Publications by authors named "Tung Viet Nguyen"

Background And Aims: Myeloperoxidase (MPO) plays a critical role in the innate immune response and has been suggested to be a surrogate marker of oxidative stress and inflammation, with elevated levels implicated in cardiovascular diseases, such as atherosclerosis and heart failure, as well as in conditions like rheumatoid arthritis and cancer. While MPO is well-known in leukocytes, its expression and function in human endothelial cells remain unclear. This study investigates MPO expression in patient-derived endothelial colony-forming cells (ECFCs) and its potential association with CAD and mitochondrial function.

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Ecotoxicological risks of perfluoroalkyl and polyfluoroalkyl substances (PFASs) in surface waters are difficult to model because data on PFASs distribution in multiple compartments (sediments, suspended particles and aqueous phase) are difficult to predict. This study quantified the distribution of 21 PFASs including PFCAs: C6-C13 perfluoroalkyl carboxylates, C4, C6, C8 and C10 perfluoroalkane sulfonates, 5 perfluorooctane sulfonamide substances (FOSAMs, including EtFOSA, FOSA, MeFOSAA, EtFOSAA, FOSAA), 2 N-alkyl perfluoroalkane sulfonamidoethanols (MeFOSE and EtFOSE), bis (perfluorooctyl) phosphinic acid (C8/C8 PFPIA), and 5:3 fluorotelomer carboxylic acid (5:3 acid) between bulk water and suspended particles in water column, and pore water and benthic sediments from a tropical urban water body. The distribution of PFASs between sorbed and dissolved phase was largely dependent on the perfluoroalkyl chain length (N).

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Understanding the sources, occurrence and sinks of perfluoroalkyl and polyfluoroalkyl substances (PFASs) in the urban water cycle is important to protect and utilize local water resources. Concentrations of 22 target PFASs and general water quality parameters were determined monthly for a year in filtered water samples from five tributaries and three sampling stations of an urban water body. Of the 22 target PFASs, 17 PFASs were detected with a frequency >93% including PFCAs: C4-C12 perfluoroalkyl carboxylates, C4, C6, C8, and C10 perfluoroalkane sulfonates, perfluorooctane sulfonamides and perfluorooctane sulfonamide substances (FOSAMs), C10 perfluoroalkyl phosphonic acid (C10 PFPA), 6:2 fluorotelomer sulfonic acid (6:2 FTSA) and C8/C8 perfluoroalkyl phosphinic acid (C8/C8-PFPIA).

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The results of an inter-laboratory comparison exercise to determine cytostatic anticancer drug residues in surface water, hospital wastewater and wastewater treatment plant effluent are reported. To obtain a critical number of participants, an invitation was sent out to potential laboratories identified to have the necessary knowledge and instrumentation. Nine laboratories worldwide confirmed their participation in the exercise.

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The degradation of perfluorochemicals (PFCs) by hydroxyl radical ((·)OH) follows complex pathways resulting in stable products. Kinetic models are needed to predict the product distribution of (·)OH-initiated PFC degradation under environmental and treatment conditions. The bimolecular rate constants were measured in water for the reaction of (·)OH and N-ethyl perfluorooctane sulfonamidoethanol (N-EtFOSE), and intermediates, N-ethyl perfluorooctane sulfonamidoacetate (N-EtFOSAA), N-ethyl perfluorooctane sulfonamide (N-EtFOSA) and perfluorooctane sulfonamidoacetate (FOSAA).

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Direct and indirect (sensitized) photolysis of p-tert-octylphenol (OP), 4-octylphenoxy-acetic acid (OP1EC), and ibuprofen (IBU) were investigated in laboratory water and surface water under simulated and natural sunlight conditions. Photodegradation obeyed apparent-first order kinetics with rates increasing in the presence of NO₂⁻, NO₃⁻, and humic acid (HAC). The bimolecular rate constants, k″, were determined for the reactions of OP and OP1EC with hydroxyl radical (·OH) using photolyzed hydrogen peroxide (H₂O₂) as the hydroxyl radical (·OH) and IBU as the reference compound.

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