Mccurdylundsgaard4737

In comparison to the traditional titration method, the proposed DPD method was more convenient to operate, required less samples and digestion reagents (i.e., KMnO4 and H2SO4) and could be employed for online monitor.The widespread use of triclosan in personal care products as an antimicrobial agent is leading to its alarming tissue-bioaccumulation including human brain. However, knowledge of its potential effects on the vertebrate nervous system is still limited. Here, we hypothesized that sublethal triclosan concentrations are potent enough to alter motor neuron structure and function in zebrafish embryos exposed for prolonged duration. In this study, zebrafish embryos were used as vertebrate-animal model. NPS-2143 purchase Prolonged exposure (up to 4 days) of 0.6 mg/L (LC50, 96 h) and 0.3 mg/L ( less then LC50, Sublethal) triclosan produced aberrations in motor neuron innervations in skeletal muscles and reduced touch-evoked escape response in zebrafish larvae. This suggests motor dysfunction in treated embryos. To further explore the mechanisms of triclosan induced neurotoxicity, we determined the enzyme activity of acetylcholinesterase (AChE) and the expression of acetylcholinesterase (ache), myelin basic protein (mbp) and synapsin IIa (syn2a) genes which play an important role in the neural development and synaptic transmission. The ache and syn2a genes were down-regulated in triclosan treated larvae without any significant changes in mbp gene expression. At functional level, we observed a decrease in the AChE activity. Furthermore, docking results showed that triclosan can form a stable interaction with binding pocket of AChE and perhaps it can compete with natural acetylcholine for direct binding to AChE thereby inhibiting it and affecting cholinergic transmission. Therefore, triclosan can be regarded as a neurotoxic agent even at sublethal concentrations. Overall, the growing toxicological evidence against triclosan including ours suggest caution in its widespread use.Exploration of novel advanced oxidation systems with high efficiency toward radical generation is of significant importance due to the extensive and versatile application of reactive species in the wastewater treatment. Herein we report a simple UV-catalytic homogeneous advanced oxidation system (UV/Fe3+/hydrogen sulfite (BS)), which is capable of generating abundant radicals (e.g., SO3-, SO4-, SO5- and HO) in the aqueous environment. Sulfamethoxazole (SMX) degradation using this system was tested. Results indicated that SMX could be degraded effectively by UV/Fe3+/BS and sulfate radical (SO4-) and hydroxyl radical (HO•) were verified to be presented in this system and be contributive to SMX removal. The acidic pH (4.0) and a low BS/Fe3+ ratio (101) were suitable for SMX degradation. The presence of fulvic acid (FA) and HCO3- strongly inhibited the degradation of SMX, but obvious acceleration was observed in the presence of NO3- due to its contribution on additional radical generation by photosensitization. Based on the detected transformation products through LC-MS analysis, the degradation pathway of SMX by UV/Fe3+/BS was proposed including hydroxylation and bond cleavage.

Perfluoroalkyl substances (PFASs) are a class of manmade chemicals commonly used in consumer product manufacturing. Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are two of the most highly studied PFASs. Both are present in the blood of the most Americans. PFASs are associated with intermediate cardiovascular disease (CVD) outcomes, but their relationship with obesity, a risk factor for intermediate and advanced CVD, remains largely unconfirmed. In this context, we aimed to explore the relationship between PFASs and both overweight/obesity and abdominal obesity among children.

We examine associations between PFOA and PFOS levels, and Body Mass Index (BMI) and waist circumference (WC) in a representative sample (N=2473) of US children, aged 12-18 years from the Centers for Disease Control and Prevention's National Health and Nutrition Examination Survey 1999-2012. Overweight/obesity is defined as age-, sex-specific BMI z-score ≥ 85th percentile; abdominal obesity is defined as age-, sex-specific waist circumference ≥90th percentile.

Associations between PFASs and anthropometric outcomes show a dose-response relationship overall. For overweight/obese BMI z-score, findings indicate OR=1.42 and 95% CI 0.85-2.38 for quartile 2 of PFOA exposure; OR=2.22 (95% CI 1.20-4.13) for quartile 3 of PFOA exposure; and OR=2.73 (95% CI1.10-6.74) for quartile 4 of PFOA exposure.

Findings indicate an association between elevated PFOA and overweight/obesity among children after multivariable adjustment.

Findings indicate an association between elevated PFOA and overweight/obesity among children after multivariable adjustment.Iron sulfide (FeS) is an important scavenger for hexavalent molybdate (Mo(VI)) in an anoxic environment; it plays a crucial role in the mobilization and transformation of Mo(VI), although the underlying reaction mechanisms between Mo(VI) and FeS remain unclear. This study investigates the Mo(VI) reaction kinetics with the amorphous FeS over a pH range 5.0-9.0 and Mo's chemical form on the FeS surface. It is found that the Mo(VI) reaction kinetics with FeS follow a pseudo first-order model, and the reaction rate constant (kobs) increases with a decrease in the pH value. The kobs at pH 5.0 is 0.027 min-1, which is about 38 times higher than that at pH 9.0. The rapid Mo(VI) removal under acidic conditions is due to quick Mo(VI) transformation into stable MoS2 and thiomolybdate (MoVOxSy). The amount of MoS2 formed on the surface of FeS increases with a decrease in the pH value. Under neutral and alkaline conditions, Mo(VI) is not transformed into MoS2 by FeS because the precipitation of iron oxy-hydroxide passivates the active sites of FeS. The study also investigates the effect of the initial dosage of FeS (20-200 mg L-1) and Mo(VI) (10-50 mg L-1) on the reaction kinetics of Mo(VI) with FeS. The results provides important information on the environmental fate of Mo(VI) in the anoxic environment containing amorphous FeS.