ライフサイエンスコーパス: Vt.

1 Vt, peak airway pressure, positive end-expiratory pressu

2 nt and nondependent lung regions (Vt%dep and Vt%(nondep)), regional tidal volumes (Vt(dep) and Vt(non

3 oxygenation, end-expiratory lung volume, and Vt, without affecting DeltaP(L).

4 PV was defined as Vt <=8 ml/kg predicted body weight and positive end-expi

5 There was a linear relationship between Vt, driving pressure, transpulmonary pressure, and the i

6 etermined by driving pressure rather than by Vt, then the effect of ventilation with lower Vt on mort

7 ncrease in EELI of >10% of the corresponding Vt (46.2%; IQR, 23.9-60.9%).

8 ystic Vt (P = 0.015) but not total lung cyst Vt (P = 0.8).

9 here was variability between individual cyst Vt, with 22% of cysts demonstrating negative Vt.

10 Trans-epithelial potential difference (Vt) measurements are routinely carried out on nasal epit

11 nity for Vh and in their ability to displace Vt, suggesting that the strengths of these interactions

12 d either with only its vinculin tail domain (Vt), with all residues in its closed conformation, with

13 to interactions between the Vcn tail domain (Vt) and filamentous (F)-actin.

14 sphosphate (PIP(2)) through its tail domain (Vt) to drive recruitment, activation, and focal adhesion

15 ) and to actin filaments at its tail domain (Vt).

16 erentiates it from the vinculin tail domain (Vt).

17 Its tail domain, Vt, is crucial for vinculin activation and focal adhesio

18 ranspulmonary pressure (DeltaPl), expiratory Vt, and respiratory rate were recorded on admission and

19 redictor (frequency-tidal volume ratio, or f/Vt) in a weaning protocol.

20 Including a weaning predictor (f/Vt) in a protocol prolonged weaning time.

21 results from movement of domain 1 away from Vt; the open II conformation results from complete disso

22 w Vt; RR, 0.66; [95% CI, 0.49-0.88] vs. high Vt) but was rated with lower certainty because VV ECMO w

23 ives: To compare the effects of low Vt, high Vt, high positive end-expiratory pressure (PEEP), prone

24 ainty; RR, 0.77 [95% CI, 0.65-0.91] vs. high Vt; moderate certainty).

25 TB between 1 and 4 years of age had impaired Vt (-9.32 ml [95% CI, -14.89 to -3.75 ml]) and time to p

26 At 60 W, a 50% smaller increase in Vt (P < 0.001) in response to added DS in COPD compared

27 [CI], 1.13-2.28 per 1-ml/kg PBW decrease in Vt; P = 0.008).

28 d maximal effort during deflation) increased Vt (51 [38-64] ml), increased inspiratory and mean-expir

29 with delayed expiratory relaxation increased Vts (128 [86-170] ml) and increased inspiratory and mean

30 g with early expiratory relaxation increased Vts (88 [64-113] ml) and inspiratory transpulmonary pres

31 ive end-expiratory pressure [PEEP] 0) or low Vt (6 ml/kg; PEEP 3 cm H(2)O; 3 h) in supine or prone po

32 ted with very high (24 ml/kg; PEEP 0) or low Vt (6-7 ml/kg; PEEP 3 cm H(2)O).

33 thing, cardiac arrhythmias) or doubtful (low Vt).

34 Objectives: To compare the effects of low Vt, high Vt, high positive end-expiratory pressure (PEEP

35 lung currently revolve around the use of low Vt, ostensibly to avoid volutrauma, together with positi

36 confidence interval (CI), 0.60-0.92] vs. low Vt; high certainty).

37 iately (RR, 0.91 [95% CI, 0.81-1.03] vs. low Vt; low certainty; RR, 0.77 [95% CI, 0.65-0.91] vs. high

38 worst (RR, 1.19 [95% CI, 1.02-1.37] vs. low Vt; moderate certainty), and we found no support for hig

39 e best (RR, 0.78 [95% CI, 0.58-1.05] vs. low Vt; RR, 0.66; [95% CI, 0.49-0.88] vs. high Vt) but was r

40 as the training data set (ARMA [High vs. Low Vt], ALVEOLI [Assessment of Low Vt and Elevated End-Expi

41 n group with RT received significantly lower Vt (7 vs. 10 ml/kg) and higher RR (45 vs. 31 breaths/min

42 Lower Vt, lower driving pressure ( P), lower respiratory rates

43 cal trial demonstrating the benefit of lower Vts, the use of Vts of 6 ml/kg predicted body weight (ba

44 essure positively correlated with total lung Vt (P = 0.027) and noncystic Vt (P = 0.015) but not tota

45 Ventilator pressure increases noncystic lung Vt, but inspiratory time does not correlate with Vt of n

46 Increased bone marrow Vt, on the other hand, suggests hematopoietic activation

47 ships between ionic permeabilities and nasal Vt, giving insights into the physiology of CF disease th

48 with total lung Vt (P = 0.027) and noncystic Vt (P = 0.015) but not total lung cyst Vt (P = 0.8).

49 = 5) or 7 d (n = 3) after injury normalized Vt, f, and the respiratory response to 7% CO2.

50 end-expiratory pressure [PEEP], 5 cm H(2)O; Vt, 10 ml/kg; respiratory rate, 20 bpm), 2) conventional

51 conventional-protective (PEEP, 10 cm H(2)O; Vt, 6 ml/kg; respiratory rate, 20 bpm), and 3) near-apne

52 itration resulted in significant declines of Vt (mean +/- SEM, 9.3 +/- 0.6 to 5.6 +/- 0.2 ml/kg; P <

53 15 patients had pendelluft involving >10% of Vt; pendelluft was mitigated by CPAP and further by NIV.

54 primary ventilator variables such as the P, Vt, and RR.Methods: We obtained data on ventilatory vari

55 es Vt and also increases amiloride-sensitive Vt, these effects are too small to account for the magni

56 rent best practice involves the use of small Vt, low plateau and driving pressures, and high levels o

57 ; n = 8) or a more lung-protective strategy (Vt: 6-8 ml/kg; n = 24) with adjustments in RR to facilit

58 interactions between its head (Vh) and tail (Vt) domains.

59 ms of the interaction between vinculin tail (Vt) and residues 1-258 (D1), we find an absolute require

60 nd pseudo-atomic model of the vinculin tail (Vt) domain bound to F-actin.

61 h domain, which displaces the vinculin tail (Vt) domain.

62 function of the duration of ventilation, the Vt, the level of positive end-expiratory pressure (PEEP)

63 MVt binds to F-actin in a similar manner to Vt, MVt is incapable of F-actin bundling and inhibits Vt

64 uation for Vd/Vt using the clinical data: Vd/Vt = 0.32 + 0.0106 (Paco2 - ETCO2) + 0.003 (RR) + 0.0015

65 score, dead space-tidal volume fraction (Vd/Vt), and EVLWp were all significantly higher on day 1 in

66 xt]co2, dead space to tidal volume ratio (Vd/Vt), and arterial to end-tidal CO2 difference were all h

67 Pulmonary dead space fraction (Vd/Vt) is an independent predictor of mortality in acute re

68 imary end point was pulmonary dead space (Vd/Vt) at 6 hours after esophagectomy or before extubation.

69 e, 13 +/- 3.4 vs. 7.7 +/- 0.8; p = .006) (Vd/Vt, 0.68 +/- 0.07 vs. 0.58 +/- 0.07; p = .009) (EVLWp, 2

70 stic curve analysis indicated that EVLWp, Vd/Vt, and extravascular lung water (p = .0005, .009, and .

71 lure Assessment score, lung injury score, Vd/Vt, and PaO2/FIO2.

72 d to receive passive mechanical ventilation (Vt: 10 ml/kg; respiratory rate [RR]: 30-35 breaths/min;

73 The tail domain of vinculin (Vt) binds to acidic phospholipids and has been proposed

74 The tail domain of vinculin (Vt) contains a salt-insensitive binding site for acidic

75 The tail domain of vinculin (Vt) contains determinants necessary for binding and bund

76 The tail domain of vinculin (Vt) forms tight autoinhibitory interactions with the hea

77 ease that initiates degradation of vitellin (Vt) in the orthopteran Blattella germanica, and its prop

78 The distribution volume (Vt) for (18)F-UCB-H was calculated with Logan graphic an

79 Tidal Volume (Vt) and end-expiratory lung volume were assessed with el

80 rain mechanics when the global tidal volume (Vt) and inflation pressure was matched.

81 e volume of CO2 rebreathed and tidal volume (Vt).

82 rats (n = 5) showed decreased tidal volume (Vt; 0.90 +/- 0.02-0.66 +/- 0.03 ml; p < 0.05) and increa

83 EBOV inoculation, and distribution volumes (Vt) were calculated as a measure of peripheral TSPO bind

84 Lower tidal volumes (Vts) attenuate extrapulmonary organ injury in other dise

85 nts with PIP(2) membranes in comparison with Vt, we conducted mutagenesis, phospholipid-association a