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1                                              VILI indices were calculated for each recorded PCV datap
2                                              VILI progresses topographically outward from these regio
3                                 In Series 2, VILI progressed linearly with increasing DP and decreasi
4 d CO could serve to protect the lung against VILI.
5 t hypercapnic acidosis is protective against VILI in this model.
6 an increase in lung D2 is protective against VILI.
7 ce tension will increase and atelectasis and VILI will occur.
8 esulting from CVtV result in atelectasis and VILI.
9 ariations in VILI severity were dampened and VILI-induced mortality at CT0 was reduced compared with
10 mAb 2 h after initiation of septic shock and VILI (12 h).
11 rity of lung injury in each rat/porcine ARDS/VILI model (~ 50% reduction) including reduction in seru
12                        Each rat/porcine ARDS/VILI model was strongly associated with evidence of seve
13  exchange, while an A2BAR agonist attenuated VILI.
14 A2BARs located on the lung tissue attenuated VILI-induced albumin leakage and pulmonary edema.
15 al a role for A2BAR signaling in attenuating VILI and implicate this receptor as a potential therapeu
16  the literature documenting that CVtV causes VILI and reviews the mechanisms by which it occurs.
17  mechanism(s) that recruit leukocytes during VILI have not been elucidated.
18 a suggest that NETs form in the lungs during VILI, contribute to the disease process, and thus may be
19  increase in extravascular lung water during VILI development contributed to the observed decrease in
20 elevation of pulmonary cAMP levels following VILI, suggesting that A2BAR agonist treatment protects b
21 l power alone is insufficient to account for VILI.
22    Expression profiling of lung tissues from VILI-challenged GADD45a(-/-) mice revealed strong dysreg
23  and whether the stress index could identify VILI better than compliance.
24 pliance and alveolar protein accumulation in VILI.
25 nhaled CO exerts antiinflammatory effects in VILI via the p38 mitogen-activated protein kinase pathwa
26 ic function of heme oxygenase-1 induction in VILI, we determined whether low concentration of inhaled
27 LysM(Bmal1-/-) mice, circadian variations in VILI severity were dampened and VILI-induced mortality a
28 V) may overdistend lung regions and initiate VILI compared to physiologically-analogous negative pres
29 unintended ventilator induced lung injuries (VILI).
30 nitiation of ventilator-induced lung injury (VILI) (4 h).
31 ociated with ventilator-induced lung injury (VILI) are unexplored.
32 ine model of ventilator-induced lung injury (VILI) correlated with injury and was reduced in hypercap
33 o understand ventilator-induced lung injury (VILI) during positive pressure ventilation, mechanisms o
34  to minimize ventilator-induced lung injury (VILI) for any given lung remains controversial and poorl
35 olism during ventilator-induced lung injury (VILI) in mice.
36 ects against ventilator-induced lung injury (VILI) in vivo, we subjected 12 anesthetized, paralyzed r
37              Ventilator-induced lung injury (VILI) is a major cause of morbidity and mortality in int
38              Ventilator-induced lung injury (VILI) is a major complication of mechanical ventilation.
39              Ventilator-induced lung injury (VILI) is a major complication of mechanical ventilation;
40              Ventilator-induced lung injury (VILI) is characterized by inflammation.
41              Ventilator-induced lung injury (VILI) is currently ascribed to volutrauma and/or atelect
42 The onset of ventilator-induced lung injury (VILI) is linked to a number of possible mechanisms.
43 r, MV causes ventilator-induced lung injury (VILI), a condition characterized by increased permeabili
44 use model of ventilator-induced lung injury (VILI), NETs were found in the lung microvasculature, and
45  can lead to ventilator-induced lung injury (VILI), which contributes to a 30 to 40% mortality rate.
46 d to prevent ventilator-induced lung injury (VILI).
47 velopment of ventilator-induced lung injury (VILI).
48 ity known as ventilator-induced lung injury (VILI).
49 ventilator-induced inflammatory lung injury (VILI).
50 nt models of ventilator-induced lung injury (VILI).
51 mation after ventilator-induced lung injury (VILI).
52 to influence ventilator-induced lung injury (VILI).
53 F attenuated ventilator-induced lung injury (VILI).
54 n also cause ventilator-induced lung injury (VILI).
55 nderstanding ventilator-induced lung injury (VILI).
56 ut may evoke ventilator-induced lung injury (VILI).
57  cervix after application of Lugol's iodine (VILI), 46.3% (95% CI, 34.0%-58.5%) of respondents report
58 ) or visual inspection using Lugol's iodine (VILI), high-risk human papillomavirus DNA test (Hybrid C
59 hat inhaled CO might be useful in minimizing VILI.
60 RD events may thus be crucial for mitigating VILI.
61 study, to ameliorate lung damage in a murine VILI model.
62 circadian clock modulates severity of murine VILI via the core clock component BMAL1 (basic helix-loo
63 +RR constant, result in different degrees of VILI in healthy (Series 1) and hydrochloric acid-injured
64 al energy dissipation as key determinants of VILI progression.
65 of energy dissipation as key determinants of VILI.
66 epithelial deformation in the development of VILI, we have developed an in vitro system in which chan
67  hypothesis for encapsulating the drivers of VILI may be for clinical applications, we acknowledge th
68                   There are various forms of VILI, including volutrauma (i.e., injury caused by overd
69              Here we present a hypothesis of VILI pathogenesis that potentially serves as a basis upo
70 context are in accord with the importance of VILI, and appear to show age-related susceptibility to V
71  to be a major component in the mechanism of VILI.
72 altered alveolar mechanics as a mechanism of VILI.
73  ADAM17 is an important proximal mediator of VILI; its inhibition is one mechanism of hypercapnic pro
74 G attenuates injury in this ex vivo model of VILI via mechanisms that prevent increases in permeabili
75 on was obtained in a two-hit murine model of VILI where pharmacological inhibition of ADAM17 reduced
76 ygenase-1 mRNA and protein in a rat model of VILI.
77 c microvascular leak of the present model of VILI.
78 investigated their role in a murine model of VILI.
79 n myeloid cells is an important modulator of VILI.
80 h CXCR2 are important in the pathogeneses of VILI.
81  has been proposed to assess the presence of VILI.
82              Understanding the principles of VILI energetics may provide valuable insights and guidan
83                             The relevance of VILI in the pediatric intensive care unit population is
84 l Care Perspective analyzes the relevance of VILI to the pediatric population, and addresses why pedi
85  - has been proposed to estimate the risk of VILI.
86 se settings to identify the lowest values of VILI indices that could be achieved in both modes while
87 yses to local mechanics to discern potential VILI mechanisms interdependent on both ventilation mode
88 ssed as 4DP+RR, has been proposed to predict VILI risk.
89 esis is based on evidence demonstrating that VILI begins in isolated lung regions manifesting a Perme
90                         We hypothesized that VILI would cause systemic microvascular leak that is dep
91 n the tissue-protective effects of CO in the VILI model.
92 nts might be less susceptible than adults to VILI.
93 were found in hypothyroid WT mice exposed to VILI compared with euthyroid mice, indicating that the l
94                              Mice exposed to VILI recapitulated the serum TH findings of acute illnes
95 proposed ventilator settings expose lungs to VILI during EVLP and whether the stress index could iden
96 rently proposed for EVLP may expose lungs to VILI.
97 res in pathological lungs expose pathways to VILI in PPV versus NPV, and insights can be used to info
98 n to directly evaluate their relationship to VILI.
99            Here, we profiled the response to VILI in mice with genetic deletions of each of the 4 ade
100 ne and cytokine profiles seen in response to VILI, demonstrating a role for T(3) in the treatment of
101 role of caveolin-1 in lung susceptibility to VILI in mice.
102 2KO mice exhibited greater susceptibility to VILI than WT mice, as evidenced by poorer alveoli integr
103 appear to show age-related susceptibility to VILI, although a conclusive link between use of large Vt
104 Caveolin-1 null mice are more susceptible to VILI.
105  ECHO attendees compared with newcomers (VIA/VILI: 63.2% [95% CI, 47.4%-78.9%] vs 33.3% [95% CI, 16.0
106 re sensitive for CIN2+/CIN3+ compared to VIA/VILI (relative sensitivity for CIN2+ = 1.72, 95% CI 1.28
107        Triage of HC2-positive women with VIA/VILI reduced the number of colposcopy referrals, but wit
108  profoundly susceptible to high tidal volume VILI, with increases in microvascular permeability and b
109  the morbidity and mortality associated with VILI.

 
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