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'Pseudomonas aeruginosa' is a Gram-negative bacterium of the proteobacteria class, and one of the most common causes of nosocomial infections. For example, it causes chronic pneumonia in cystic fibrosis patients. Patient sputum contains 2-heptyl-4-hydroxyquinoline N-oxide [HQNO] and 'Pseudomonas' quorum sensing molecules such as the 'Pseudomonas' quinolone signal [PQS]. It is known that HQNO inhibits the enzyme activity of mitochondrial and bacterial complex III at the Qi (quinone reduction) site, but the target of PQS is not known. In this work we have shown that PQS has a negative effect on mitochondrial respiration in HeLa and A549 cells. It specifically inhibits the complex I of the respiratory chain. In vitro analyses showed a partially competitive inhibition with respect to ubiquinone at the IQ site. In competing studies with Rotenone, PQS suppressed the ROS-promoting effect of Rotenone, which is typical for a B-type inhibitor. Prolonged incubation with PQS also had an effect on the activity of complex III., Finanziert über die DEAL-Vereinbarung mit Wiley 2019-2022.

Lima1 is an extensively studied prognostic marker of malignancy and is also considered to be a tumour suppressor, but its role in a developmental context of non-transformed cells is poorly understood. Here, we characterise the expression pattern and examined the function of Lima1 in mouse embryos and pluripotent stem cell lines. We identify that Lima1 expression is controlled by the naïve pluripotency circuit and is required for the suppression of membrane blebbing, as well as for proper mitochondrial energetics in embryonic stem cells. Moreover, forcing Lima1 expression enables primed mouse and human pluripotent stem cells to be incorporated into murine pre-implantation embryos. Thus, Lima1 is a key effector molecule that mediates the pluripotency control of membrane dynamics and cellular metabolism., How pluripotency transcription factors regulate the cellular architecture and energetics has remained largely unknown. Here the authors identify Lima1 as a key effector that mediates the pluripotency control of membrane dynamics and cellular metabolism.

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A new mitochondria-targeted probe MitoCLox was designed as a starting compound for a series of probes sensitive to cardiolipin (CL) peroxidation. Fluorescence microscopy reported selective accumulation of MitoCLox in mitochondria of diverse living cell cultures and its oxidation under stress conditions, particularly those known to cause a selective cardiolipin oxidation. Ratiometric fluorescence measurements using flow cytometry showed a remarkable dependence of the MitoCLox dynamic range on the oxidation of the sample. Specifically, MitoCLox oxidation was induced by low doses of hydrogen peroxide or organic hydroperoxide. The mitochondria-targeted antioxidant 10-(6′-plastoquinonyl)decyltriphenyl-phosphonium (SkQ1), which was shown earlier to selectively protect cardiolipin from oxidation, prevented hydrogen peroxide-induced MitoCLox oxidation in the cells. Concurrent tracing of MitoCLox oxidation and membrane potential changes in response to hydrogen peroxide addition showed that the oxidation of MitoCLox started without a delay and was complete during the first hour, whereas the membrane potential started to decay after 40 minutes of incubation. Hence, MitoCLox could be used for splitting the cell response to oxidative stress into separate steps. Application of MitoCLox revealed heterogeneity of the mitochondrial population; in living endothelial cells, a fraction of small, rounded mitochondria with an increased level of lipid peroxidation were detected near the nucleus. In addition, the MitoCLox staining revealed a specific fraction of cells with an increased level of oxidized lipids also in the culture of human myoblasts. The fraction of such cells increased in high-density cultures. These specific conditions correspond to the initiation of spontaneous myogenesis in vitro, which indicates that oxidation may precede the onset of myogenic differentiation. These data point to a possible participation of oxidized CL in cell signalling and differentiation.

Masteroppgave(MSc) in Master of Science in Business, Business law, tax and accounting - Handelshøyskolen BI, 2017 The purpose of this thesis is to get insight into how the Norwegian economy is affected by changes in oil prices, with emphasis on the 2014 oil bust. We also study if this effect differs between Norwegian industries. We use data from all registered Norwegian firms in the period from 2000 to 2015. We investigate how oil price changes affect the Norwegian economy, measured through firms’ return on assets and return on equity, by using panel data regression analysis. We perform the same regression on all industries in Norway and investigate if industries’ exposure to the oil price determines how they are affected by fluctuations in oil prices. We also include an analysis of bankruptcies in Norway during the period from 2000 to 2016 to further explore how changes in oil prices affect different industries. Finally, we investigate if negative shocks have a bigger impact on Norwegian industries than positive shocks, as proposed by the prospect theory. Testing 41 396 Norwegian companies we find that the Norwegian firm performance, as a whole, will be affected by a fall in oil price. The coefficient for oil price changes is positive, which means that firm performance, collectively, decreases when the oil price decreases. For the Norwegian industries with a statistical significant relationship between percentage change in oil price and return on assets, the oil price coefficient is positive for every industry, except two. We find that for most industries consuming oil, the economic activity plays a determinant role along with the actual price of oil. When it comes to the number of bankruptcies in Norway during our sample period, we find evidence that bankruptcies tend to move in the opposite direction of the oil price. From our last analysis we find asymmetry in response to different oil price shocks. We find that a negative event has a statistically significant effect, and that a positive event is not statistically different than zero.