Sentence examples for high oxygen exposure from inspiring English sources

The central link between pulmonary inflammation and distortion of lung development is modulated by amniotic infection and a bundle of well-established clinical therapies including steroid exposure as well as the avoidance of mechanical ventilation and high oxygen exposure [6, 8].

We found that all mTOR downstream targets were activated by acute high oxygen exposure in a time dependent manner.

This suggests that BMP2, analogously to an acute high oxygen exposure, may promote mTOR activation by down-modulating inhibitory REDD1.

Importantly, after high oxygen exposure HIF-1α was down-modulated, but after 120 min it was partially reconstituted in GBM probably by a mTOR dependent mechanism.

These results indicate that activation of Akt/mTOR dependent pro-translational pathways (p70S6K) and gliogenic and pro-survival mechanisms (Stat3) occur in response to acute high oxygen exposure.

In this study we elucidate the molecular mechanisms by which two pro-differentiating stimuli, BMP2 and acute high oxygen exposure, control HIF-1α stability.

We observed the same results when traps were injected at P7 (pre-high oxygen exposure) and analysed at P17 (Supplementary Fig S18B).

Thus, it may be most desirable to decrease FiO2 in patients receiving the highest oxygen exposure.

This study suggests that higher oxygen exposure is not associated with subsequent pulmonary dysfunction after cardiac arrest.

We examined the association between inhaled oxygen exposure and change in pulmonary function after CA. Higher oxygen exposure in the initial 24 h was strongly associated with the presence of baseline cardiopulmonary dysfunction, but was not associated with deterioration in pulmonary compliance or gas exchange in the first 48 h after ROSC.

Importantly, despite observing no association between oxygen exposure and pulmonary dysfunction, we observed significantly worse survival in the quartile of CA patients with the highest oxygen exposure (25% versus 50%, P = 0.003), which remained significant in adjusted analysis and in our propensity-adjusted analysis.