233 research outputs found
Kinetics and mechanisms of biosorption of copper ion onto waste yeast (S. cerevisiae)
No full textSpringer NetherlandsHeavy metals are the most common pollutants found in industrial effluents. Several chemical treatment methods are used to remove heavy metals from aquatic solutions. Recently, biosorption process which utilizes various microbial materials (bacteria, fungi, yeasts, algae etc.) has been preferred to remove pollutants. In this study, waste yeast taken from yeast factory in Turkey was used as (working volume of 100 ml) biosorbent in erlenmeyer batch experiments by using temperature controlled shaker and copper (II) ion biosorption was examined. The effects of initial pH (2, 3, 4, 5, 6, 7), initial copper concentrations (25, 50, 75, 100, 150, 200, 250, 300 mg L?1), biosorbent amount (1, 3, 5, 7 10 g L?1), contact time (5, 10, 15, 30, 45, 60, 90, 120, 240, 1440 min.) and temperature (20, 30, 40, 50 °C) parameters on to biosorption process were investigated. Optimum biosorption capacity was found as pH 5, 100 mg L?1 of initial copper concentration, 10 g L?1 biosorbent amount and 1440 min. of contact time. The experimental equilibrium data fitted to Freundlich and Langmuir adsorption isotherm models. Freundlich models fitted better than Langmuir models. The maximum adsorption capacity of waste yeast was determined as 7.94 mg g?1and Freundlich isotherm values n and kf were found to be 1.55 and 0.21 respectively. Pseudo-second order kinetic model was suitable for biosorption kinetics. According to calculated thermodynamic parameters (?H, ?G and ?S), biosorption of copper onto waste yeast was exothermic. As a conclusion; it was found that copper (II) removal by using waste yeast was low. Activation of biomaterial by pretreatment can be resulted in increasing of removal rate. Use of waste materials in pollution control is important for economic issue. © Springer Science+Business Media Dordrecht 2015.Sarioglu Cebeci, M.; Cumhuriyet University, Department of Environmental EngineeringTurkey; email: [email protected]
Corrosion of CrN-Coated stainless steel in a NaCl solution (w = 3 %)
No full textA CrN coating deposited by arc PVD was characterized by XRD and SEM. The in-situ measurement of the corrosion of the CrN-coated substrate was made by corrosion potential (Cor. Pot.), the polarization resistance (PR) method and electrochemical impedance spectroscopy (EIS) in a NaCl solution w = 3 % as a function of the immersion time (about 24 h). A semiconductor scale that formed on the CrN was identified by Mott-Shottky analysis as a p-type semiconductor with flat band potentials, 0.49 V (SCE). The CrN coating (0.5 μm thick) consisted of a mixture of cubic Cr and hexagonal Cr2N phases exhibiting equiaxed grains and a dense coating with a small quantity of pinholes, voids and porosities. The "transition in corrosion resistance" for the CrN coatings at an early stage was found based on Cor. Pot., PR and EIS data. The CrN did not exhibit any pitting for about 24 h, while the corrosion resistance (Rp and Rtotal) decreased rapidly with time after 5 h of incubation. The transition from high resistance (3 Mω cm2) to low resistance (0.24 Mω cm2) was explained as a result of the penetration of the electrolyte through the Cr2O3 oxide layer to the Cr2O3/CrN interface. The resistance of the CrN against pitting corrosion was explained based on the blocking character of the equiaxed, dense, CrN coating against the penetration of the electrolyte
PITTING CORROSION OF TiN-COATED STAINLESS STEEL IN 3 % NaCl SOLUTION
No full textTiN coatings deposited by arc PVD were characterized by XRD and SEM. In-situ measurements of the corrosion of the substrate and the TiN-coated substrate were made using the corrosion potential (Cor.Pot.), the polarization resistance (PR) method and electrochemical impedance spectroscopy (EIS) in a 3 % NaCl solution as a function of the immersion time. The semiconductor scale formed on the TiN was identified using a Mott-Shottky analysis as an n-type semiconductor with a flat band potential of -0.83 V vs. SCE. The TiN coating (0.5 mu m thick) consisted of cubic TiN exhibiting columnar grains, pin holes, voids and porosities. The pitting corrosion of the TiN, observed visually between I h and 2 h, was captured by EIS and PR. The electrical circuit (EC) model used for the EIS data supported the degradation of the coating through pitting corrosion, in agreement with the visual observations. The corrosion resistance (polarization resistance) determined by the polarization resistance method (R-p) and the EIS (R-total) decreased suddenly during the pitting corrosion. The corrosion resistance of the TiN-coated substrate was greater than the corrosion resistance of the substrate during the approximately 24 h of exposure
CORROSION OF CrN-COATED STAINLESS STEEL IN A NaCl SOLUTION (w=3 %)
No full textA CrN coating deposited by arc PVD was characterized by XRD and SEM. The in-situ measurement of the corrosion of the CrN-coated substrate was made by corrosion potential (Cor. Pot.), the polarization resistance (PR) method and electrochemical impedance spectroscopy (EIS) in a NaCl solution w = 3 % as a function of the immersion time (about 24 h). A semiconductor scale that formed on the CrN was identified by Mott-Shottky analysis as a p-type semiconductor with flat band potentials, 0.49 V (SCE). The CrN coating (0.5 mu m thick) consisted of a mixture of cubic Cr and hexagonal Cr2N phases exhibiting equiaxed grains and a dense coating with a small quantity of pinholes, voids and porosities. The transition in corrosion resistance for the CrN coatings at an early stage was found based on Cor. Pot., PR and EIS data. The CrN did not exhibit any pitting for about 24 h, while the corrosion resistance (R-p and R-total) decreased rapidly with time after 5 h of incubation. The transition from high resistance (3 M Omega cm(2)) to low resistance (0.24 M Omega cm(2)) was explained as a result of the penetration of the electrolyte through the Cr2O3 oxide layer to the Cr2O3/CrN interface. The resistance of the CrN against pitting corrosion was explained based on the blocking character of the equiaxed, dense, CrN coating against the penetration of the electrolyte
Analysis of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced proteome changes in 5L rat hepatoma cells reveals novel targets of dioxin action including the mitochondrial apoptosis regulator VDAC2.
No full textAs part of a comprehensive survey of the impact of the environmental pollutant and hepatocarcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the proteome of hepatic cells, we have performed a high resolution two-dimensional gel electrophoresis study on the rat hepatoma cell line 5L. 78 protein species corresponding to 73 different proteins were identified as up- or down-regulated following exposure of the cells to 1 nm TCDD for 8 h. There was an overlap of only nine proteins with those detected as altered by TCDD in our recent study using the non-gel-based isotope-coded protein label method (Sarioglu, H., Brandner, S., Jacobsen, C., Meindl, T., Schmidt, A., Kellermann, J., Lottspeich, F., and Andrae, U. (2006) Quantitative analysis of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced proteome alterations in 5L rat hepatoma cells using isotope-coded protein labels. Proteomics 6, 2407-2421) indicating a strong complementarity of the two approaches. For the majority of the altered proteins, an effect of TCDD on their abundance or posttranslational modifications had not been known before. Several observations suggest that a sizable fraction of the proteins with altered abundance was induced as an adaptive response to TCDD-induced oxidative stress that was demonstrated using the fluorescent probe dihydrorhodamine 123. A prominent group of these proteins comprised various enzymes for which there is evidence that their expression is regulated via the Keap1/Nrf2/antioxidant response element pathway. Other proteins included several involved in the maintenance of mitochondrial energy production and the regulation of the mitochondrial apoptotic pathway. A particularly intriguing finding was the up-regulation of the mitochondrial outer membrane pore protein, voltage-dependent anion channel-selective protein 2 (VDAC2), which was dependent on the presence of a functional aryl hydrocarbon receptor. The regulatability of VDAC2 protein abundance has not been described previously. In view of the recently discovered central role of VDAC2 as an inhibitor of the activation of the proapoptotic protein BAK and the mitochondrial apoptotic pathway, the present data point to a hitherto unrecognized mechanism by which TCDD may affect cellular homeostasis and survival
Differential response of the proteome induced by exposure to low-dose ionizing radiation (IR) using different dose rates and doses in human fibroblast cells
No full textPathway analysis techniques to study proteomic data from low dose/low-dose-rate irradiated cells
No full textBiological phosphorus removal in a sequencing batch reactor by using pure cultures
No full textThe aim of this study was to investigate the effect of pure cultures on the enhancement of biological phosphorus removal capability of a Sequencing Batch Reactor (SBR) inoculated initially with a mixed culture. For this purpose, three anaerobic/aerobic SBRs with mixed cultures were started in parallel and operated for a while. At the end of this period, pure cultures of Acinetobacter lwoffii, A. lwoffii-Pseudomonas aeruginosa mixture and P. aeruginosa were added into the first, second and third reactors, respectively. All reactors were operated at a constant solid retention time (SRT) of 10 days and the food/microorganism (F/M) ratio was changed between 0.43-0.50 mg COD mg(-1) VSS day(-1). The total cycle time was 14 h throughout the experimental study. The addition of A. lwoffii to the mixed culture in the first reactor significantly enhanced the biological phosphorus removal (EBPR) rate. Complete removal (E = 100%) of 20 mg 1(-1) PO4-P was achieved within 35 days of operation. Corresponding removal efficiencies obtained using A. lwoffii-P. aeruginosa mixture (second reactor) and P. aeruginosa alone (third reactor) were 25% and 20%, respectively. The COD removal efficiency was 90% in all reactors. (c) 2004 Elsevier Ltd. All rights reserved
Residual stresses in (Zr,Hf)N films (up to 11.9 at.% Hf) measured by X-ray diffraction using experimentally calculated XECs
No full textIn the present work, the residual stresses of (Zr,Hf)N films were measured using X-ray diffraction (XRD) fixed incident multiplane technique (FIM) for varying amounts of Hf addition by assuming the film was isotropic and anisotropic (Kronel model). The residual stress values calculated according to isotropic and anisotropic models were almost the same (-6 GPa). Addition up to 11.9 at.% Hf into ZrN films did not affect the level of residual stress. (C) 2004 Elsevier B.V. All rights reserved
Simultaneous inhibition of PFKFB3 and GLS1 selectively kills KRAS-transformed pancreatic cells
No full textActivating mutations of the oncogenic KRAS in pancreatic ductal adenocarcinoma (PDAC) are associated with an aberrant metabolic phenotype that may be therapeutically exploited. Increased glutamine utilization via glutaminase-1 (GLS1) is one such feature of the activated KRAS signaling that is essential to cell survival and proliferation; however, metabolic plasticity of PDAC cells allow them to adapt to GLS1 inhibition via various mechanisms including activation of glycolysis, suggesting a requirement for combinatorial anti-metabolic approaches to combat PDAC. We investigated whether targeting the glycolytic regulator 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3) in combination with GLS1 can selectively prevent the growth of KRAS-transformed cells. We show that KRAS-transformation of pancreatic duct cells robustly sensitizes them to the dual targeting of GLS1 and PFKFB3. We also report that this sensitivity is preserved in the PDAC cell line PANC-1 which harbors an activating KRAS mutation. We then demonstrate that GLS1 inhibition reduced fructose-2,6-bisphosphate levels, the product of PFKFB3, whereas PFKFB3 inhibition increased glutamine consumption, and these effects were augmented by the co-inhibition of GLS1 and PFKFB3, suggesting a reciprocal regulation between PFKFB3 and GLS1. In conclusion, this study identifies a novel mutant KRAS-induced metabolic vulnerability that may be targeted via combinatorial inhibition of GLS1 and PFKFB3 to suppress PDAC cell growth.Fil: Ozcan, Selahattin C.. Koc University Research Center For Translational Medici; TurquíaFil: Mutlu, Aydan. Bursa Uludag University; TurquíaFil: Altunok, Tugba H.. Bursa Uludag University; TurquíaFil: Gurpinar, Yunus. Bursa Uludag University; TurquíaFil: Sarioglu, Aybike. Bursa Uludag University; TurquíaFil: Guler, Sabire. Bursa Uludag University; TurquíaFil: Muchut, Robertino José. Universidad Nacional del Litoral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; ArgentinaFil: Iglesias, Alberto Alvaro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; Argentina. Universidad Nacional del Litoral; ArgentinaFil: Celikler, Serap. Bursa Uludag University; TurquíaFil: Campbell, Paul M.. The Marvin and Concetta Greenberg Pancreatic Cancer Institute; Estados UnidosFil: Yalcin, Abdullah. Bursa Uludag University; Turquí
- …
