ライフサイエンスコーパス: injured tissue

1 large baseline ischemic cores (irreversibly injured tissue).

2 zing molecular motifs unique to pathogens or injured tissue.

3 on that destroys the injurious agent and the injured tissue.

4 ought to involve adaptive changes within the injured tissue.

5 blood loss and the accumulation of fluid in injured tissue.

6 that assigns region-specific instructions to injured tissue.

7 c approach to improve healing of ischemic or injured tissue.

8 ich indicates that MSCs specifically home to injured tissue.

9 a potential barrier between the healthy and injured tissue.

10 on, of extracellular matrix (ECM) within the injured tissue.

11 4) treatment contributes to the clearance of injured tissue.

12 toration of vascular barrier function within injured tissue.

13 optosis in cells exposed to stress or in the injured tissue.

14 ive interactions that recruit those cells to injured tissue.

15 fight pathogens but also to control pain in injured tissue.

16 ecognition signals to regulate blood flow to injured tissue.

17 h accumulation and retention kinetics in the injured tissue.

18 gical processes are triggered to recover the injured tissue.

19 s invade and replace the collagen-containing injured tissue.

20 helial cells migrate across wounds to repair injured tissue.

21 and subsequent cardiomyocyte protrusion into injured tissue.

22 g and is essential for the reconstruction of injured tissue.

23 ed in serum, cerebrospinal fluid, and in the injured tissue.

24 nd has the potential to be used in repairing injured tissue.

25 y be the most common molecular feature of an injured tissue.

26 brin(ogen) cross-linking in vitro and within injured tissue.

27 t role in the repair and regeneration of the injured tissue.

28 transcriptional profiles were obtained from injured tissue.

29 ir native environment or conditions found in injured tissue.

30 Only selenide targets to injured tissue.

31 ve, often sparing and recovering some of the injured tissue.

32 nsplanted or endogenously recruited) and the injured tissue.

33 taining as well as nuclear p65 levels in the injured tissue.

34 sponders of innate immunity, neutrophils, to injured tissue.

35 chemokine receptor CCR2 for localization to injured tissue.

36 Thus, the probe samples injured tissue.

37 rect assessment of gene expression status of injured tissue.

38 s and is driven by inflammatory responses to injured tissue.

39 trauma and can trigger chemokine release in injured tissue.

40 complex molecular signatures and utility in injured tissues.

41 an emerging strategy for the replacement of injured tissues.

42 CNTF receptor (CNTFRalpha) is released from injured tissues.

43 hemokines by proteases that are activated in injured tissues.

44 and maintain normal function in diseased and injured tissues.

45 ic and therapeutic materials into tumors and injured tissues.

46 o wounding, to regenerate rather than repair injured tissues.

47 and maintain normal function in diseased and injured tissues.

48 persistence of fibroblasts/myofibroblasts in injured tissues.

49 tegy for directed stem-cell engraftment into injured tissues.

50 ted complex process leading to the repair of injured tissues.

51 largely upon detection of 3-nitrotyrosine in injured tissues.

52 ound periderm also forms to heal and protect injured tissues.

53 y recognizing molecular patterns released by injured tissues.

54 ce, consistent with deposition of the Abs in injured tissues.

55 , has been shown to drive EPC recruitment to injured tissues.

56 the invading pathogens or to the recovery of injured tissues.

57 potentially applicable to regenerating other injured tissues.

58 restores the integrity and functionality of injured tissues.

59 ished fibrosis and to regenerate chronically injured tissues.

60 n-kinin cascade system are both activated in injured tissues.

61 y sources of ECM-producing myofibroblasts in injured tissues.

62 o be recruited and properly activated within injured tissues.

63 and maintain normal function in diseased and injured tissues.

64 phocyte apoptosis during the regeneration of injured tissues.

65 inflammation and migration of fibroblasts in injured tissues.

66 ed diverse fibroblast subsets in healthy and injured tissues(1,2), but the origins and functional rol

67 in the removal and clearance of pathogens or injured tissue and a return to homeostasis.

68 t to enhance cardiomyocyte invasion into the injured tissue and along the apical surface of the wound

69 otrophin receptor p75NTR is increased in the injured tissue and axon regeneration is repressed by the

70 ere the mobilized cells are recruited to the injured tissue and contribute to vessel growth.

71 nitor cells that subsequently engraft in the injured tissue and further differentiate to reconstitute

72 sults suggest communication between directly injured tissue and non-affected tissues that are distant

73 s MSCs, and the potential of MSCs to home to injured tissue and promote corneal repair.

74 MSC selectively target injured tissue and promote functional recovery.

75 at macrophages are able to rapidly invade an injured tissue and reestablish a developmental program t

76 tgfa, is induced in endocardial cells in the injured tissue and regulates CM proliferation and repopu

77 designed to selectively release morphine in injured tissue and to prevent blood-brain barrier permea

78 nduces mitochondria-associated cell death in injured tissues and constitutes another mechanism for ex

79 Bone marrow-derived fibrocytes migrate to injured tissues and contribute to fibrogenesis, but thei

80 Activated neutrophils migrate into injured tissues and help contain microbial infections, b

81 widespread therapeutic applications in other injured tissues and opens up new avenues of research int

82 Although most mammals heal injured tissues and organs with scarring, spiny mice (Ac

83 when it develops in the microvasculature of injured tissues and organs.

84 s react promptly to signals from infected or injured tissues and produce an array of secreted protein

85 ration, can potentially restore diseased and injured tissues and whole organs.

86 due to immunoprivilege, capacity to home to injured tissue, and extensive pre-clinical support.

87 ity, exit the spleen en masse, accumulate in injured tissue, and participate in wound healing.

88 re-vascularization were characterized in the injured tissues, and each of these histologic features w

89 siologic conditions because it helps healing injured tissues, and in female populations it helps form

90 os, forming fibroblasts/mesenchymal cells in injured tissues, and initiating metastasis of epithelial

91 for EPO/EPOR cytoprotection of ischemically injured tissues, and potential EPO-mediated worsening of

92 matory mediators produced and accumulated in injured tissues, and TRPV1 activation-induced feed-forwa

93 itment of macrophages and T lymphocytes into injured tissues, and we have found that RAS activation i

94 therapeutic bone regeneration, the defect or injured tissues are frequently inflamed with an abnormal

95 heart had increased ANXA1 expression in the injured tissue, associated mainly with the infiltrated l

96 novel approaches were developed to classify injured tissues at different time points.

97 CNS to minimize primary damage and to repair injured tissues, but it ultimately generates harmful eff

98 ay important roles in repair/regeneration of injured tissues, but their roles in pathological fibrosi

99 Tumor was differentiated from radiation-injured tissue by histopathology (n = 13) or 1-y clinica

100 ionated ventricular myocardium, localizes to injured tissues by binding to leaky microvasculature, an

101 and other sources have been shown to repair injured tissues by differentiating into tissue-specific

102 Injured tissues can replace damaged cells by proliferati

103 at the anaphylatoxins C3a and C5a present in injured tissues contribute to the recruitment of MSCs an

104 roduced by hMSCs in response to signals from injured tissues, delayed the onset of spontaneous autoim

105 stinct stem/progenitor cell pools repopulate injured tissue depending on the extent of the injury, an

106 f-injury based on the 2 models used, but the injured tissue dictates the systemic cytokine response.

107 An hour after a simulated blast, injured tissues displayed altered intracellular calcium

108 AURKB deficiency during regeneration of the injured tissues: disrupted cell cycle progression, repre

109 omyocyte invasion of the collagen-containing injured tissue during cardiac regeneration.

110 to penetrate basement membranes and remodel injured tissue during inflammation.

111 genous bioelectric state by depolarizing the injured tissue during the first 3 h of regeneration alte

112 ways that regulate neutrophil recruitment to injured tissues during noninfectious inflammation remain

113 e endogenous activation signals liberated by injured tissues even in the absence of infection.

114 e expression of proinflammatory cytokines by injured tissues exacerbates the inflammatory cascade, in

115 imulated with conditioned medium from spinal-injured tissue explants.

116 o revealed considerably more versican in the injured tissue extract.

117 A myriad of destructive processes unfold in injured tissue following ischemia-reperfusion.

118 sue-resident cells and those that infiltrate injured tissue from the periphery during noninfectious i

119 the chemokine receptor CCR2 to gain entry to injured tissues from the bloodstream, are purportedly ne

120 The behavior of BMDCs in injured tissue has a profound effect on repair, but the

121 While the role of inflammation in the injured tissue has been examined in some detail, the con

122 successful, the cellular environment of the injured tissue has to be able to nurture new hair cells.

123 , the absence of an adequate blood supply to injured tissues has been hypothesized to contribute to t

124 Expression of pro-inflammatory cytokines by injured tissues has been shown to exacerbate the inflamm

125 adaptive because both can persist long after injured tissues have healed and inflammation has resolve

126 scular fibrin(ogen) deposits are observed in injured tissues; however, the mechanisms regulating fibr

127 The injured tissue in apoE(-/-) mice also showed a more pron

128 reduced bleeding and facilitated healing of injured tissue in both prophylactic and immediate treatm

129 t are required for the healing and repair of injured tissues in adult animals.

130 eukocytes from the vascular compartment into injured tissues in response to inflammatory stimuli.

131 associated molecular pattern released by the injured tissues in trauma and sepsis settings, which tri

132 formed blood vessels that revascularize the injured tissue, in ccn2a mutants CM proliferation and re

133 have been associated with delayed healing in injured tissues, inappropriate femoral fractures, and os

134 y adult epithelium but upregulated in select injured tissues, including fibrotic lung.

135 tions that underlie their reparative role in injured tissues, including the regulation of the cellula

136 Brought into the injured tissue initially by migrated neutrophils, and th

137 Regeneration of injured tissue is a dynamic process, critically dependen

138 an amniotic mesenchymal stromal cells to the injured tissue is not necessary for the release of bioac

139 Restoring blood flow to the site of injured tissue is often a necessary prerequisite for mou

140 The environment of injured tissue is thus thought to restrict the regenerat

141 tive agents accelerating healing of infected injured tissues is crucial.

142 pression of stromal cell-derived factor-1 in injured tissue leads to improved end-organ function.

143 ing of diffuse-injured circuits into diffuse-injured tissue likely establishes maladaptive circuits r

144 GCSF-stimulated neutrophils to migrate into injured tissue may be impaired.

145 hat vascular survival and growth in ischemia-injured tissue may be stimulated by suppressing PHD2 in

146 une signals from infectious organisms and/or injured tissues may activate peripheral neuronal pain si

147 ng that an excess of TGF-beta in inflamed or injured tissues may alter mast cell expression of gelati

148 he affinity of (64)Cu-bis-DOTA-hypericin for injured tissues may be attributed to the breakdown of th

149 ions of gelsolin, a protein that responds to injured tissue, might be a predictor of patient outcomes

150 and increased the levels of LC3(+) puncta in injured tissue of Nod2(-/-) mice.

151 Neutrophil recruitment to sites of injured tissue or infection has been well studied, and m

152 usively intracellular (except in diseased or injured tissues), our data show that schistosomes displa

153 betics could contribute to limited repair of injured tissue, particularly when combined with other kn

154 ior of neutrophils that target and adhere to injured tissues, preventing inflammation and neointima f

155 Signals that target inflammatory cells to injured tissue probably direct MSC to injury sites.

156 ic release of neuropeptides into infected or injured tissue, producing neurogenic inflammation.

157 odulating monocytes/macrophages (Mo/MPhi) in injured tissues, promoting their switch to an anti-infla

158 t in plasma, which are observed in fluids of injured tissues, purified and recombinant gelsolin augme

159 In healthy individuals, injured tissues rapidly repair themselves following dama

160 o the migration of reprogrammed cells to the injured tissue, reducing regional cardiac strain and imp

161 ical roles, such as increasing blood flow to injured tissues, reducing leukocyte adherence, and inhib

162 and confirmed that DRP1 has a vital role in injured tissue regeneration.

163 We hypothesize that injured tissues release mediators that increase the prod

164 fferentiation of stem cells, responsible for injured tissue repair, and simultaneously discourage bac

165 osis FAP-a(+)(myo)fibroblasts disappear from injured tissues, replaced by cells with a normal FAP-a(-

166 In response to ischemic insult, injured tissues secrete several chemo-cytokines, includi

167 hich activate peripheral opioid receptors in injured tissue.SIGNIFICANCE STATEMENT Interleukin-4 (IL-

168 of normal tissues such as proteoglycans and injured tissues such as cell-associated cytokines with r

169 tor cells may provide powerful therapies for injured tissues such as the lung and heart.

170 ally inhibited ERK1/2 phosphorylation in the injured tissue, suggesting it may act through a combinat

171 local synthesis and secretion of FBG in the injured tissue, supporting the hypothesis that productio

172 hereby conferring specificity to stressed or injured tissues that produce adenosine.

173 treating degenerative diseases by 'seeding' injured tissues, the regenerative capacity of stem cells

174 modulation of remodeling, or preservation of injured tissue through paracrine mechanisms is actively

175 ways is the ability of MSCs to interact with injured tissue through the release of soluble bioactive

176 Inflammation promotes regeneration of injured tissues through poorly understood mechanisms, so

177 ing on skin and mucosa, but poised to invade injured tissue to cause local infections.

178 controlling the local environment within the injured tissue to optimize tissue regeneration via the t

179 Immunohistochemistry was performed on injured tissue to reveal patterns of caspase-3 and UCP-2

180 ate the vascular epithelial lining or expose injured tissues to endothelial cells (ECs) with unique h

181 by the cells being activated by signals from injured tissues to express an anti-inflammatory protein

182 active during repair processes that restore injured tissues to normal, reduced fibrinolytic activity

183 en the immune injury exceeds the capacity of injured tissues to regenerate and repair.

184 Leukocytes migrating into injured tissues tonically release DAMPs, including the h

185 Macrophages infiltrating an inflamed or injured tissue undergo development of coordinated sets o

186 In this study, we show that fibroblasts in injured tissues undertake the clearance of collectins by

187 me metabolism, is produced at high levels in injured tissue via induction of heme-oxygenase-1 activit

188 ion of cell-cell junctions seen in wild-type injured tissue was absent in matrilysin-null samples.

189 r, both critical for monocyte recruitment to injured tissues, was decreased.

190 be a useful source of cells for treatment of injured tissues where smooth muscle plays an important r

191 TH17 cells and CX3CR1(+) monocytes into the injured tissue, which was accompanied by increased RIPK3

192 sions may serve as a means to rapidly repair injured tissue while preserving the capacity to regenera

193 ne or cytokine treatment alone, treatment of injured tissue with either 1 ng/ml IL-1alpha or 100 ng/m

194 degenerating neurons in the traumatic brain-injured tissue with the absence of staining in our sham-

195 important for T cells to access inflamed or injured tissues with abrupt topographical changes.

196 ly regulates neutrophil retention within the injured tissues with consequences for neutrophil clearan

197 ent mesenchymal stem cells; MSCs) can repair injured tissues with little evidence of engraftment or d

198 adipose tissue, which resembles chronically injured tissue, with immune cell infiltration and remode