Cavitation-erosion wear-resistance of strengthened surfaces of strucutral steels in the food-processing production medium

Розглянуто вплив термоциклічної обробки (ТЦО), іонного азотування і полімерних покриттів на кавітаційно-ерозійну зносостійкість конструкційних сталей. Отримані результати пояснюються фізико-механічними, електрохімічними характеристиками досліджених матеріалів з покриттями.To improve cavitation and erosion wear-resistance of metals methods of surface strengthening must be used. For this reason the paper studies the influence of thermo-cyclic treatment (TCT), ion nitriding and polymer coatings on cavitation and erosion wear-resistance of C 45, 15Cr3 and 41 Cr 4 steels. Thermo-cyclic treatment of C 45, 15Cr3 and 41 Cr 4 steels was conducted using pendulum and medium-temperature approaches. Ion nitriding of normalized and temro-cycled samples of C 45 and 41 Cr 4 steels was conducted taking advantage of hydrogen-free nitriding machine and in a nitrogen-argon mixture at 500 and 560 оС. Coatings made of polypropylene PPR2 and fluorine plastic PTFE4 were sprayed on C 45 steel by the electrostatic method and colliquated in the furnace at the temperature 200...280 оС. The thickness of polymer coating was within 200...250 mkm. Research on cavitation and erosion wear-resistance has been done taking advantage of the magnetic strictional pulsator (MSP) in neutral, acidic and alkaline environmnet (3% NaCl, serum and milk). The results of the study have shown that TCT of structural steels improves the mechanical properties of plasticity, small-and multicyclic durability, corrosion resistance and, approximately by 35%, cavitation and erosion wear-resistance under the primary influence of corrosion damage factor. The developed technology of low temperature nitriding of structural carbon steels increases their cavitation and erosion wear-resistance in 1.15, 1.63, 1.65 and 1.84 times in the 3% aqua of sodium chloride, serum, milk and lactic acid respectively, that is by 10...32% higher compared with the conventional methods of nitriding. Polymer coating based on polypropylene and PTFE allow to increase in 2 times the cavitation and erosion wear-resistance of C 45 steel in a neutral (3% NaCl) and more than in 40 times - in acidic solutions. Especially effective is the application of polymeric coverages in a sour environment, where the increase of cavitation firmness presents more than in 40 times. Thus application of fluoroplastic for making of cavitation firmness detailsincreases their wearproofness more than in 50, and from a polypropylene – 60 times

Lactate dehydrogenase A silencing in IDH mutant gliomas

BackgroundMutations of the isocitrate dehydrogenase 1 and 2 gene (IDH1/2) were initially thought to enhance cancer cell survival and proliferation by promoting the Warburg effect. However, recent experimental data have shown that production of 2-hydroxyglutarate by IDH mutant cells promotes hypoxia-inducible factor (HIF)1α degradation and, by doing so, may have unexpected metabolic effects.MethodsWe used human glioma tissues and derived brain tumor stem cells (BTSCs) to study the expression of HIF1α target genes in IDH mutant ((mt)) and IDH wild-type ((wt)) tumors. Focusing thereafter on the major glycolytic enzyme, lactate dehydrogenase A (LDHA), we used standard molecular methods and pyrosequencing-based DNA methylation analysis to identify mechanisms by which LDHA expression was regulated in human gliomas.ResultsWe found that HIF1α-responsive genes, including many essential for glycolysis (SLC2A1, PDK1, LDHA, SLC16A3), were underexpressed in IDH(mt) gliomas and/or derived BTSCs. We then demonstrated that LDHA was silenced in IDH(mt) derived BTSCs, including those that did not retain the mutant IDH1 allele (mIDH(wt)), matched BTSC xenografts, and parental glioma tissues. Silencing of LDHA was associated with increased methylation of the LDHA promoter, as was ectopic expression of mutant IDH1 in immortalized human astrocytes. Furthermore, in a search of The Cancer Genome Atlas, we found low expression and high methylation of LDHA in IDH(mt) glioblastomas.ConclusionTo our knowledge, this is the first demonstration of downregulation of LDHA in cancer. Although unexpected findings, silencing of LDHA and downregulation of several other glycolysis essential genes raise the intriguing possibility that IDH(mt) gliomas have limited glycolytic capacity, which may contribute to their slow growth and better prognosis

Sensitivity to temozolomide in brain tumor initiating cells

Molecular alterations in glioblastoma have the potential to guide treatment. Here, we explore the relationship between temozolomide (TMZ) response and O6-methylguanine DNA methyltransferase (MGMT) status in brain tumor initiating cells (BTICs). Methylation, expression, and sensitivity were assessed in 20 lines; associations were evaluated by Fisher's exact test. Some BTICs were sensitive. Sensitivity to TMZ was only associated with protein expression (P = .001). There were atypical BTICs including TMZ-resistant lines in which the methylation-specific PCR reaction revealed both methylated and unmethylated bands. BTICs are not uniformly resistant to TMZ; some are sensitive. MGMT status does not predict TMZ response with high precision

Lactate dehydrogenase A silencing in IDH mutant gliomas

BACKGROUND: Mutations of the isocitrate dehydrogenase 1 and 2 gene (IDH1/2) were initially thought to enhance cancer cell survival and proliferation by promoting the Warburg effect. However, recent experimental data have shown that production of 2-hydroxyglutarate by IDH mutant cells promotes hypoxia-inducible factor (HIF)1α degradation and, by doing so, may have unexpected metabolic effects. METHODS: We used human glioma tissues and derived brain tumor stem cells (BTSCs) to study the expression of HIF1α target genes in IDH mutant ((mt)) and IDH wild-type ((wt)) tumors. Focusing thereafter on the major glycolytic enzyme, lactate dehydrogenase A (LDHA), we used standard molecular methods and pyrosequencing-based DNA methylation analysis to identify mechanisms by which LDHA expression was regulated in human gliomas. RESULTS: We found that HIF1α-responsive genes, including many essential for glycolysis (SLC2A1, PDK1, LDHA, SLC16A3), were underexpressed in IDH(mt) gliomas and/or derived BTSCs. We then demonstrated that LDHA was silenced in IDH(mt) derived BTSCs, including those that did not retain the mutant IDH1 allele (mIDH(wt)), matched BTSC xenografts, and parental glioma tissues. Silencing of LDHA was associated with increased methylation of the LDHA promoter, as was ectopic expression of mutant IDH1 in immortalized human astrocytes. Furthermore, in a search of The Cancer Genome Atlas, we found low expression and high methylation of LDHA in IDH(mt) glioblastomas. CONCLUSION: To our knowledge, this is the first demonstration of downregulation of LDHA in cancer. Although unexpected findings, silencing of LDHA and downregulation of several other glycolysis essential genes raise the intriguing possibility that IDH(mt) gliomas have limited glycolytic capacity, which may contribute to their slow growth and better prognosis