In vivo
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Panton-Valentine leukocidin (PVL) is a cytotoxin that causes leukocyte destruction and lung necrosis. Managing respiratory failure and acute respiratory distress syndrome secondary to PVL-expressing Staphylococcus aureus pneumonia and its associated lung necrosis with mechanical ventilation is challenging. We report a patient with life-threatening PVL-expressing S. aureus-associated pneumonia who was rescued using extracorporeal membrane oxygenation (ECMO). ⋯ This case demonstrates that early induction of ECMO support can be a reasonable therapeutic option for PVL-S. aureus-associated pneumonia. This patient's successful outcome might be attributable to early establishment of ECMO to prevent ventilation-induced lung injury.
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The aim of this comparative study was to assess the impact of two different settings of tidal volume (Vt) on the function and morphology of the mechanically ventilated lungs during a 12-h period. ⋯ Mechanical ventilation with a Vt of 6 ml/kg induces minimal histological lung parenchymal changes in terms of proliferation and apoptosis. Positive pressure mechanical ventilation with Vt of 10 ml/kg does not protect lung tissue and induces substantial proliferative and apoptotic changes within the lung parenchyma. Positive pressure mechanical ventilation with Vt of 10 ml/kg does not guarantee protection of healthy pulmonary tissue in the absence of a priming pulmonary insult.
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Genetic polymorphism is a strong risk factor for coronary artery disease (CAD). In the present study, our aim was to evaluate angiotensin-converting enzyme (ACE) gene I/D polymorphism and interleukin-4 (IL-4) gene Intron 3 variable number of tandem repeat (VNTR) polymorphism in CAD. ⋯ Although, there is no correlation between IL4 VNTR polymorphism and ACE gene polymorphism and CAD, there is a strong association between CAD and co-existence of IL-4 VNTR and ACE gene polymorphisms in the Turkish population.