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To induce VILI, mice were ventilated with HVt ventilation of Vt 25 mL/Kg, respiratory rate 50 bpm and PEEP of 2 cmH2O for four hours.
Untreated wild-type mice, IL-1αβ knockout and caspase-1 knockout mice, pralnacasan (a selective caspase-1 inhibitor -treated minhibitor -treatedcyte-derived chemicene (KC)-treated mice and cyclophosphanti-keratinocyte-deriveddepleted wild-type mice were ventilated using clinically relevant ventilator settings (tidal volume 8 ml/KC -treated
After preparation, a recruitment maneuver was performed (increasing of the airway pressure to 30 cmH2O), and mice were ventilated for 4 hours with the following ventilator settings: Mice were ventilated with a tidal volume of 9 ml/kg, respiratory rate of 160 per minute, and I E ratio of either 1 2 or 1 1 (LVT 1 2; LVT 1 1).
In a separate series of experiments, anesthetised and tracheostomised mice were ventilated with a custom-made mouse ventilator (8 9 ml/kg tidal volume, 2.5 cmH2O positive end-expiratory pressure (PEEP), respiratory rate 120), with a carotid arterial line inserted for blood sampling, fluid infusion (0.4 ml/hr saline containing 10 U/ml heparin) and monitoring arterial blood pressure [16].
Adult male wild-type and Tpl2-deficient mice were ventilated with normal or high tidal volume for 4 h.
Healthy wild-type (WT) and RAGE knockout (KO) mice were ventilated with relatively low (approximately 7.5 ml/kg) or high (approximately 15 ml/kg) tidal volume.
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However, we have previously shown that the inflammatory response is aggravated when mice are ventilated with these parameters for a longer period of time or when higher tidal volumes are used, suggesting that the inflammatory response is mainly ventilation-induced.
To assess the physiological relevance of MMP8 in VILI, mmp8 gene deleted mice (mmp8−/−) were ventilated and their lung injury parameters were compared to wild-type mice.
In the first study [ 10], wildtype or c-jun N-terminal kinase (JNK -deficient knockout mice (JNK -deficientventilated with high Vt (30 mL/knockout two different fractions of inspired oxygen: 21% O2 (roomicer) or greater than 95% O2 (hyperoxia).
Healthy C57Bl/6 mice (n = 66) or BALB/c mice (n = 66) were ventilated (tidal volume = 7.5 ml/kg or 15 ml/kg; positive end-expiratory pressure = 2 cmH2O; fraction of inspired oxygen = 0.5) for five hours.
BALB/c mice (n = 84) were ventilated for 5 hours with low (7.5 ml/kg) or high (15 ml/kg) tidal volume, a positive end-expiratory pressure of 2 cmH2O and a fraction of inspired oxygen of 50%.
More suggestions(16)
individuals were ventilated
mice were indicated
mice were classified
mice were allocated
mice were assigned
studies were ventilated
mice were arranged
mice were distributed
mice were disaggregated
mice were differentiated
mice were split
mice were sacrificed
mice were killed
mice were hunted
mice were euthanized
mice were injected
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