tissues.

46 and reduced immune cell infiltration within ischemic tissues.

47 s leukocyte trafficking in IL-6-inflamed and ischemic tissues.

48 physiologic angiogenesis and angiogenesis in ischemic tissues.

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

50 physiologic angiogenesis and angiogenesis in ischemic tissues.

51 on of the regeneration process in peripheral ischemic tissues.

52 red for inflammatory cell recruitment to the ischemic tissues.

53 (hEPCs) participate in neovascularization of ischemic tissues.

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

55 source for restoring endothelial function in ischemic tissues.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 Since acidosis is a hallmark of ischemic tissue and tumors, the hypoxia specificity of [

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

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

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

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

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

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

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

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

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

80 y increased fibrin(ogen) accumulation in the ischemic tissue, and plasma VWF content and activity, an

81 s have potential to augment cell survival in ischemic tissues, and promote ischemic tissue regenerati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 (EVs) may induce pro-regenerative effects in ischemic tissues by delivering bioactive molecules, incl

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

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

99 ved of oxygen, subsequent reperfusion of the ischemic tissue can lead to oxidative damage due to exce

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

101 nthesis to augment wound healing by rescuing ischemic tissues caused by peripheral artery disease.

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

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

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

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

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

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

108 First, ischemic tissue damage was systematically assessed by tw

109 P levels, and thereby reduce the severity of ischemic tissue damage.

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

111 trauma and hemorrhage, reperfusion magnifies ischemic tissue damage.

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

113 applications such as tissue engineering and ischemic tissue disorders.

114 may have a reduced ability to revascularize ischemic tissues due to abnormal production of circulati

115 ular supply and metabolic equilibrium to the ischemic tissue during ischemic retinopathies, a dysregu

116 Reperfusion of ischemic tissues elicits an acute inflammatory response

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

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

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

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

121 and the damage resulting from reperfusion of ischemic tissue following stroke or organ transplant.

122 f genes for several proangiogenic factors in ischemic tissues following iPS-miR-126-EV transplantatio

123 Neutrophil infiltration to ischemic tissues following reperfusion worsens injury.

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

125 Therapies to revascularize ischemic tissue have long been a goal for the treatment

126 mal cell functions or restoring perfusion to ischemic tissues have been limited.

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

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

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

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

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

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

133 resent a novel acellular tool for therapy of ischemic tissues in vivo.

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

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

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

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

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

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

140 Reperfusion of ischemic tissue induces an acute inflammatory response t

141 Reperfusion of ischemic tissue induces significant tissue damage in mul

142 -occlusions, i.e. microstokes, could lead to ischemic tissue infarctions and cognitive deficits.

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

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

145 Ischemic tissue injury contributes to significant morbid

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

147 Because ischemic tissue injury provides a potential source for N

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

149 he interruption of blood supply and provokes ischemic tissue injury.

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

151 lates downstream CXCL12 expression following ischemic tissue injury.

152 initiate intravascular occlusion leading to ischemic tissue injury.

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

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

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

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

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

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

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

160 Revascularization of ischemic tissues is a major barrier to restoring tissue

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

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

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

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

165 s for the treatment of ischemic rest pain or ischemic tissue loss.

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

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

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

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

170 Nitrite significantly increased ischemic tissue NO bioavailability along with concomitan

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

172 evated reactive oxygen species production in ischemic tissues occurs as a result of accumulation of t

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

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

175 For the ischemic tissues of the scleroderma hand the prerequisit

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

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

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

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

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

181 ll survival in ischemic tissues, and promote ischemic tissue regeneration in a safer and more efficie

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

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

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

185 eutic tools that ablate or inhibit GPR39 for ischemic tissue repair under metabolic stress.

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

187 e development of protein-based therapies for ischemic tissue repair, also beyond the sole application

188 ng their functional properties essential for ischemic tissue repair, including proliferation, metabol

189 tic needs for arterial revascularization and ischemic tissue repair.

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

191 ify HS sulfation as a therapeutic target for ischemic tissue repair.

192 L as a KIT receptor ligand in the context of ischemic tissue repair.

193 inflammatory mitochondrial metabolism during ischemic tissue repair.

194 late regenerative processes underlying post-ischemic tissue repair.

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

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

197 Reperfusion injury of ischemic tissue represents an acute inflammatory respons

198 Ischemic tissues require mechanisms to alert the immune

199 y of HIF-CSC might be a promising option for ischemic tissue restoration.

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

201 Blockade of EC apoptosis may promote ischemic tissue revascularization by preserving ECs with

202 In ischemic tissues, stress kinases such as c-Jun N-termina

203 cularization strategies for the treatment of ischemic tissues such as ischemic heart disease.

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

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

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

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

208 sociation suggests that sepsis disturbs post-ischemic tissue survival and brain remodeling.

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

210 -specific deletion of CXCL12 (eKO) modulates ischemic tissue survival, altering tissue repair and tum

211 e revascularization by preserving ECs within ischemic tissue that retain the capacity to reassemble a

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

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

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

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

216 Identifying ischemic tissue to direct tissue sampling towards ischem

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

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

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

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

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

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

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

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

225 % of baseline, and endogenous VEGF levels in ischemic tissue were increased.

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

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

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

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

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

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

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

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

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

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