231 research outputs found

    Konstrukcija laboratorijske opreme za proizvodnju bioplina

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    The aim of the paper is building of the mini digester for biogas production from energy plants. The basic structure is of welded construction from stainless steel. The mini digester consists of twelve units so that four tests simultaneously with three repetitions can be performed. Each unit consists of an eudiometer, fermenter containing the substrate and a levelling bottle for surplus closing liquid. Other components ensuring correct functioning of the mini digester are the pump and heater with thermostat, the thermometer, barometer, eudiometer clamps. Finally, some measurements with energy plants according DIN 38414 were made.Osnovna namjera istraĆŸivanja bila je izgradnja mini digestora za proizvodnju bioplina od energetskih biljaka. Osnovna struktura digestora zavarena je od nehrđajućeg čelika. Mini digestor sastavljen je od dvanaest jedinica, tako da se ujedno mogu izvoditi četiri pokusa sa tri ponavljanja. Svaka jedinica sastavljena je od eudiometra, fermentora, koji sadrĆŸi supstrat i nivojne posude za spremanje suviĆĄne tekućine. Drugi sastavni dijelovi koji omogućavaju pravilno funkcioniranje mini digestora su pumpa sa grijaćem i termostatom, termometar, barometar te stezaljke eudiometra. Na kraju smo izveli mjerenja proizvodnje bioplina od energetskih biljaka po standardu DIN 38414

    EphB1 recruits c-Src and p52Shc to activate MAPK/ERK and promote chemotaxis

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    Eph receptors and their ligands (ephrins) play an important role in axonal guidance, topographic mapping, and angiogenesis. The signaling pathways mediating these activities are starting to emerge and are highly cell- and receptor-type specific. Here we demonstrate that activated EphB1 recruits the adaptor proteins Grb2 and p52Shc and promotes p52Shc and c-Src tyrosine phosphorylation as well as MAPK/extracellular signal–regulated kinase (ERK) activation. EphB1-mediated increase of cell migration was abrogated by the MEK inhibitor PD98059 and Src inhibitor PP2. In contrast, cell adhesion, which we previously showed to be c-jun NH2-terminal kinase (JNK) dependent, was unaffected by ERK1/2 and Src inhibition. Expression of dominant-negative c-Src significantly reduced EphB1-dependent ERK1/2 activation and chemotaxis. Site-directed mutagenesis experiments demonstrate that tyrosines 600 and 778 of EphB1 are required for its interaction with c-Src and p52Shc. Furthermore, phosphorylation of p52Shc by c-Src is essential for its recruitment to EphB1 signaling complexes through its phosphotyrosine binding domain. Together these findings highlight a new aspect of EphB1 signaling, whereby the concerted action of c-Src and p52Shc activates MAPK/ERK and regulates events involved in cell motility

    Number of severe bleeding complications according to classification used: Is unified classification of bleeding complications really necessary?

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    Background: To compare the number of severe periprocedural bleeding complications from the total number of bleeding complications associated with diagnostic selective coronary an­giography or percutaneous coronary intervention (PCI) when using different classifications (TIMI, GUSTO, PLATO, BARC) and to relate these classifications to real hemodynamic status of evaluated patients. Methods: We analyzed data from 106 patients who underwent invasive procedure for ischemic heart disease (selective coronary angiography/PCI) and suffered from any type of bleeding complication. Results: The number of bleeding according to impacts on hemodynamic status and consequent treatment shows that 54.7% of all bleedings did not need any specific therapy. Bleeding leading to death, hemorrhagic shock, hemodynamic instability, administration of blood transfusion, surgical procedure and local treatment occurred in 6.6%, 1.9%, 5.7%, 14.2%, 2.8%, and 14.2%, respectively. The results comparing bleeding classifications demonstrate that the rate of severe bleeding complications may increase up to 4 times when different classifications are used on the same group of patients (TIMI 9.4%, GUSTO 15.1%, PLATO 39.2% and BARC 35.9%). The power of association between severe bleeding determined by these classifications and real hemodynamic compromise using Kendall’s tau-c correlation is –0.4106 (95% CI –0.599 to –0.222), –0.5355 (95% CI –0.718 to –0.353), –0.5513 (95% CI –0.729 to –0.374) and –0.7552 (95% CI –0.897 to –0.612) for TIMI, GUSTO, PLATO and BARC, respectively. Conclusions: The data show significant dependence of percentage of severe periprocedural bleeding complications on selected classification. The strongest association between severe bleeding and real hemodynamic status was found for BARC classification as this classification seems to be promising for future general use

    The Multifunctional Sorting Protein PACS-2 Controls Mitophagosome Formation in Human Vascular Smooth Muscle Cells through Mitochondria-ER Contact Sites.

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    Mitochondria-associated ER membranes (MAMs) are crucial for lipid transport and synthesis, calcium exchange, and mitochondrial functions, and they also act as signaling platforms. These contact sites also play a critical role in the decision between autophagy and apoptosis with far reaching implications for cell fate. Vascular smooth muscle cell (VSMC) apoptosis accelerates atherogenesis and the progression of advanced lesions, leading to atherosclerotic plaque vulnerability and medial degeneration. Though the successful autophagy of damaged mitochondria promotes VSMC survival against pro-apoptotic atherogenic stressors, it is unknown whether MAMs are involved in VSMC mitophagy processes. Here, we investigated the role of the multifunctional MAM protein phosphofurin acidic cluster sorting protein 2 (PACS-2) in regulating VSMC survival following a challenge by atherogenic lipids. Using high-resolution confocal microscopy and proximity ligation assays, we found an increase in MAM contacts as in PACS-2-associated MAMs upon stimulation with atherogenic lipids. Correspondingly, the disruption of MAM contacts by PACS-2 knockdown impaired mitophagosome formation and mitophagy, thus potentiating VSMC apoptosis. In conclusion, our data shed new light on the significance of the MAM modulatory protein PACS-2 in vascular cell physiopathology and suggest MAMs may be a new target to modulate VSMC fate and favor atherosclerotic plaque stability

    Identifying the anti-inflammatory response to lipid lowering therapy: a position paper from the working group on atherosclerosis and vascular biology of the European Society of Cardiology

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    Dysregulated lipid metabolism induces an inflammatory and immune response leading to atherosclerosis. Conversely, inflammation may alter lipid metabolism. Recent treatment strategies in secondary prevention of atherosclerosis support beneficial effects of both anti-inflammatory and lipid-lowering therapies beyond current targets. There is a controversy about the possibility that anti-inflammatory effects of lipid-lowering therapy may be either independent or not of a decrease in low-density lipoprotein cholesterol. In this Position Paper, we critically interpret and integrate the results obtained in both experimental and clinical studies on anti-inflammatory actions of lipid-lowering therapy and the mechanisms involved. We highlight that: (i) besides decreasing cholesterol through different mechanisms, most lipid-lowering therapies share anti-inflammatory and immunomodulatory properties, and the anti-inflammatory response to lipid-lowering may be relevant to predict the effect of treatment, (ii) using surrogates for both lipid metabolism and inflammation as biomarkers or vascular inflammation imaging in future studies may contribute to a better understanding of the relative importance of different mechanisms of action, and (iii) comparative studies of further lipid lowering, anti-inflammation and a combination of both are crucial to identify effects that are specific or shared for each treatment strategy
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