ライフサイエンスコーパス: endothelial injury

1 e complement activation, likely triggered by endothelial injury.

2 in part, by less severe lung epithelial and endothelial injury.

3 respectively, aHUS is characterized by renal endothelial injury.

4 in the pathogenesis of diseases that involve endothelial injury.

5 osure to hand-held vibrating tools may cause endothelial injury.

6 tributes to the cellular injury in shock and endothelial injury.

7 ting arterial lesion growth in conditions of endothelial injury.

8 geting as a drug delivery strategy to reduce endothelial injury.

9 ythrocyte, provokes inflammation, and causes endothelial injury.

10 improves renal and lung function by reducing endothelial injury.

11 otid artery following experimentally induced endothelial injury.

12 predispose to atherosclerosis by inflicting endothelial injury.

13 ts with active SLE may represent a marker of endothelial injury.

14 r CAD, may cause atherosderosis by oxidative endothelial injury.

15 ic systems, neutrophil release products, and endothelial injury.

16 ant role in platelet adhesion to the site of endothelial injury.

17 ese findings likely represent sepsis-induced endothelial injury.

18 n cytolytic activity may contribute to graft endothelial injury.

19 tory response that in turn causes functional endothelial injury.

20 ischemia-reperfusion (I-R) occurs because of endothelial injury.

21 lial barrier and in preventing lung vascular endothelial injury.

22 s in the promoters of other genes induced by endothelial injury.

23 lity, multiple markers of ICU morbidity, and endothelial injury.

24 A pathogenic consequence of hyperoxia is endothelial injury.

25 t blocking APC-mediated pathways or inducing endothelial injury.

26 hanges were accompanied by evidence of acute endothelial injury.

27 e the restoration of vascular function after endothelial injury.

28 tly in response to systemic inflammation and endothelial injury.

29 dothelial cell regeneration in rabbits after endothelial injury.

30 renchyma, and decreased hepatic ischemia and endothelial injury.

31 as well as pulmonary epithelial and systemic endothelial injury.

32 MN activation and recruitment at the site of endothelial injury.

33 , ICU morbidity, and biochemical evidence of endothelial injury.

34 t, but had little effect on antibody-induced endothelial injury.

35 ics of inflammation, hypercoagulability, and endothelial injury.

36 athway dysregulation and is characterized by endothelial injury.

37 tory T-cell (Treg) activity fails to control endothelial injury.

38 mpaired reannealing of endothelial AJs after endothelial injury.

39 elopment of neointimal hyperplasia following endothelial injury.

40 or simply reveals the presence of underlying endothelial injury.

41 C reparative function after diabetes-related endothelial injury.

42 ession in vivo and noninvasive assessment of endothelial injury.

43 ame concentrated in the adventitia following endothelial injury.

44 the protective effects of olive oil against endothelial injuries.

45 ur groups of C57BL/6 mice underwent denuding endothelial injury 1 day after systemic injection of rec

46 their adhesion at the site of laser-induced endothelial injury, a necessary step leading to the gene

47 in a mouse model of type 1 diabetes promotes endothelial injury accelerating the progression of glome

48 terleukin-8 (anti-IL-8) therapy reduces lung endothelial injury after acid instillation, there is no

49 ng the postoperative days, presumably due to endothelial injuries and the infusion of vWF concentrate

50 Epithelial and endothelial injury and a cascade of immune and interstit

51 adhesion molecule-1 (sVCAM-1) is a marker of endothelial injury and a potent predictor of cardiovascu

52 mportant role in the mechanism of glomerular endothelial injury and activation and the formation of m

53 uremic syndrome (D+HUS) is characterized by endothelial injury and activation of inflammatory cytoki

54 ory cytokines, alveolar fluid clearance, and endothelial injury and activation.

55 We hypothesized that microvascular endothelial injury and attendant interstitial edema woul

56 hat because AMR is associated with allograft endothelial injury and C4d deposition, plasma microvesic

57 eases and renal fibrosis are associated with endothelial injury and capillary rarefaction.

58 important missing piece is the link between endothelial injury and complement activation.

59 NETs may serve as a mechanistic link between endothelial injury and complement activation.

60 sociation with this condition, the extent of endothelial injury and dysfunction has been difficult to

61 Endothelial injury and dysfunction precede accelerated a

62 y investigated whether biomarkers related to endothelial injury and endothelial repair discriminate b

63 These MPs induce endothelial injury and facilitate acute vaso-occlusive e

64 thin 5 d; the histology was characterized by endothelial injury and fibrin thrombi.

65 have shown that smoke inhalation causes lung endothelial injury and formation of pulmonary edema, the

66 marker of classic complement activation and endothelial injury and has been described in preliminary

67 of these studies suggest new mechanisms for endothelial injury and impaired vascular function associ

68 lveolar fluid clearance could be due to lung endothelial injury and increased fluid flux from the blo

69 nt in the pathogenesis of diseases linked to endothelial injury and inflammation in smokers.

70 sition was accompanied by extensive vascular endothelial injury and intravascular release of von Will

71 diabetic D2 mice demonstrated early signs of endothelial injury and loss of fenestrae.

72 d suggest that cross talk between glomerular endothelial injury and podocytes leads to defects and de

73 e of this study was to assess how indices of endothelial injury and repair change during different st

74 ause the mechanisms by which FeCl(3) induces endothelial injury and subsequent thrombus formation are

75 ides mechanistic insight into toxin-mediated endothelial injury and suggests new therapeutic approach

76 se data suggest that NETs contribute to lung endothelial injury and that targeting NET formation may

77 their use is limited by the resulting acute endothelial injury and the long-term development of inti

78 Systemic organ endothelial injury and V(O2)-D(O2) relationship alterati

79 relationship, if any, between systemic organ endothelial injury and V(O2)-D(O2) relationship alterati

80 This was due to hepatic ischemia, endothelial injury, and activation of neutrophils, Kupff

81 hondrial reactive oxygen species generation, endothelial injury, and ICAM-1 expression after LPS admi

82 flammation, alveolar epithelial and systemic endothelial injury, and the development of acute lung in

83 g coronary artery by creation of a stenosis, endothelial injury, and thrombus formation followed by t

84 n end products and surfactant protein D) and endothelial injury (angiopoietin-2) and inflammation (in

85 due to features of PAH: in situ thrombi and endothelial injury, angioproliferative remodeling, and r

86 rs reduced extravascular lung water and lung endothelial injury as measured by protein permeability (

87 To detect endothelial injury at the early and reversible stage of

88 It was shown that ELIPs specifically enhance endothelial injury/atheroma components.

89 ium of the diabetic retina, which results in endothelial injury, blood-retina barrier breakdown, and

90 has been widely associated with tubular and endothelial injury but rarely has been shown to induce p

91 le in the process of platelet adhesion after endothelial injury by serving as a bridge between consti

92 advanced glycation end products and systemic endothelial injury by the urine albumin-creatinine ratio

93 To determine endothelial injury component enhancement, anti-fibrinoge

94 he vascular system and its inhibition due to endothelial injury contributes to cardiovascular disease

95 ition of nitric oxide-mediated vasodilation, endothelial injury due to increased release of free fatt

96 than reactive oxygen species as mediators of endothelial injury during ANCA-associated systemic vascu

97 accompanied by increased pulmonary vascular endothelial injury, enhanced pulmonary accumulation of n

98 Ventilation with either 6 or 3 ml/kg reduced endothelial injury equally as measured by plasma vWf:Ag

99 fts in C6+ recipients demonstrated extensive endothelial injury evidenced by release of von Willebran

100 lement plays a significant role in mediating endothelial injury following oxidative stress.

101 matory condition precipitated in response to endothelial injury from various environmental challenges

102 ific integrin Mac-1, neutrophil recruitment, endothelial injury, glomerular thrombosis, and acute ren

103 in initial platelet accumulation at sites of endothelial injury, however, is the subject of debate.

104 timulated leukocyte shape change at sites of endothelial injury; however, only thrombi were capable o

105 on and fibrin generation after laser-induced endothelial injury in a single developing thrombus.

106 iopoietin-2 is a proinflammatory mediator of endothelial injury in animal models, and increased plasm

107 ir, representing a novel mechanism promoting endothelial injury in CAD patients.

108 d inflation--on alveolar epithelial and lung endothelial injury in experimental acute lung injury.

109 whereas both CPAP-30 and STEP-30/30 yielded endothelial injury in extrapulmonary acute lung injury.

110 This mechanism may well be relevant to acute endothelial injury in inflammation and other pathologica

111 of LOX-1 in monocyte adhesion to HCAECs and endothelial injury in response to ox-LDL.

112 yte-dependent and -independent mechanisms of endothelial injury in sepsis.

113 These findings suggest that endothelial injury in the absence of sufficient circulat

114 cular imaging and quantitative evaluation of endothelial injury in the choriocapillaris of live anima

115 ffects of WEB and GB in reducing LPS-induced endothelial injury in the choroid indicate an important

116 f hepatocytes in viral hepatitis and also in endothelial injury in the cold perfusion-warm reperfusio

117 y rise of Ang-2 emphasizes the importance of endothelial injury in the early pathogenesis of ALI.

118 roduces noninvasive subclinical detection of endothelial injury in the iris vasculature, providing a

119 idence for the role of potential triggers of endothelial injury in the pathophysiology of CAV and dis

120 se, suggesting that in vivo diabetes-related endothelial injury in the retina may be due to glucose-i

121 iciency of eNOS-derived NO causes glomerular endothelial injury in the setting of diabetes and result

122 th, replicating the characteristics of acute endothelial injury in transfused lungs in vivo.

123 findings shed light on a novel mechanism of endothelial injury in transplant-TMA and may therefore g

124 study was to investigate the role of PAF in endothelial injury in uveitis.

125 imaging agents for noninvasive detection of endothelial injury in vivo.

126 ly, reendothelialization after focal carotid endothelial injury in WT mice was significantly increase

127 c Organ Dysfunction score, and biomarkers of endothelial injury, including angiopoietin-2, von Willeb

128 irculatory events included hepatic ischemia, endothelial injury, including with gene expression array

129 expression may be an important mechanism of endothelial injury induced by TNF-alpha.

130 Endothelial injury is a major manifestation of septic sh

131 Endothelial injury is central to the development of pulm

132 As endothelial injury is central to the pathogenesis of vas

133 Endothelial injury is central to the pathogenesis of vas

134 Endothelial injury is considered critical for progressio

135 Vascular endothelial injury is responsible for many of the clinic

136 The mechanism of endothelial injury is still elusive, yet endothelial apo

137 Endothelial injury is the first step in atherosclerosis,

138 ear adaptation, which promotes shear-induced endothelial injury, is a newly identified dysfunction sp

139 exposure can result in hemolysis and direct endothelial injury leading to HUS phenotype.

140 -mediated dilatation (R = -0.3, P < 0.01) or endothelial injury marker von Willebrand factor (R = +0.

141 Our data indicate that the degree of endothelial injury may also be an important component of

142 This review focuses on epithelial and endothelial injury mediators, interactions, and targets

143 Utilizing a mouse endothelial injury model we show that thrombin cleavage

144 Using a laser-induced endothelial injury model, we examined thrombus formation

145 Glomerular inflammation correlates with endothelial injury, monocyte influx, and IL-6 and IL-bet

146 mice were studied in a model of transluminal endothelial injury of the femoral artery.

147 Stimuli that can cause endothelial injury or death include environmental stress

148 Endothelial injury plays a central role in the pathophys

149 elial cells and ameliorated diabetes-induced endothelial injury, podocyte loss, albuminuria, and glom

150 which are biomarkers of lung epithelial and endothelial injury previously found to be prognostic in

151 Diabetic NGRs showed substantial retinal endothelial injury, primarily in the microvessels, inclu

152 ed rat lungs upon I/R in order to assess the endothelial injury produced.

153 posure accelerated lethal pulmonary vascular endothelial injury, reduced the inspired oxygen threshol

154 injury, but the signaling pathways mediating endothelial injury remain incompletely understood.

155 Although endothelial injury represents the final common pathway o

156 O by HIV-1 Tat plays a pivotal role in brain endothelial injury, resulting in the irreversible loss o

157 rved with kidneys obtained from NHBDs is the endothelial injury seen on protocol core biopsies after

158 ted ECs may promote adhesion of platelets to endothelial injury sites to assure wound healing, simult

159 ctivation (elastase/alpha 1 antitrypsin) and endothelial injury (soluble thrombomodulin).

160 ficantly higher sensitivity for detection of endothelial injury than singly conjugated MSs (rPSGL-1-

161 In a rabbit model of arterial endothelial injury, the infusion of 51Cr-labeled micropa

162 oncerning its pathogenesis focus on vascular endothelial injury, the oxidation of low-density lipopro

163 (polymorphonuclear leukocytes, PMNs) mediate endothelial injury, thrombosis, and vascular remodeling.

164 In an in vivo model of light/dye-induced endothelial injury/thrombosis in the cremasteric venules

165 nterior descending coronary artery stenosis, endothelial injury, thrombus formation and thrombolysis.

166 a regulator of arterial thrombosis following endothelial injury through effects on vascular wall IGF-

167 eleased by intravascular hemolysis initiates endothelial injury through nitric oxide (NO) scavenging

168 mote platelet activation, leukocyte-mediated endothelial injury, tissue damage, and death.

169 Studies using a model of endothelial injury to the carotid artery reveal that the

170 derived toxins (or possibly other sources of endothelial injury), together with additional genetic su

171 Using mouse models of endothelial injury (traumatic or ischemia reperfusion),

172 Brain endothelial injury was measured with cytotoxicity and di

173 ets; however, time to vessel occlusion after endothelial injury was significantly shorter in Pf4-Lox(

174 trial of gene therapy to reduce CTL-mediated endothelial injury, we stably transduced early passage H

175 n Willebrand factor (a traditional marker of endothelial injury) were measured in 931 subjects with a

176 challenge resulted in more severe glomerular endothelial injury, whereas the glomerular injury after

177 This suggests that the virus may initiate endothelial injury, which is believed to be an early eve

178 e used for 1% of births yet may also lead to endothelial injury with long-term adverse consequences f

179 Electron microscopy showed endothelial injury within 6 hours following CP, and, aft

180 We observed extensive endothelial injury without Kupffer cell or hepatocyte da

181 Endothelial injury worsens over time on dialysis but imp