ライフサイエンスコーパス: cardiac injury

1 ndicator of neuromuscular skeletal muscle or cardiac injury).

2 ed that PAI-1 also regulates fibrosis during cardiac injury.

3 ac function and ventricular dilatation after cardiac injury.

4 rving cardiac function after acute ischaemic cardiac injury.

5 te immunity and ischemia/reperfusion-induced cardiac injury.

6 the biomarker of choice for the diagnosis of cardiac injury.

7 have potential as therapeutics to attenuate cardiac injury.

8 including ischemia/reperfusion (I/R)-induced cardiac injury.

9 sternal reentry is more likely to result in cardiac injury.

10 ely used in clinics as a serum biomarker for cardiac injury.

11 oting endogenous revascularization following cardiac injury.

12 milar protective effects against DOX-induced cardiac injury.

13 gnaling in a cardioprotective role following cardiac injury.

14 -adrenergic receptor agonist known to induce cardiac injury.

15 n unusual capacity to regenerate after acute cardiac injury.

16 radiation techniques may reduce the risk of cardiac injury.

17 el or sustained neovascularization following cardiac injury.

18 Angiopoietin-1 limits ischemia-induced cardiac injury.

19 ments for clinical or ECG signs of potential cardiac injury.

20 ceptibility of the HFE gene knockout mice to cardiac injury.

21 ric oxide and superoxide in various forms of cardiac injury.

22 and Bl.Tg.Ealpha [IA+ IE+]) had substantial cardiac injury.

23 accumulation of Ca2+, has been implicated in cardiac injury.

24 itivity and specificity for the detection of cardiac injury.

25 a variety of experimental models of ischemic cardiac injury.

26 le in gap junction remodeling in response to cardiac injury.

27 e known to be a major target during ischemic cardiac injury.

28 gesting mitochondria as the critical site of cardiac injury.

29 are capable of heart regeneration following cardiac injury.

30 e treatment of older patients suffering from cardiac injury.

31 omyocytes in vitro as well as in vivo during cardiac injury.

32 yte recruitment to the heart following acute cardiac injury.

33 ndent cardiac troponin elevation to indicate cardiac injury.

34 93 is important for tissue oxygenation after cardiac injury.

35 l and smooth muscle cells in vitro and after cardiac injury.

36 nt for the enhanced protective effects after cardiac injury.

37 a LOF both lead to unresolved scarring after cardiac injury.

38 n contributing to the detrimental effects of cardiac injury.

39 unt a strong regenerative response following cardiac injury.

40 educe reactive oxygen species (ROS) -induced cardiac injury.

41 al-cell-like phenotype after acute ischaemic cardiac injury.

42 egenerative and nonregenerative responses to cardiac injury.

43 d a potential therapeutic target in ischemic cardiac injury.

44 itical mechanism in the maternal response to cardiac injury.

45 yte Ca(2)(+) homeostasis and survival during cardiac injury.

46 ung injury; 4) The role of exosomes in acute cardiac injury; 5) The role of exosomes in acute kidney

47 After cardiac injury, activated cardiac myofibroblasts can inf

48 STAT3 are significantly more susceptible to cardiac injury after doxorubicin treatment than age-matc

49 diac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convinci

50 choice in screening patients for a possible cardiac injury after penetrating chest trauma by detecti

51 with non-small-cell lung cancer (NSCLC), yet cardiac injury after treatment is a significant concern.

52 enerate intracellular Na+ and Ca2+ overload, cardiac injury and arrhythmia in the heart.

53 yocardium, is activated to proliferate after cardiac injury and can contribute vascular support cells

54 Doxorubicin causes cardiac injury and cardiomyopathy in children with acute

55 tudying the role of alpha-E-catenin in human cardiac injury and cardiomyopathy in the future.

56 dualize treatment by immediately identifying cardiac injury and cardiomyopathy.

57 ance of studying the role of PINCHs in human cardiac injury and cardiomyopathy.

58 kine-dependent dysfunction during both acute cardiac injury and chronic cardiac pathologies.

59 an produce the serious side effects of acute cardiac injury and chronic congestive heart failure.

60 Potential cardiac injury and danger to viable grafts from repeated

61 or PINCH2 in myocardium leads to exacerbated cardiac injury and deterioration in cardiac function aft

62 rculating histone levels have been linked to cardiac injury and dysfunction in experimental models an

63 is involved in the regulation of I/R-induced cardiac injury and dysfunction via antithetical regulati

64 ne, a matrix metalloproteinase inhibitor, on cardiac injury and functional recovery in a swine model

65 lly increased cTnT may represent subclinical cardiac injury and have important clinical implications,

66 imal elevations in biomarkers of subclinical cardiac injury and hemodynamic stress modify the associa

67 ion administration of doxycycline attenuates cardiac injury and improves functional recovery in newbo

68 ed by doxorubicin and also protected against cardiac injury and loss of function.

69 Here, we have found that cardiac injury and mortality in models of myocardial inf

70 n early heart failure phenotypes, preventing cardiac injury and neurohormonal activation.

71 , is critical for control of immune-mediated cardiac injury and polymorphonuclear leukocyte inflammat

72 luronan, heparan sulfate) are upregulated on cardiac injury and regulate key processes in the remodel

73 d splenic T cells in HF are primed to induce cardiac injury and remodeling, and retain this memory on

74 idence of new physiological phenomena during cardiac injury and repair as well as cardiac drug-mediat

75 in the infarcted heart; however, its role in cardiac injury and repair remains controversial.

76 al conditioning may result in a reduction of cardiac injury and support rapid recovery after major su

77 ion is an early event in doxorubicin-induced cardiac injury and that titin degradation occurs by acti

78 te NF-kappaB signaling as a key node between cardiac injury and tissue regeneration.

79 contribute importantly to remodeling during cardiac injury and/or inflammation.

80 o atherosclerosis, thrombosis, inflammation, cardiac injury, and fibrosis are introduced in the conte

81 k stratification, diagnosis and prognosis of cardiac injury, and multiple forms of cardiovascular dis

82 ocyte mechanical interactions develop during cardiac injury, and that cardiac conduction may be impai

83 erexpression of Hsp20 inhibits DOX-triggered cardiac injury, and these beneficial effects appear to b

84 PKG Ialpha disulfide formation triggers cardiac injury, and this initiation of maladaptive signa

85 At the moment, the most specific markers for cardiac injury are cardiac troponin I (cTnI) and cardiac

86 known to induce oxidative stress and thereby cardiac injury, as a model cardiotoxic compound and obse

87 Dexrazoxane prevents or reduces cardiac injury, as reflected by elevations in troponin T

88 cardiomyocytes to proliferate in response to cardiac injury, as well as transplantation of cardiomyoc

89 ocardium of diabetic rodents suggesting that cardiac injury associated with PKCbeta2 activation, diab

90 aluable in understanding the pathogenesis of cardiac injury associated with retroviral infection in a

91 mice that resulted in higher viral loads and cardiac injury at day 8 after infection.

92 Also, the response to cardiac injury at postnatal day 15 is intermediate betwe

93 stigated the influence of O-GlcNAc levels on cardiac injury at the cellular level.

94 x4 expression, indicating that AngII worsens cardiac injury, at least in part by enhancing Nox4 expre

95 um measurements of cardiac troponin T (cTnT; cardiac injury biomarker), N-terminal pro-brain natriure

96 In contrast, four out of five postoperative cardiac injury biomarkers (NT-proBNP, H-FABP, hs-cTnT, a

97 of urine kidney injury biomarkers and plasma cardiac injury biomarkers in adverse events, we conducte

98 A significant increase in cardiac injury biomarkers was observed at 18-24 hours in

99 ith the appearance of microscopic injury and cardiac injury biomarkers.

100 rophages are crucial for tissue repair after cardiac injury but are not well characterized.

101 flammatory cytokines released in response to cardiac injury by chemotherapy or acute ischemia.

102 IF is expressed in cardiomyocytes and limits cardiac injury by enhancing AMPK activity during ischemi

103 mice/tandem dimer Tomato (tdTomato) mice to cardiac injury by permanent ligation of the left anterio

104 After acute cardiac injury, c-kit(+) cells retain their endothelial

105 r inflammation, neurohumoral activation, and cardiac injury can predict appropriate shocks and all-ca

106 After cardiac injury, cardiac progenitor cells are acutely red

107 ncreased the myocyte resistance to the acute cardiac injury caused by enteroviral infection.

108 antly increased CVB3 levels in the heart and cardiac injury compared with controls.

109 r rates of morbidity and mortality following cardiac injury compared with WT; however, adaptive cardi

110 indings suggest that bacterial pneumonia and cardiac injury contribute to fatal outcomes after infect

111 To treat cardiac injuries created by myocardial infarcts, current

112 treatment of ischemia with genes that limit cardiac injury due to hypoxia.

113 Cardiac injury due to inadequate energy production from

114 role of MIF in regulating JNK activation and cardiac injury during experimental ischemia/reperfusion

115 ry circulation, and this resulted in greater cardiac injury during ischemia-reperfusion.

116 Induction of autophagy and cardiac injury during the reperfusion phase was signific

117 Following cardiac injury, early immune cell responses are essentia

118 decreases in miR-101a levels at the onset of cardiac injury enhanced CM proliferation.

119 Prior studies of hepatic and cardiac injury examined limited repertoires of UPR eleme

120 ignificance of radiotherapy (RT) -associated cardiac injury for stage III non-small-cell lung cancer

121 d applied it to identify early biomarkers of cardiac injury from the blood of patients undergoing a t

122 The role of NHE1 in cardiac injury has prompted interest in the development

123 inding protein (HFABP) as an early marker of cardiac injury holds a promising future with studies ind

124 ge, which may in turn lead to a reduction in cardiac injury, hypertrophy, fibrosis, remodeling, and s

125 as that a sternotomy was unnecessary and the cardiac injury, if present, had sealed.

126 cribes a 10-min surgical procedure to induce cardiac injury in 1-d-old neonatal mice.

127 diac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance spor

128 To investigate cardiac injury in borrelia carditis, we used antibody-de

129 : use of biomarkers for early recognition of cardiac injury in children receiving chemotherapy, devel

130 Cardiac injury in mammals and amphibians typically leads

131 Cardiac injury in mice expressing cyclin D1 or D3 result

132 In contrast, cardiac injury in mice expressing cyclin D2 did not alte

133 le of ABCC6 in the calcification response to cardiac injury in mice.

134 apoptosis plays a critical role in mediating cardiac injury in the setting of viral myocarditis and i

135 as increased in some mutant mice and reduced cardiac injury in these animals.

136 e coronary syndrome, indicating unrecognized cardiac injury in these settings.

137 This study shows that E. coli OMVs induce cardiac injury in vitro and in vivo, in the absence of b

138 ays, play a pivotal role in the reduction of cardiac injury induced by mechanical stress or ischemia

139 ammatory and apoptotic responses may promote cardiac injury initiated by passively acquired autoantib

140 dings indicate that (1) beta-agonist-induced cardiac injury is associated with activation of the ASK1

141 Cardiac injury is common in asphyxiated neonates and is

142 of Grem2 and BMP-signaling inhibitors after cardiac injury is currently unknown.

143 ectly contribute to neovascularization after cardiac injury is not known.

144 for the treatment of heart tissue damaged by cardiac injury is to develop strategies for restoring he

145 in regulating immune cell responses to acute cardiac injury is unknown.

146 er development of efficient therapeutics for cardiac injury, it is essential to uncover molecular mec

147 PK-DN mice subjected to MI/R endured greater cardiac injury (larger infarct size, more apoptosis, and

148 njury, excessive hemorrhage, and inadvertent cardiac injury leading to morbidity and mortality.

149 Genetic ablation of MMP-9 attenuated cardiac injury, left ventricle dilation, and fibrosis in

150 unit clinician, including new biomarkers of cardiac injury like troponin T and I.

151 hol-induced cardiac fibrosis and more severe cardiac injury, making the MT-KO mouse model of alcohol-

152 Serial measurements of cardiac injury markers were not obtained.

153 Several components of the cardiac injury microenvironment have been identified, ye

154 We sought to determine whether subclinical cardiac injury might also occur in acute liver failure.

155 A murine cardiac injury model was performed by subcutaneous infus

156 In contrast, data analyses for mammalian cardiac injury models indicated that inflammation and me

157 s or via cell transplantation in preclinical cardiac injury models.

158 , and albumin) and five plasma biomarkers of cardiac injury (NT-proBNP, H-FABP, hs-cTnT, cTnI, and CK

159 (93%) randomized to sternotomy had either no cardiac injury or a tangential injury.

160 Although rare instances of cardiac injury or arrhythmias have been reported in acut

161 death in the western world, develops when a cardiac injury or insult impairs the ability of the hear

162 2 hours post-MI but had no effect on initial cardiac injury or structure.

163 factor (CTGF) is upregulated in response to cardiac injury or with transforming growth factor beta (

164 roptosis, is critically involved in ischemic cardiac injury, pathological cardiac remodeling, and hea

165 artery disease reduced renal dysfunction and cardiac injury, potentially resulting in improved surviv

166 Fibrosis resulting from cardiac injury presents a major challenge to restoring h

167 Because the mammalian heart scars following cardiac injury, recent work showing that cardiac fibrobl

168 gonucleotide miR-494 increased I/R-triggered cardiac injury relative to the administration of mutant

169 cardiac remodeling, but its precise role in cardiac injury remains controversial.

170 dings indicate that epicardium modulates the cardiac injury response by conditioning the subepicardia

171 lpha (Mapk14 gene) is known to influence the cardiac injury response, but its direct role in orchestr

172 Cardiac injury resulted in a approximately 6.45-fold exp

173 mine whether fibroblast activation following cardiac injury results in a distinct electrophysiologica

174 These data demonstrate cardiac injury results in significant electrophysiologic

175 a subgroup of patients with more complicated cardiac injuries such as coronary artery injuries, septa

176 nt of mesenchymal stem cells (MSC) following cardiac injury, such as myocardial infarction, plays a c

177 emic inflammatory diseases, cancer, and post-cardiac injury syndromes).

178 Following cardiac injury, the epicardium is activated organ-wide i

179 yocytes can reenter the cell cycle following cardiac injury, the myocardium is largely thought to be

180 ferative expansion, transforming subclinical cardiac injury to overt heart failure.

181 proliferation of spared cardiomyocytes after cardiac injury to regenerate lost heart muscle.

182 ith a penetrating chest wound and a possible cardiac injury to the Groote Schuur Hospital Trauma Cent

183 Acute ischaemic cardiac injury upregulates Wnt1 that is initially expres

184 s a biomarker of doxorubicin-induced chronic cardiac injury was evaluated in the spontaneously hypert

185 Cardiac injury was induced in neonatal and adult hearts

186 Cardiac injury was induced in the adult feline heart by

187 e cardiomyocyte proliferative response after cardiac injury was lost in G3 Terc(-/-) newborns but res

188 ad to a possible false-positive diagnosis of cardiac injury when skeletal muscle pathology is present

189 is conserved in the mouse and observed after cardiac injury, where it promotes wound healing and redu

190 3 nm); two greatly reduced ischemia-induced cardiac injury with an IC50 of approximately 200 nm and

191 We investigated the role of CTRP9 in cardiac injury with loss-of-function genetic manipulatio

192 neumoniae invades the myocardium and induces cardiac injury with necroptosis and apoptosis, followed

193 of immune cell localization following acute cardiac injury, with deficient leukocyte infiltration in