The Regional Policy of the European Union and its Impact on the Functioning of Polish Economy

W pracy przedstawiono, w jaki sposób Unia Europejska wpływa na funkcjonowanie polskiej gospodarki. Zaprezentowano wielorakie znaczenie pomocy unijnej, która oddziałuje pozytywnie na funkcjonowanie kraju. Ukazano, że fundusze unijne mają niewątpliwy wpływ na rozwój oraz funkcjonowanie zarówno gospodarki międzynarodowej, jak i krajowej, szczególnie gospodarki regionalnej. Opracowanie zostało przygotowane na podstawie literatury przedmiotu metodą analizy i syntezy zebranego materiału.The paper presents the EU affects the functioning of the Polish economy. Presented multiple importance of the EU aid, which has a positive effect on the functioning of the country. It shows that EU funds have a definite influence on the development and functioning of both the international and the country economy, particularly the regional economy. The study was prepared on the literature method of analysis and synthesis of the collected material

The Effect of Boron Content on Wetting Kinetics in Si-B Alloy/h-BN System

In this work, the effect of boron content on the high-temperature wetting behavior in the Si-B alloy/h-BN systems was experimentally examined. For this reason, hypoeutectic, eutectic and hypereutectic Si-B alloys (Si-1B, Si-3.2B and Si-5.7B wt.%, respectively) were produced by electric arc melting method and then subjected to sessile drop/contact heating experiments with polycrystalline h-BN substrates, at temperatures up to 1750 °C. Similar to pure Si/h-BN system, wetting kinetics curves calculated on a basis of in situ recorded drop/substrate images point toward non-wetting behavior of all selected Si-B alloy/h-BN couples. The highest contact angle values of ~ 150° were obtained for hypoeutectic and eutectic Si-B alloys in the whole examined temperature range. © 2018, The Author(s)

The NADPH oxidase Nox4 restricts the replicative lifespan of human endothelial cells

The free radical theory of aging proposes that ROS (reactive oxygen species) are major driving forces of aging, and are also critically involved in cellular senescence. Besides the mitochondrial respiratory chain, alternative sources of ROS have been described that might contribute to cellular senescence. Noxs (NADPH oxidases) are well-known sources of superoxide, which contribute to the antimicrobial capabilities of macrophages, a process involving the prototypical member of the family referred to as Nox2. However, in recent years non-phagocytic homologues of Nox2 have been identified that are involved in processes other than the host defence. Superoxide anions produced by these enzymes are believed to play a major role in signalling by MAPKs (mitogen-activated protein kinases) and stress-activated kinases, but could also contribute to cellular senescence, which is known to involve oxygen radicals. In HUVECs (human umbilical vein endothelial cells), Nox4 is predominantly expressed, but its role in replicative senescence of HUVECs remains to be elucidated. Using shRNA (small-hairpin RNA)-mediated knockdown of Nox4, implicating lentiviral vectors, we addressed the question of whether lifelong depletion of Nox4 in HUVECs would influence the senescent phenotype. We found a significant extension of the replicative lifespan of HUVECs upon knockdown of Nox4. Surprisingly, mean telomere length was significantly reduced in Nox4-depleted cells. Nox4 depletion had no discernable influence on the activity of MAPKs and stress-activated kinases, but reduced the degree of oxidative DNA damage. These results suggest that Nox4 activity increases oxidative damage in HUVECs, leading to loss of replicative potential, which is at least partly independent of telomere attrition

Calcium Signals Are Affected by Ciprofloxacin as a Consequence of Reduction of Mitochondrial DNA Content in Jurkat Cells

The effects of ciprofloxacin on mitochondrial DNA (mtDNA) content, oxygen consumption, mitochondrial membrane potential, cellular ATP formation, and capacitative Ca(2+) entry into Jurkat cells were investigated. In cells incubated for several days with 25 μg/ml ciprofloxacin, a 60% reduction of mtDNA content, inhibition of the respiratory chain, and a significant decrease in mitochondrial membrane potential were observed. These changes led to a decrease in the calcium buffering capacity of mitochondria which, in turn, resulted in a gradual inhibition of the capacitative Ca(2+) entry. On days 4, 7, and 11 of incubation with ciprofloxacin, the initial rates of Ca(2+) entry were reduced by 33%, 50%, and 50%, respectively. Ciprofloxacin caused a transient decrease in the cellular capability for ATP formation. In cells incubated for 15 min with glucose, pyruvate, and glutamine as exogenous fuel, ciprofloxacin reduced ATP content by 16% and 35% on days 4 and 7, respectively, of incubation with the drug. However, on day 11 of incubation with ciprofloxacin, a recovery of cellular ATP formation was observed. In conclusion, long-term exposure of Jurkat cells to ciprofloxacin at a concentration of 25 μg/ml seriously affects cellular energy metabolism and calcium homeostasis

The regulatory role of mitochondria in capacitative calcium entry

AbstractCapacitative regulation of calcium entry is a major mechanism of Ca2+ influx into electrically non-excitable cells, but it also operates in some excitable ones. It participates in the refilling of intracellular calcium stores and in the generation of Ca2+ signals in excited cells. The mechanism which couples depletion of intracellular calcium stores located in the endoplasmic reticulum with opening of store-operated calcium channels in the plasma membrane is not clearly understood. Mitochondria located in close proximity to Ca2+ channels are exposed to high Ca2+ concentration, and therefore, they are able to accumulate this cation effectively. This decreases local Ca2+ concentration and thereby affects calcium-dependent processes, such as depletion and refilling of the intracellular calcium stores and opening of the store-operated channels. Finally, mitochondria modulate the intensity and the duration of calcium signals induced by extracellular stimuli. Ca2+ uptake by mitochondria requires these organelles to be in the energized state. On the other hand, Ca2+ flux into mitochondria stimulates energy metabolism. To sum up, mitochondria couple cellular metabolism with calcium homeostasis and signaling