Models for enzymatic nucleotide cleavage

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Factors affecting the Faradaic efficiency of Fe(0) electrocoagulation

Electrocoagulation (EC) using Fe(0) electrodes is a low cost water treatment technology that relies on efficient production of Fe(II) from the electrolytic dissolution of Fe(0) electrodes (i.e. a high Faradaic efficiency). However, the (electro)chemical factors that favor Fe(0) oxidation rather than O2 evolution during Fe(0) EC have not been identified. In this study, we combined electrochemical methods, electron microscopy and Fe measurements to systematically examine the interdependent effects of current density (i), anodic interface potential (EA) and solution chemistry on the Faradaic efficiency. We found that Fe(0) oxidation was favored (Faradaic efficiency >0.85) in chloride and bromide solutions at all i, whereas carbonate, phosphate, citrate, and nitrate solutions lead to Faradaic efficiencies <0.1. The anodic reaction (i.e. Fe(0) oxidation or O2 evolution) only depended on i in the sulfate and formate solutions. Experiments in binary-anion solutions revealed that molar ratios of [HCO3−]/[Cl−] near 100 and [NO3−]/[Cl−] near 20 separated the electrochemical domains of Fe(0) oxidation and O2 evolution in the EC system. These molar ratios were supported by experiments in synthetic groundwater solutions. We also found that the EA vs i curves for solutions with poor Faradaic efficiency overlapped but were situated 2–4 V vs Ag/AgCl higher than those of solutions with high Faradaic efficiency. Therefore, the position of the EA vs i curve, rather than the EA alone, can be used to determine unambiguously the reaction occurring on the Fe(0) anode during EC treatment

Factors affecting the Faradaic efficiency of Fe(0) electrocoagulation

Electrocoagulation (EC) using Fe(0) electrodes is a low cost water treatment technology that relies on efficient production of Fe(II) from the electrolytic dissolution of Fe(0) electrodes (i.e. a high Faradaic efficiency). However, the (electro)chemical factors that favor Fe(0) oxidation rather than O2 evolution during Fe(0) EC have not been identified. In this study, we combined electrochemical methods, electron microscopy and Fe measurements to systematically examine the interdependent effects of current density (i), anodic interface potential (EA) and solution chemistry on the Faradaic efficiency. We found that Fe(0) oxidation was favored (Faradaic efficiency >0.85) in chloride and bromide solutions at all i, whereas carbonate, phosphate, citrate, and nitrate solutions lead to Faradaic efficiencies <0.1. The anodic reaction (i.e. Fe(0) oxidation or O2 evolution) only depended on i in the sulfate and formate solutions. Experiments in binary-anion solutions revealed that molar ratios of [HCO3−]/[Cl−] near 100 and [NO3−]/[Cl−] near 20 separated the electrochemical domains of Fe(0) oxidation and O2 evolution in the EC system. These molar ratios were supported by experiments in synthetic groundwater solutions. We also found that the EA vs i curves for solutions with poor Faradaic efficiency overlapped but were situated 2–4 V vs Ag/AgCl higher than those of solutions with high Faradaic efficiency. Therefore, the position of the EA vs i curve, rather than the EA alone, can be used to determine unambiguously the reaction occurring on the Fe(0) anode during EC treatment

Epidermal Growth Factor Receptor Dependence of Radiation-induced Transcription Factor Activation in Human Breast Carcinoma Cells

Ionizing radiation (1–5 Gy) activates the epidermal growth factor receptor (EGFR), a major effector of the p42/44 mitogen-activated protein kinase (MAPK) pathway. MAPK and its downstream effector, p90 ribosomal S6 kinase (p90RSK), phosphorylate transcription factors involved in cell proliferation. To establish the role of the EGFR/MAPK pathway in radiation-induced transcription factor activation, MDA-MB-231 human breast carcinoma cells were examined using specific inhibitors of signaling pathways. Gel-shift analysis revealed three different profile groups: 1) transcription factors that responded to both radiation (2 Gy) and epidermal growth factor (EGF) (CREB, Egr, Ets, and Stat3); 2) factors that responded to radiation, but not EGF (C/EBP and Stat1); and 3) those that did not respond significantly to either radiation or EGF (AP-1 and Myc). Within groups 1 and 2, a two- to fivefold maximum stimulation of binding activity was observed at 30–60 min after irradiation. Interestingly, only transcription factors that responded to EGF had radiation responses significantly inhibited by the EGFR tyrosine kinase inhibitor, AG1478; these responses were also abrogated by farnesyltransferase inhibitor (FTI) or PD98059, inhibitors of Ras and MEK1/2, respectively. Moreover, radiation-induced increases in CREB and p90RSK phosphorylation and activation of Stat3 and Egr-1 reporter constructs by radiation were all abolished by AG1478. These data demonstrate a distinct radiation response profile at the transcriptional level that is dependent on enhanced EGFR/Ras/MAPK signaling