ライフサイエンスコーパス: injured tissue

1 large baseline ischemic cores (irreversibly injured tissue).

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

3 ir native environment or conditions found in injured tissue.

4 that assigns region-specific instructions to injured tissue.

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

6 ich indicates that MSCs specifically home to injured tissue.

7 a potential barrier between the healthy and injured tissue.

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

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

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

11 ive interactions that recruit those cells to injured tissue.

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

13 ecognition signals to regulate blood flow to injured tissue.

14 Only selenide targets to injured tissue.

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

16 nsplanted or endogenously recruited) and the injured tissue.

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

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

19 chemokine receptor CCR2 for localization to injured tissue.

20 Thus, the probe samples injured tissue.

21 rect assessment of gene expression status of injured tissue.

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

23 transcriptional profiles were obtained from injured tissue.

24 trauma and can trigger chemokine release in injured tissue.

25 zing molecular motifs unique to pathogens or injured tissue.

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

27 ought to involve adaptive changes within the injured tissue.

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

29 persistence of fibroblasts/myofibroblasts in injured tissues.

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

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

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

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

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

35 o be recruited and properly activated within injured tissues.

36 and maintain normal function in diseased and injured tissues.

37 phocyte apoptosis during the regeneration of injured tissues.

38 inflammation and migration of fibroblasts in injured tissues.

39 an emerging strategy for the replacement of injured tissues.

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

41 hemokines by proteases that are activated in injured tissues.

42 and maintain normal function in diseased and injured tissues.

43 ic and therapeutic materials into tumors and injured tissues.

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

45 and maintain normal function in diseased and injured tissues.

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

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

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

49 MSC selectively target injured tissue and promote functional recovery.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 Injured tissues can replace damaged cells by proliferati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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