ライフサイエンスコーパス: alveolar fluid

1 ired for active near-isosmolar absorption of alveolar fluid.

2 in the recognition of Aspergillus conidia in alveolar fluid.

3 roteoglycan, and KC, a CXC chemokine, in the alveolar fluid.

4 Active, near-isosmolar alveolar fluid absorption (Jv) was measured in in situ p

5 Active alveolar fluid absorption was measured in an in situ lun

6 Inhibition of ENaC by amiloride reproduced alveolar fluid and Cl(-) secretion that were again CFTR-

7 tibodies, we found H3.3 in the airway lumen, alveolar fluid, and plasma of COPD samples.

8 ected in resident macrophages and monocytes, alveolar fluid, and the endothelium of blood vessels in

9 may contribute significantly in maintaining alveolar fluid balance and in resolving airspace edema.

10 plays a critical role in the maintenance of alveolar fluid balance.

11 ant ion channels that maintain bronchial and alveolar fluid balance: the cystic fibrosis transmembran

12 energic agonists accelerate the clearance of alveolar fluid by increasing the expression and activity

13 tant, or hyaluronan, normally present in the alveolar fluids, can enhance adsorption in the presence

14 Of the patients, 56% had impaired alveolar fluid clearance (< 3%/h), 32% had submaximal cl

15 mild pulmonary oedema (24/29 [83%]), intact alveolar fluid clearance (17/23 [74%]), and normal or mi

16 ith serial samples, there was a high rate of alveolar fluid clearance (19 +/- 9%/h, mean +/- SD).

17 lar epithelial dysfunction, as determined by alveolar fluid clearance (AFC) and intra-alveolar levels

18 Furthermore, measurement of alveolar fluid clearance (AFC) demonstrated that A2BAR s

19 h acute lung injury (ALI) who retain maximal alveolar fluid clearance (AFC) have better clinical outc

20 Moreover, induced Na,K-ATPase improved alveolar fluid clearance (AFC) in IAV-infected mice.

21 of the NO donor, DETANONOate, would decrease alveolar fluid clearance (AFC) in the rabbit in vivo.

22 nfected with M. pulmonis for measurements of alveolar fluid clearance (AFC) in vivo and isolation of

23 reactive byproducts inhibit Na(+)-dependent alveolar fluid clearance (AFC) in vivo and the activity

24 Alveolar fluid clearance (AFC) is necessary for the reso

25 Whether these receptors are essential for alveolar fluid clearance (AFC) or if other mechanisms ar

26 Alveolar fluid clearance (AFC), an index of active Na(+)

27 Alveolar fluid clearance (AFC), an index of alveolar act

28 A(2a)R- or A(3)R-specific agonists increased alveolar fluid clearance (AFC), whereas physiologic conc

29 g the inhibition of the c-AMP stimulation of alveolar fluid clearance (ALC) in rats.

30 3) and in patients with an absence of intact alveolar fluid clearance (p =.03).

31 ing demonstrated a positive correlation with alveolar fluid clearance (Spearman rank correlation [r(s

32 aspiration-induced lung injury by increasing alveolar fluid clearance and decreasing endothelial perm

33 hese data suggest that claudin-4 may promote alveolar fluid clearance and demonstrate that the amount

34 subunit plasmid showed a twofold increase in alveolar fluid clearance and Na(+),K(+)-ATPase activity

35 ce to lung injury, db/db mice had diminished alveolar fluid clearance and reduced Na,K-ATPase functio

36 In isolated perfused lungs, alveolar fluid clearance and secretion were determined b

37 panied by a 2.4-fold increase in the rate of alveolar fluid clearance at 4 hrs in the salmeterol-trea

38 Recently, we showed that impairment of alveolar fluid clearance because of inhibition of epithe

39 with control, LTD4 (1 x 10(-11) M) increased alveolar fluid clearance by 41% (p < 0.001) in isolated,

40 in BALB/c mice increased amiloride-sensitive alveolar fluid clearance by approximately 30%, consisten

41 ung and restored the normal up-regulation of alveolar fluid clearance by catecholamines after prolong

42 e lung prevented the normal up-regulation of alveolar fluid clearance by catecholamines following hem

43 Alveolar fluid clearance contributes to graft function a

44 Intact alveolar fluid clearance correlated with less histologic

45 Because a decrease in net alveolar fluid clearance could be due to lung endothelia

46 Alveolar fluid clearance driven by active epithelial Na(

47 The two patients with no net alveolar fluid clearance had persistent hypoxemia and mo

48 Patients with maximal alveolar fluid clearance had significantly lower mortali

49 edema and acute lung injury, we measured net alveolar fluid clearance in 79 patients with acute lung

50 ring the beta- adrenergic agonist-stimulated alveolar fluid clearance in acute lung injury, an effect

51 The unimpaired alveolar fluid clearance in AQP5-null mice indicates tha

52 nfection has been shown to reduce Na+-driven alveolar fluid clearance in BALB/c mice in vivo.

53 g injury and the loss of claudin-4 decreases alveolar fluid clearance in mice.

54 in contrast to hydrostatic pulmonary edema, alveolar fluid clearance in patients with acute lung inj

55 K-ATPase in alveolar epithelial cells and on alveolar fluid clearance in rat lungs.

56 The high rates of alveolar fluid clearance indicate that the fluid transpo

57 red in the majority of patients, and maximal alveolar fluid clearance is associated with better clini

58 Airway and alveolar fluid clearance is mainly governed by vectorial

59 However, impaired alveolar fluid clearance is present in most of the patie

60 Measurement of alveolar fluid clearance may be useful to assess the sev

61 ins (including ZO-1) was not associated with alveolar fluid clearance or claudin-4 levels.

62 nction protein claudin-4 are associated with alveolar fluid clearance or clinical measures of lung fu

63 Maximal cAMP-dependent alveolar fluid clearance rate was 32.9 +/- 10.9 %/hr (p

64 Alveolar fluid clearance rates were measured in ex vivo

65 ts with acute lung injury (ALI) have reduced alveolar fluid clearance that has been associated with h

66 , and isoproterenol 10(-6) M each stimulated alveolar fluid clearance to a level comparable to maxima

67 -grade human mesenchymal stem cells restored alveolar fluid clearance to a normal level, decreased in

68 across the alveolar epithelium and restored alveolar fluid clearance to normal.

69 th hydrostatic pulmonary edema, in whom mean alveolar fluid clearance was 13%/h; only 25% had impaire

70 Mean alveolar fluid clearance was 6%/h.

71 Basal alveolar fluid clearance was 7.6 +/- 2.2 %/hr.

72 Net alveolar fluid clearance was calculated from sequential

73 Alveolar fluid clearance was calculated from serial samp

74 Compared with basal rates, alveolar fluid clearance was increased by both racemic a

75 Alveolar fluid clearance was measured by change in conce

76 Alveolar fluid clearance was measured in anesthetized, v

77 Alveolar fluid clearance was measured in living ventilat

78 Alveolar fluid clearance was measured in vivo.

79 r without electroporation, and 3 days later, alveolar fluid clearance was measured.

80 Alveolar fluid clearance was preserved in SP-C-GM mice i

81 Acute lung injury with maximal alveolar fluid clearance were more likely to be female (

82 nce, fibrinogenesis, inflammatory cytokines, alveolar fluid clearance, and endothelial injury and act

83 human lungs, mesenchymal stem cells restored alveolar fluid clearance, reduced inflammation, and exer

84 Concomitantly, we observed a reversal of alveolar fluid clearance, suggesting that reversed trans

85 eduction of Na,K-ATPase expression decreases alveolar fluid clearance, which in turn leads to pulmona

86 by reducing lung inflammation and enhancing alveolar fluid clearance.

87 nary edema by up-regulating sodium-dependent alveolar fluid clearance.

88 genous catecholamines did not correlate with alveolar fluid clearance.

89 in and an approximately 50% reduction in net alveolar fluid clearance.

90 id instillation led to a 50% decrease in net alveolar fluid clearance.

91 ANTU-induced edema formation by potentiating alveolar fluid clearance.

92 eolar epithelial fluid transport measured as alveolar fluid clearance.

93 ndothelial barrier permeability and restored alveolar fluid clearance.

94 mechanisms may contribute to the decrease in alveolar fluid clearance.

95 bited both basal and beta agonist-stimulated alveolar fluid clearance.

96 is, neutrophil activation and clearance, and alveolar fluid clearance.

97 elial permeability to protein, and decreased alveolar fluid clearance.

98 ed elevated lung inflammation and attenuated alveolar fluid clearance.

99 a level comparable to maximal cAMP-dependent alveolar fluid clearance.

100 samples were associated with slower rates of alveolar fluid clearance.

101 istent with permeability edema and increased alveolar fluid export.

102 high concentrations of IL-8 were present in alveolar fluids from patients with ARDS and were associa

103 ive ion transport that is needed to maintain alveolar fluid homeostasis during pulmonary edema.

104 gamma-aminobutyric acid receptors involving alveolar fluid homeostasis in adult lungs.

105 hat betaAR signaling may not be required for alveolar fluid homeostasis in uninjured lungs.

106 Alveolar fluid homeostasis is regulated by Na+/K+-ATPase

107 fluid from the fetal lung and in reabsorbing alveolar fluid in the injured adult lung.

108 Light microscopy showed gross alveolar fluid in three apneic dogs, and electron micros

109 ute respiratory distress syndrome (ALI/ARDS) alveolar fluid induces KGF and fibroblast genes importan

110 The deficiency of total GSH in the alveolar fluid may predispose lung allografts to extrace

111 Production of TNF-alpha in lung alveolar fluids of mice infected with B. dermatitidis wa

112 tion of either hyaluronan (normally found in alveolar fluid) or polyethylene glycol to subphases cont

113 ht heart catheterization and the sampling of alveolar fluid protein are sometimes necessary.

114 med with wet/dry lung weight ratios, and the alveolar fluid protein concentration was measured after

115 for up to 24 h and then measured changes in alveolar fluid reabsorption (AFR) and Na,K-ATPase functi

116 nce of poor alveolar ventilation and impairs alveolar fluid reabsorption (AFR) by promoting Na,K-ATPa

117 We found that alveolar fluid reabsorption after 1 hour was impaired by

118 Hypoxia inhibits alveolar fluid reabsorption and decreases Na,K-ATPase ac

119 c alpha(1) agonist, phenylephrine, increased alveolar fluid reabsorption by 54 and 40%, respectively,

120 ion in rat lungs prevented the impairment of alveolar fluid reabsorption caused by hypoxia.

121 gest that beta-adrenergic agonists increased alveolar fluid reabsorption in rats ventilated with HVT

122 losis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolated and continuo

123 Alveolar fluid reabsorption increased approximately twof

124 We report here that NE increased alveolar fluid reabsorption via the activation of both a

125 The hypocapnia-mediated decrease of alveolar fluid reabsorption was associated with decrease

126 The effect of low PCO2 on alveolar fluid reabsorption was reversible because clear

127 veolar epithelial Na,K-ATPase and increasing alveolar fluid reabsorption, cysteinyl leukotrienes may,

128 -adrenergic receptor agonists have a role in alveolar fluid reabsorption, via Na,K-ATPase, in the alv

129 pocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption.

130 bitor, prevented the NE-mediated increase in alveolar fluid reabsorption.

131 s that reduce alveolar inflammation, enhance alveolar fluid removal, and reduce pulmonary fibrosis wi

132 fluid and showed that PRELP can be found in alveolar fluid, resident macrophages/monocytes, myofibro

133 The mechanisms of alveolar fluid resorption are different from those of al

134 Alveolar fluid resorption into the vessels is brought ab

135 ort across the alveolar epithelium, and thus alveolar fluid resorption, is regulated by apical Na+ ch

136 and the Na,K-ATPase giving rise to increased alveolar fluid resorption.

137 drostatic pressure induced ouabain-sensitive alveolar fluid secretion that coincided with transepithe

138 (+)-K(+)-Cl(-) cotransporters (NKCC) blocked alveolar fluid secretion, and lungs of CFTR(-/-) mice we

139 ort may promote lung edema by driving active alveolar fluid secretion.

140 ALI/ARDS alveolar fluid suppresses KGF expression, in part, due t

141 otein concentration and neutrophil counts in alveolar fluid through bronchoalveolar lavage, reduced e