Project description:Human A549 lung epithelial cells were exposed directly at the air-liquid interphase towards combustion aerosols of wood burning. The goal was to compare the responses towards different wood and burning conditions. Beech log woods were burnt in a modern masonry heater, soft wood pellets were burnt in a pellet boiler.
Project description:Bio-electrospray, the direct jet-based cell handling apporach, is able to handle a wide range of cells. Studies at the genomic, genetic, and the physiological level have shown that, post-treatment, cellular integrity is unperturbed and a high percentage (>70%, compared to control) of cells remain viable. Although, these results are impressive, it may be argued that cell based systems are oversimplistic. This study utilizing a well characterised multicellular model organism, the non-parasitic nematode Caenorhabditis elegans. Nematodes were subjected to bio-electrosprays to demonstrate that bio-electrosprays can be safely applied to nematodes.
Project description:Adipogenesis is one of the most intensively studied models of cellular differentiation, and transcriptional activities involved in the process have been extensively investigated. We analyzed transcripts differentially expressed between hen preadipocytes treated with adipogenic cocktail containing 500 nM dexamethasone, 0.5 mM 3-isobutyl-1-methylxanthine, 20 µg/mL insulin and 300 μM OA (DMIOA) and non-treated control cells and transcripts differentially expressed between preadipocytes treated with DMIOA alone and those treated with a combination of DMIOA and 20(S)-hydroxycholesterol (DMIOA + 20(S)) using Affymetrix GeneChip® Chicken Genome Array containing 28,000 transcripts. Preadipocytes were isolated from hen abdominal tissue, cultured and treated with DMIOA, DMIOA+Retinoic Acid
Project description:Smoking cigarettes is harmful to the cardiovascular system. Considerable attention has been paid to the reduced harm potential of alternative nicotine-containing inhalable products such as e-cigarettes. We investigated the effects of E-vapor aerosols or cigarette smoke (CS) on atherosclerosis progression, cardiovascular function, and molecular changes in the heart and aorta of female ApoE−/− mice. The mice were exposed to aerosols from three different E-vapor formulations: (1) carrier (propylene glycol and vegetable glycerol), (2) base (carrier and nicotine) or (3) test (base and flavor) or to CS from 3R4F reference cigarettes for up to 6 months. Concentrations of CS and base or test aerosols were matched at 35 µg nicotine/L. Exposure to CS, compared with sham-exposed fresh air controls, accelerated atherosclerotic plaque formation, while no such effect was seen for any of the three E-vapor aerosols. Molecular changes indicated disease mechanisms related to oxidative stress and inflammation in general, plus changes in calcium regulation, and altered cytoskeletal organization and microtubule dynamics in the left ventricle. While ejection fraction, fractional shortening, cardiac output, and isovolumic contraction time remained unchanged following E-vapor aerosols exposure, the nicotine-containing base and test aerosols caused an increase in isovolumic relaxation time similar to CS. A nicotine-related increase in pulse wave velocity and arterial stiffness was also observed, but it was significantly lower for base and test aerosols than for CS. These results demonstrate that in comparison with CS, E-vapor aerosols induce substantially lower biological responses associated with smoking-related cardiovascular diseases.