Rotary mechanism with the enhanceable indexes of efficiency for orbital forging process

Загальна ефективність виробництва залежить від застосування сучасних технологічних процесів та ефективного і технологічного обладнання. Основним показником ефективності обладнання є коефіцієнт корисної дії. Треба враховувати показники надійності, продуктивності, матеріалоємності. Основним вузлом обладнання є механізм орбітального руху. Його робота пов’язана з виникненням і здоланням сил тертя. Якраз ця обставина суттєво впливає на корисне застосування підведеної енергії. Існують декілька базових конструкцій орбітальних механізмів. Проведений аналіз їх роботи, визначені недоліки та шляхи їх усунення. Мета статті полягає в створенні ефективного обладнання та обґрунтуванні проведених інновацій. Їх застосування забезпечує максимальну ефективність і продуктивність, а також мінімальну собівартість виробництва. Стаття є результатом експериментальних та теоретичних досліджень, що проводяться на кафедрі механіки пластичності матеріалів та ресурсозберігаючих процесів Національного технічного університету України «КПІ».General efficiency of production depends on the use of modern technological processes and effective technological equipment. The basic index of efficiency of equipment is an output-input ratio. It is necessary to take into account descriptions of reliability and productivity. The basic knot of equipment is a mechanism of orbital motion. His work flows with an origin and overcoming of forces of friction. His work flows with an origin and overcoming of forces of friction. This circumstance substantially influences on the useful use of energy. There are a few base constructions of orbital mechanisms. The analysis of their work is conducted, failings and ways of their removal are certain. The purpose of the article consists of creation of effective equipment and ground of the offered innovations. Their use provides maximal efficiency and reliability, and also minimum production cost. The article is the result of experimental and theoretical researches which are conducted on the department of mechanics of plasticity of materials and resource-safe processes of the National technical university of Ukraine «KPI».Общая эффективность производства зависит от использования современных технологических процессов и эффективного технологического оборудования. Основным показателем эффективности оборудования является коэффициент полезного действия. Необходимо учитывать характеристики надежности и производительности. Основным узлом оборудования является механизм орбитального движения. Его работа протекает с возникновением и преодолением сил трения. Это обстоятельство существенно влияет на полезное использование энергии. Существуют несколько базовых конструкций орбитальных механизмов. Проведен анализ их работы, определены недостатки и пути их устранения. Цель статьи состоит в создании эффективного оборудования и обосновании предложенных инноваций. Их использование обеспечивает максимальную эффективность и надежность, а также минимальную себестоимость производства. Статья является результатом экспериментальных и теоретических исследований, которые выполняются на кафедре механики пластичности материалов и ресурсосберегающих процессов Национального технического университета Украины "КПИ"

HOCl-modified phosphatidylcholines induce apoptosis and redox imbalance in HUVEC-ST cells

Electrophilic attack of hypochlorous acid on unsaturated bonds of fatty acyl chains is known to result mostly in chlorinated products that show cytotoxicity to some cell lines and were found in biological systems exposed to HOCl. This study aimed to investigate more deeply the products and the mechanism underlying cytotoxicity of phospholipid-HOCl oxidation products, synthesized by the reaction of HOCl with 1-stearoyl-2-oleoyl-, 1-stearoyl-2-linoleoyl-, and 1-stearoyl-2-arachidonyl-phosphatidylcholine. Phospholipid chlorohydrins were found to be the most abundant among obtained products. HOCl-modified lipids were cytotoxic towards HUVEC-ST (endothelial cells), leading to a decrease of mitochondrial potential and an increase in the number of apoptotic cells. These effects were accompanied by an increase of the level of active caspase-3 and caspase-7, while the caspase-3/-7 inhibitor Ac-DEVD-CHO dramatically decreased the number of apoptotic cells. Phospholipid-HOCl oxidation products were shown to affect cell proliferation by a concentration-dependent cell cycle arrest in the G/G phase and activating redox sensitive p38 kinase. The redox imbalance observed in HUVEC-ST cells exposed to modified phosphatidylcholines was accompanied by an increase in ROS level, and a decrease in glutathione content and antioxidant capacity of cell extracts

Alkylation of the Tumor Suppressor PTEN Activates Akt and β-Catenin Signaling: A Mechanism Linking Inflammation and Oxidative Stress with Cancer

PTEN, a phosphoinositide-3-phosphatase, serves dual roles as a tumor suppressor and regulator of cellular anabolic/catabolic metabolism. Adaptation of a redox-sensitive cysteinyl thiol in PTEN for signal transduction by hydrogen peroxide may have superimposed a vulnerability to other mediators of oxidative stress and inflammation, especially reactive carbonyl species, which are commonly occurring by-products of arachidonic acid peroxidation. Using MCF7 and HEK-293 cells, we report that several reactive aldehydes and ketones, e.g. electrophilic α,β-enals (acrolein, 4-hydroxy-2-nonenal) and α,β-enones (prostaglandin A2, Δ12-prostaglandin J2 and 15-deoxy-Δ-12,14-prostaglandin J2) covalently modify and inactivate cellular PTEN, with ensuing activation of PKB/Akt kinase; phosphorylation of Akt substrates; increased cell proliferation; and increased nuclear β-catenin signaling. Alkylation of PTEN by α,β-enals/enones and interference with its restraint of cellular PKB/Akt signaling may accentuate hyperplastic and neoplastic disorders associated with chronic inflammation, oxidative stress, or aging

Cell signalling by oxidized lipids and the role of reactive oxygen species in the endothelium

Abstract The controlled formation of ROS (reactive oxygen species) and RNS (reactive nitrogen species) is now known to be critical in cellular redox signalling. As with the more familiar phosphorylation-dependent signal transduction pathways, control of protein function is mediated by the post-translational modification at specific amino acid residues, notably thiols. Two important classes of oxidant-derived signalling molecules are the lipid oxidation products, including those with electrophilic reactive centres, and decomposition products such as lysoPC (lysophosphatidylcholine). The mechanisms can be direct in the case of electrophiles, as they can modify signalling proteins by post-translational modification of thiols. In the case of lysoPC, it appears that secondary generation of ROS/RNS, dependent on intracellular calcium fluxes, can cause the secondary induction of H 2 O 2 in the cell. In either case, the intracellular source of ROS/RNS has not been defined. In this respect, the mitochondrion is particularly interesting since it is now becoming apparent that the formation of superoxide from the respiratory chain can play an important role in cell signalling, and oxidized lipids can stimulate ROS formation from an undefined source. In this short overview, we describe recent experiments that suggest that the cell signalling mediated by lipid oxidation products involves their interaction with mitochondria. The implications of these results for our understanding of adaptation and the response to stress in cardiovascular disease are discussed

Rac1 modification by an electrophilic 15-deoxy Δ12,14-prostaglandin J2 analog

Vascular endothelial cells (ECs) are important for maintaining vascular homeostasis. Dysfunction of ECs contributes to cardiovascular diseases, including atherosclerosis, and can impair the healing process during vascular injury. An important mediator of EC response to stress is the GTPase Rac1. Rac1 responds to extracellular signals and is involved in cytoskeletal rearrangement, reactive oxygen species generation and cell cycle progression. Rac1 interacts with effector proteins to elicit EC spreading and formation of cell-to-cell junctions. Rac1 activity has recently been shown to be modulated by glutathiolation or S-nitrosation via an active site cysteine residue. However, it is not known whether other redox signaling compounds can modulate Rac1 activity. An important redox signaling mediator is the electrophilic lipid, 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2). This compound is a downstream product of cyclooxygenase and forms covalent adducts with specific cysteine residues, and induces cellular signaling in a pleiotropic manner. In this study, we demonstrate that a biotin-tagged analog of 15d-PGJ2 (bt-15d-PGJ2) forms an adduct with Rac1 in vitro at the C157 residue, and an additional adduct was detected on the tryptic peptide associated with C178. Rac1 modification in addition to modulation of Rac1 activity by bt-15d-PGJ2 was observed in cultured ECs. In addition, decreased EC migration and cell spreading were observed in response to the electrophile. These results demonstrate for the first time that Rac1 is a target for 15d-PGJ2 in ECs, and suggest that Rac1 modification by electrophiles such as 15d-PGJ2 may alter redox signaling and EC function