Post B37Ri0bTtWREwrGDse by AlainPetit77@gigaohm.bio
 (DIR) More posts by AlainPetit77@gigaohm.bio
 (DIR) Post #B37Ri0bTtWREwrGDse by AlainPetit77@gigaohm.bio
       2026-02-08T15:01:54.738971Z
       
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       Detecting Pulmonary Oxygen Toxicity Using eNose Technology and Associations between Electronic Nose and Gas Chromatography–Mass Spectrometry DataAbstract: Exposure to oxygen under increased atmospheric pressures can induce pulmonaryoxygen toxicity (POT). Exhaled breath analysis using gas chromatography–mass spectrometry (GC–MS) has revealed that volatile organic compounds (VOCs) are associated with inflammation and lipoperoxidation after hyperbaric–hyperoxic exposure. Electronic nose (eNose) technology would be more suited for the detection of POT, since it is less time and resource consuming. However, it is unknown whether eNose technology can detect POT and whether eNose sensor data can be associated with VOCs of interest. In this randomized cross-over trial, the exhaled breath from divers who had made two dives of 1 h to 192.5 kPa (a depth of 9 m) with either 100% oxygen or compressed air was analyzed, at several time points, using GC–MS and eNose. We used a partial least square discriminant analysis, eNose discriminated oxygen and air dives at 30 min post dive with an area under the receiver operating characteristics curve of 79.9% (95%CI: 61.1–98.6; p = 0.003). A two-way orthogonal partial least square regression (O2PLS) model analysis revealed an R2 of 0.50 between targeted VOCs obtained by GC–MS and eNose sensor data. The contribution of each sensor to the detection of targeted VOCs was also assessed using O2PLS. When all GC–MS fragments were included in the O2PLS model, this resulted in an R2 of 0.08. Thus, eNose could detect POT 30 min post dive, and the correlation between targeted VOCs and eNose data could be assessed using O2PLS.
       
 (DIR) Post #B37Ri67DOxnG2j98XQ by AlainPetit77@gigaohm.bio
       2026-02-08T15:12:02.001718Z
       
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       Mechanistic role of cytochrome P450 (CYP)1B1 in oxygen-mediated toxicity in pulmonary cells: a novel target for prevention of hyperoxic lung injuryABSTRACTSupplemental oxygen, which is routinely administered to preterm infants with pulmonaryinsufficiency, contributes to bronchopulmonary dysplasia (BPD) in these infants. Hyperoxia alsocontributes to the development of acute lung injury (ALI) and acute respiratory distresssyndrome (ARDS) in adults. The mechanisms of oxygen-mediated pulmonary toxicity are notcompletely understood. Recent studies have suggested an important role for cytochrome P450(CYP)1A1/1A2 in the protection against hyperoxic lung injury. The role of CYP1B1 in oxygen-mediated pulmonary toxicity has not been studied. In this investigation, we tested thehypothesis that CYP1B1 plays a mechanistic role in oxygen toxicity in pulmonary cells in vitro.In human bronchial epithelial cell line BEAS-2B, hyperoxic treatment for 1-3 days led todecreased cell viability by about 50-80%. Hyperoxic cytotoxicity was accompanied by anincrease in levels of reactive oxygen species (ROS) by up to 110%, and an increase of TUNEL-positive cells by up to 4.8-fold. Western blot analysis showed hyperoxia to significantly down-regulated CYP1B1 protein level. Also, there was a decrease of CYP1B1 mRNA by up to 38%and Cyp1b1 promoter activity by up to 65%. On the other hand, CYP1B1 siRNA appeared torescue the cell viability under hyperoxia stress, and overexpression of CYP1B1 significantlyattenuated hyperoxic cytotoxicity after 48 h of incubation. In immortalized lung endothelial cellsderived from Cyp1b1-null and wild-type mice, hyperoxia increased caspase 3/7 activities in atime-dependent manner, but endothelial cells lacking the Cyp1b1 gene showed significantlydecreased caspase 3/7 activities after 48 and 72 h of incubation, implying that CYP1B1 mightpromote apoptosis in wild type lung endothelial cells under hyperoxic stress. In conclusion, ourresults support the hypothesis that CYP1B1 plays a mechanistic role in pulmonary oxygentoxicity, and CYP1B1-mediated apoptosis could be one of the mechanisms of oxygen toxicity.Thus, CYP1B1 could be a novel target for preventative and/or therapeutic interventions againstBPD in infants and ALI/ARDS in adults.2
       
 (DIR) Post #B37RiBqm50CvpTV5kG by AlainPetit77@gigaohm.bio
       2026-02-08T15:58:17.710527Z
       
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       A SIMPLE CLINICAL PREDICTIVEINDEX FOR OBJECTIVE ESTIMATES OFMORTALITY IN ACUTE LUNG INJURY(ALI)Jason D. Christie