Hardening of leading edges of turbine blades by electrospark alloying

With a purpose of creating anti-erosion protection on turbine rotor blades the experiments in electrospark alloying using electrodes made of different materials: Т15К6 hard alloy and 15Х11МФШ steel were conducted. Reduction of the roughness of a surface layer having a uniform thickness was achieved upon its hardening with a steel electrode. The electrospark alloying process was perfected. Tests of mechanical properties of blade samples hardened with steel revealed overmatch of GOST requirements for strength and ductility. Increasing of surface layer microhardness was also achieved. For anti-erosion protection of leading edges of the turbine rotor blades it is recommended to replace the applied electrode made of Т15 К6 alloy with the one made of 15Х11МФШ steel.Для формування протиерозійного захисту робочих лопаток турбіни проведені експерименти з електроіскрового легування електродами з різних матеріалів: твердого сплаву Т15К6 і сталі 15Х11МФШ. Досягнуто зменшення шорсткості поверхневого шару, отриманого легуванням сталевим электродом, при однаковій товщині поверхневого шару. Відпрацьовано режим електроіскрового легування. Випробування механічних властивостей зразків лопаток, зміцнених сталлю, показали перевищення вимог ДСТУ з характеристик міцності та пластичності. Досягнуто також підвищення мікротвердості поверхневого шару. Рекомендована заміна електрода із сплаву Т15К6, що використовується, на електрод із сталі 15Х11МФШ, для захисту від ерозії вхідних кромок робочих лопаток турбін.Для формирования противно эрозионной защиты рабочих лопаток турбины проведены эксперименты по электроискровому легированию электродами из различных материалов: твердого сплава Т15К6 и стали 15Х11МФШ. Достигнуто уменьшение шероховатости поверхностного слоя при одинаковой его толщине после упрочнения стальным электродом. Отработан режим электроискрового легирования. Испытания механических свойств образцов лопаток, упрочненных сталью, показали превышение требований ГОСТ по прочности и пластичности. Достигнуто также повышение микротвердости поверхностного слоя. Рекомендована замена применяемого электрода из сплава Т15 К6 на электрод из стали 15Х11МФШ для защиты от эрозии входных кромок рабочих лопаток турбин

Atherogenic effects of Chlamydia pneumoniae: refuting the innocent bystander hypothesis.

Item does not contain fulltextOBJECTIVE: Serologic evidence of Chlamydia pneumoniae infection and atherosclerosis was first demonstrated in patients with ischemic heart disease in 1988. Subsequently, the organism has been detected in several cardiovascular lesions. Outside of observational reports, few studies mechanistically link vascular infection with C. pneumoniae and atherogenesis. To better define its pathophysiologic role, we examined the influence of C. pneumoniae infection of human vascular smooth muscle cells on vascular smooth muscle cell proliferation, cell-cycle protein expression, and inflammatory cytokine release. METHODS: Human aortic vascular smooth muscle cells were inoculated with C. pneumoniae in culture. Proliferation was assessed by mitochondrial activity, direct cell counting, and immunohistochemical staining for proliferating cell nuclear antigen. Electromobility gel shift assays probed for the antiproliferative cell-cycle protein p53. Supernatants were assayed for the mitogens interleukin-6 and interleukin-8 by enzyme-linked immunosorbent assay. RESULTS: After C. pneumoniae inoculation, vascular smooth muscle cell proliferation increased 2-fold by mitochondrial activity and more than 3-fold by cell numbers. C. pneumoniae infection promoted a 3-fold increase in proliferating cell nuclear antigen expression, which was associated with decreased nuclear binding of p53. Compared with control, C. pneumoniae inoculation resulted in a 2.5-fold increase in released interleukin-6 and interleukin-8. In each experiment, the influence of C. pneumoniae was abrogated by concomitant treatment with the macrolide antibiotic azithromycin. CONCLUSIONS: C. pneumoniae induced human vascular smooth muscle cell proliferation and proliferating cell nuclear antigen expression, down-regulated p53, and promoted release of prototypical atherogenic cytokines. These in vitro findings indicate that C. pneumoniae is more than an innocent bystander, rather it is a pathophysiologic participant in atherogenesis warranting elimination

Atherogenic effects of Chlamydia pneumoniae: refuting the innocent bystander hypothesis.

Item does not contain fulltextOBJECTIVE: Serologic evidence of Chlamydia pneumoniae infection and atherosclerosis was first demonstrated in patients with ischemic heart disease in 1988. Subsequently, the organism has been detected in several cardiovascular lesions. Outside of observational reports, few studies mechanistically link vascular infection with C. pneumoniae and atherogenesis. To better define its pathophysiologic role, we examined the influence of C. pneumoniae infection of human vascular smooth muscle cells on vascular smooth muscle cell proliferation, cell-cycle protein expression, and inflammatory cytokine release. METHODS: Human aortic vascular smooth muscle cells were inoculated with C. pneumoniae in culture. Proliferation was assessed by mitochondrial activity, direct cell counting, and immunohistochemical staining for proliferating cell nuclear antigen. Electromobility gel shift assays probed for the antiproliferative cell-cycle protein p53. Supernatants were assayed for the mitogens interleukin-6 and interleukin-8 by enzyme-linked immunosorbent assay. RESULTS: After C. pneumoniae inoculation, vascular smooth muscle cell proliferation increased 2-fold by mitochondrial activity and more than 3-fold by cell numbers. C. pneumoniae infection promoted a 3-fold increase in proliferating cell nuclear antigen expression, which was associated with decreased nuclear binding of p53. Compared with control, C. pneumoniae inoculation resulted in a 2.5-fold increase in released interleukin-6 and interleukin-8. In each experiment, the influence of C. pneumoniae was abrogated by concomitant treatment with the macrolide antibiotic azithromycin. CONCLUSIONS: C. pneumoniae induced human vascular smooth muscle cell proliferation and proliferating cell nuclear antigen expression, down-regulated p53, and promoted release of prototypical atherogenic cytokines. These in vitro findings indicate that C. pneumoniae is more than an innocent bystander, rather it is a pathophysiologic participant in atherogenesis warranting elimination

Regulation of Staphylococcus epidermidis-induced IFN-7 in whole human blood: the role of endogenous IL-18, IL-12, IL-1, and TNF

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Genèse des politiques sportives publiques : le cas français

L'Etat, les collectivités publiques et le sport de compétition en France. L'image sociale élitiste du sport avant 1914, cause de l'intérêt tardif de l'Etat et des communes (préférence pour la gymnastique) - Politiques d'incitations (1913-1935) - L'Etat et les premiers contrôles des institutions sportives (1936-1957) - La politique de planification : l'Etat providence (1958-1980) - Décentralisation et désengagement de l'Etat (1981-...

Regulation of Staphylococcus epidermidis-induced IFN-gamma in whole human blood: the role of endogenous IL-18, IL-12, IL-1, and TNF.

Item does not contain fulltextInterleukin 12 (IL-12) and IL-18 act synergistically to stimulate interferon gamma (IFN-gamma) production; moreover, IL-1 and tumor necrosis factor (TNF) may also augment IFN-gamma synthesis. We have investigated the relative contributions of these cytokines in the production of IFN-gamma and TNF by the Gram-positive bacterium Staphylococcus epidermidis, using the specific cytokine inhibitors IL-18 binding protein (IL-18BP), IL-1 receptor antagonist (IL-1Ra), anti-IL-12 antibodies (anti-IL-12 Ab), and TNF binding protein. Inhibition of caspase-1 reduced IFN-gamma and IL-1beta levels (by 80 and 67%, respectively) when heat-killed S. epidermidis was added to whole human blood cultures. IL-18BP reduced S. epidermidis-induced IFN-gamma (77% maximal suppression). In contrast, blocking IL-1 receptors by IL-1Ra had no effect on IFN-gamma production. Blocking endogenous IL-12 and TNF reduced IFN-gamma production by 69 and 36%. S. epidermidis-induced TNF-alpha was inhibited by IL-18BP and IL-1Ra, but not anti-IL-12 Ab, whereas IL-8 production was unaffected by any of the specific cytokine blocking agents. In conclusion, S. epidermidis stimulates IFN-gamma which is IL-18, IL-12 and TNF-dependent, but IL-1 independent

Modern Trends of Organic Chemistry in Russian Universities

This review is devoted to the scientific achievements of the departments of organic chemistry in higher schools of Russia within the past decade. © 2018, Pleiades Publishing, Ltd

Modern Trends of Organic Chemistry in Russian Universities

© 2018, Pleiades Publishing, Ltd. This review is devoted to the scientific achievements of the departments of organic chemistry in higher schools of Russia within the past decade