ライフサイエンスコーパス: Vt.

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

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

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

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

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

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

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

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

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

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

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

12 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 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

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

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

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

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

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

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

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

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

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

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

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

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