ライフサイエンスコーパス: lung edema

1 or mechanism that prevents the resolution of lung edema.

2 three-fold (p = 0.009), without significant lung edema.

3 , a worse LV remodeling index, and increased lung edema.

4 same large global strain, constantly produce lung edema.

5 s a unique therapeutic target in cardiogenic lung edema.

6 Na(+) channels (ENaCs) promotes cardiogenic lung edema.

7 e are also protected from ventilator-induced lung edema.

8 receptor inhibitor attenuated leptin-induced lung edema.

9 ccumulation, and vascular leakage leading to lung edema.

10 ation of neutrophils to the lungs as well as lung edema.

11 glutathione and increases endotoxin-mediated lung edema.

12 ity index are two promising early markers of lung edema.

13 lial dysfunction, increased lung stress, and lung edema.

14 jury is characterized histopathologically by lung edema and a neutrophil predominate leukocyte extrav

15 ntricular remodeling after I/R, with reduced lung edema and activation of stress/pro fibrotic genes.

16 secretion may constitute a pathomechanism in lung edema and aimed to identify underlying molecular pa

17 In addition, lung edema and cytokine-induced neutrophil chemoattracta

18 TRPV4 channels, which play a central role in lung edema and dysfunction after IR.

19 currently being developed as a treatment for lung edema and has been shown to reduce extravascular lu

20 Hypoxia has been shown to cause lung edema and impair lung edema clearance.

21 channels to pulmonary pathologies, including lung edema and lung injury.

22 CD47(-/-) neutrophils significantly reduced lung edema and neutrophil infiltration, thus demonstrati

23 ficient in Trpv4 (Trpv4(-/-)) developed less lung edema and protein leak than their wild-type litterm

24 ngiotensin-(1-7) blocked the protection from lung edema and protein leak, whereas A779 restored the i

25 gas exchange and lung compliance, prevented lung edema and pulmonary hypertension, and preserved ren

26 h should reflect the underlying lung injury (lung edema and recruitability).

27 occludin, improved viral clearance, reduced lung edema, and augmented survival in infected mice.

28 neutrophil accumulation, the development of lung edema, and increased pulmonary production of IL-1be

29 ar gap formation between lung ECs, sustained lung edema, and multi-organ dysfunction that drives ARDS

30 onclusion Brixia, radiographic assessment of lung edema, and percentage opacification scores all reli

31 ction, decreasing pulmonary permeability and lung edema, and promoting tissue repair.

32 pif(-/-) mice showed greater hypertrophy and lung edema as well as reduced survival in response to su

33 Acute epithelial lung injury, lung edema, bacteremia, and mortality were evaluated qua

34 Lung edema, bronchoalveolar lavage interleukin (IL)-6, a

35 nce (AFC) is necessary for the resolution of lung edema but is impaired in most patients with ARDS.

36 AQP1 facilitates hydrostatically driven lung edema but is not required for active near-isosmolar

37 th by altering vasoreactivity and increasing lung edema, but the acute effects of superoxide dismutas

38 ed transepithelial ion transport may promote lung edema by driving active alveolar fluid secretion.

39 g of gas exchange and histology suggest that lung edema can result from recurrent OAs.

40 s chamber dilation, ventricular dysfunction, lung edema, cardiac fibrosis, and apoptosis.

41 provide a novel treatment option to prevent lung edema caused by S. aureus alpha-toxin.

42 However, the effects of VALI on lung edema clearance and alveolar epithelial cells' Na,K

43 Dopamine (DA) increases lung edema clearance by stimulating vectorial Na+ flux a

44 Active Na+ transport and lung edema clearance decreased by approximately 44% in r

45 Lung edema clearance decreased by up to approximately 60

46 he importance of its role in contributing to lung edema clearance has been demonstrated.

47 However, the effects of this toxin on lung edema clearance have not been previously studied.

48 ine (TERB) and isoproterenol (ISO) increased lung edema clearance in control nonventilated rats (from

49 Lung edema clearance in control rats was 0.50 +/- 0.02 m

50 agonists increase active Na(+) transport and lung edema clearance in normal rat lungs by stimulating

51 to test whether DA (10(-)5 M) would increase lung edema clearance in rats exposed to 100% O2 for 64 h

52 ether beta-adrenergic agonists could restore lung edema clearance in rats ventilated with HVT (40 ml/

53 njury, decreases active sodium transport and lung edema clearance in rats.

54 DA increased lung edema clearance in room air breathing rats (from 0.

55 We studied lung edema clearance in the isolated-perfused rat lung m

56 t air spaces, the active Na(+) transport and lung edema clearance increased by approximately 53% as c

57 st that increased active Na(+) transport and lung edema clearance induced by aldosterone is probably

58 We previously reported that lung edema clearance was stimulated by dopamine (DA).

59 Paralleling the impairment in lung edema clearance we found a decrease in Na,K-ATPase

60 paminergic D(1) agonist fenoldopam increased lung edema clearance, but quinpirole (a specific dopamin

61 as been shown to cause lung edema and impair lung edema clearance.

62 terone may be used as a strategy to increase lung edema clearance.

63 alveolar epithelial cells and thus increases lung edema clearance.

64 n important role in active Na+ transport and lung edema clearance.

65 Lung edema, cytokines, and neutrophil counts were reduce

66 One of the lung edema dogs expired of acute heart failure in the se

67 f the PAR1-specific peptide TFLLRN increases lung edema during high-tidal-volume ventilation, and thi

68 k of ethanol ingestion significantly reduced lung edema during perfusion ex vivo.

69 reshold doses of TNF, which alone induced no lung edema, exacerbated S1P-induced edema and impaired s

70 attenuated cardiac dysfunction, hypertrophy, lung edema, fibrosis, and gene expression changes relati

71 Lung edema formation in this model was the result of mar

72 s in annealing AJs and thereby in preventing lung edema formation induced by endotoxin (LPS).

73 infection caused loss of CFTR that promoted lung edema formation through intracellular chloride ion

74 tion, which was associated with increases in lung edema formation, airway obstruction, and vascular e

75 stischemic lungs during reperfusion, reduces lung edema formation, and improves pulmonary function du

76 Data showed that lung edema formation, lung microvascular permeability, a

77 ion of proinflammatory cytokines and reduced lung edema formation.

78 However, rhAPC failed to prevent lung edema formation.

79 to the disruption of endothelial barrier and lung edema formation; however, the molecular mechanism o

80 Lung edema forms (possibly as an all-or-none response) d

81 Lung edema, hemorrhage, and leukocyte infiltration were

82 n, as reflected by significant reductions in lung edema, hemorrhage, and thrombosis.

83 b (AZD5423) displayed a potent inhibition of lung edema in a rat model of allergic airway inflammatio

84 of cardiopulmonary resuscitation-associated lung edema in animals and in patients with out-of-hospit

85 lung wet by dry ratio indicates there is no lung edema in DeltaECS mice.

86 n-regulation increases survival and prevents lung edema in mice induced by bleomycin exposure-a lung

87 Hydrostatic lung edema in response to acute increases in pulmonary a

88 significantly upregulated and contribute to lung edema in ventilator-induced lung injury.

89 on of tight junctions in the lung and causes lung edema in vivo, which is prevented by genetic defici

90 ling cascade in the induction of PAF-induced lung edema, in that stimulation of ASM causes recruitmen

91 propionate) and prolonged the inhibition of lung edema, indicating potential for once-daily treatmen

92 activation of endothelial TRPV4 channels and lung edema, inflammation, and dysfunction.

93 g endothelial cell cytotoxicity in vitro and lung edema, intra-alveolar hemorrhage, and mortality in

94 by inflammation, vascular permeability, and lung edema, is the major cause of primary graft dysfunct

95 four groups had similar lung weights (i.e., lung edema), lung wet-to-dry ratios, and pathological va

96 MIP-2 in lung lavage, neutrophil influx, and lung edema measured at 48 h.

97 p47(phox-/-) mice, and an isolated perfused lung edema model that all point to a relationship betwee

98 distress syndrome, can be inactivated during lung edema, most likely by serum proteins.

99 sing the modified Radiographic Assessment of Lung Edema (mRALE) score.

100 from acute lung injury as evident by reduced lung edema, myeloperoxidase activity, histological lung

101 Similarly, LPS induced increases in lung edema, myeloperoxidase-concentrations, and pulmonar

102 PS-, acid-, and sepsis-induced ALI abolished lung edema, neutrophil infiltration, and tissue damage,

103 In PI3-Kgamma(-/-) mice, lung edema, neutrophil recruitment, nuclear translocatio

104 p < 0.05 vs. control), but did not decrease lung edema or improve CL.

105 protein concentration, BAL LDH activity, and lung edema (p < 0.05).

106 lung injury, as determined by development of lung edema, pulmonary neutrophil accumulation, histology

107 lung injury, as determined by development of lung edema, pulmonary neutrophil accumulation, lung IL-1

108 lligence (AI) and Radiographic Assessment of Lung Edema (RALE) scores from frontal chest radiographs

109 eporting systems (radiographic assessment of lung edema [RALE], Brixia, and percentage opacification)

110 ion, high-tidal volume ventilation increased lung edema score and caused gas-exchange deterioration.

111 tients that have difficulty breathing due to lung edema, trauma, or general anesthesia.

112 ary gas exchange, whereas the development of lung edema was not affected.

113 e dehydrogenase (LDH) activity and increased lung edema was significantly associated with liver injur

114 activity (evaluated in the Sephadex model of lung edema) with reduced systemic toxicity (evaluated by