Enhancement of UV-assisted TiO2 degradation of ibuprofen using Fenton hybrid process at circumneutral pH

A synergistic UV/TiO2/Fenton (PCF) process is investigated for the degradation of ibuprofen (IBP) at circumneutral pH. The IBP decay in the PCF process is much faster than that with the conventional UV, UV/H2O2, Fenton, photo-Fenton, and photocatalysis processes. The kinetics analysis showed that the IBP decay follows a two-stage pseudo-first order profile, that is, a fast IBP decay (k(1)) followed by a slow decay (k(2)). The effects of various parameters, including initial pH level, dosage of Fenton's reagent and TiO2, wavelength of UV irradiation, and initial IBP concentration, are evaluated. The optimum pH level, [Fe2+](0), [Fe2+](0)/[H2O2](0) molar ratio, and [TiO2](0) are determined to be approximately 4.22, 0.20 mmol/L, 1/40, and 1.0 g/L, respectively. The IBP decay at circumneutral pH (i.e., 6.0-8.0 for wastewater) shows the same IBP decay efficiency as that at the optimum pH of 4.22 after 30 min, which suggests that the PCF process is applicable for the treatment of wastewater in the circumneutral pH range. The lnk(1) and lnk(2) are observed to be linearly correlated to 1/pH(0), [IBP](0), [H2O2](0), [H2O2](0)/[Fe2+](0) and ln[TiO2](0). Mathematical models are therefore derived to predict the IBP decay. (C) 2018, Dalian Institute of Chemical Physics, Chinese Academy of Sciences. Published by Elsevier B.V. All rights reserved

Enhanced photocatalytic degradation of ciprofloxacin over Bi2O3/(BiO)(2)CO3 heterojunctions: Efficiency, kinetics, pathways, mechanisms and toxicity evaluation

In this study, the degradation of antibiotic ciprofloxacin (CIP) over Bi2O3/(BiO)(2)CO3 heterojunctions under simulated solar light irradiation (SSL-Bi2O3/(BiO)(2)CO3) was examined for the first time. The results showed that the Bi2O3/(BiO)(2)CO3 heterojunctions dramatically improved CIP decay efficiency. The effect of parameters showed that the CIP decay was optimized with the Bi2O3/(BiO)(2)CO3 dosage of 0.5 g/L and a wide pH range of 4.0-8.3, based on which, a kinetic model was derived to predict the remaining CIP concentration. It was found that the presence of anions like SO42-, NO3- and HCO3- decelerated the CIP decay, while the co-existence of Cl- accelerated the CIP decay. Six degradation intermediates were identified by ultra-performance liquid chromatography coupled with mass analyzer (UPLC/MS) and ion chromatographic (IC) analysis, and the decay pathways and degradation mechanism of CIP were proposed by combining the experiment data with theoretical calculation of frontier electron densities. Hydroxyl radical's reaction, photo-hole (h(+)) oxidation and reductive defluorination were found to involve in the CIP decay. The efficient alleviation on total organic carbon (TOC) and toxicity indicated that the complete mineralization and de-toxicity are possible by this system with sufficient reaction time

Evidence linking exposure of fish primary macrophages to antibiotics activates the NF-kB pathway.

Low doses of antibiotics are ubiquitous in the marine environment and may exert negative effects on non-target aquatic organisms. Using primary macrophages of common carp, we investigated the mechanisms of action following exposure to several common antibiotics; cefotaxime, enrofloxacin, tetracycline, sulfamonomethoxine, and their mixtures, and explored the immunomodulatory effects associated with the nuclear factor-κB (NF-κB) signaling pathway. A KEGG pathway analysis was conducted using the sixty-six differentially expressed genes found in all treatments, and showed that exposure to 100 μg/L of antibiotics could affect regulation of the NF-κB signaling pathway, suggesting that activation of NF-κB is a common response in all four classes of antibiotics. In addition, the four antibiotics induced nf-κb and NF-κB-associated cytokines expression, as verified by qPCR, however, these induction responses by four antibiotics were minor when compared to the same concentration of LPS treatment (100 μg/L). Antagonists of NF-κB blocked many of the immune effects of the antibiotics, providing evidence that NF-κB pathways mediate the actions of all four antibiotics. Moreover, exposure to environmentally relevant, low levels (0.01-100 μg/L) of antibiotics induced a NF-κB-mediated immune response, including endogenous generation of ROS, activity of antioxidant enzymes, as well as expression of cytokine and apoptosis. Moreover, exposure to mixtures of antibiotics presented greater effects on most tested immunological parameters than exposure to a single antibiotic, suggesting additive effects from multiple antibiotics in the environment. This study demonstrates that exposure of fish primary macrophages to low doses of antibiotics activates the NF-kB pathway

Comparison of Different LGM-Based Methods with MAR and MNAR Dropout Data

The missing not at random (MNAR) mechanism may bias parameter estimates and even distort study results. This study compared the maximum likelihood (ML) selection model based on missing at random (MAR) mechanism and the Diggle–Kenward selection model based on MNAR mechanism for handling missing data through a Monte Carlo simulation study. Four factors were considered, including the missingness mechanism, the dropout rate, the distribution shape (i.e., skewness and kurtosis), and the sample size. The results indicated that: (1) Under the MAR mechanism, the Diggle–Kenward selection model yielded similar estimation results with the ML approach; Under the MNAR mechanism, the results of ML approach were underestimated, especially for the intercept mean and intercept slope (μi and μs). (2) Under the MAR mechanism, the 95% CP of the Diggle–Kenward selection model was lower than that of the ML method; Under the MNAR mechanism, the 95% CP for the two methods were both under the desired level of 95%, but the Diggle–Kenward selection model yielded much higher coverage probabilities than the ML method. (3) The Diggle–Kenward selection model was easier to be influenced by the non-normal degree of target variable's distribution than the ML approach. The level of dropout rate was the major factor affecting the parameter estimation precision, and the dropout rate-induced difference of two methods can be ignored only when the dropout rate falls below 10%

Effects of a particular heptapeptide on the IFN-α-sensitive CML cells

Abstract: Using the phage display biopanning technique, we have previously identified a heptapeptide KLWVIPQ which specifically bind to the surface of the IFN-α sensitive but not the IFN-α-resistant CML cells. The effects of this heptapeptide to the IFN-α-sensitive CML cells were investigated in the present study. IFN-α-sensitive KT-1/A3 and IFN-α-resistant KT-1/A3R CML cells were transfected by pEGFP KLWVIPQ expression vector and/or induced by IFN-α. WST-1 cell proliferation assay, flow cytometry and western blotting were performed to determine the effects of this heptapeptide and/or IFN-α on CML cells. The viability of the KT-1/A3 cells w as inhibited and apoptosis was induced by either expression of the heptapeptide KLWVIPQ or IFN-α treatment with concurrent up-regulation of P53 and down-regulation of P210bcr/abl. However, these effects were not observed in the IFN-α-resistant KT-1/A3R cells. These results suggest that the heptapeptide KLWVIPQ shares a similar mechanism w ith IFN-α in the regulat ion of CML cell growth and apoptosis, implying that the heptapeptide KLWVIPQ could be a novel target to go further into mechanisms of IFN-α sensitivity and/or resistance in CML

Cocaine- and amphetamine-regulated transcript promotes the differentiation of mouse bone marrow-derived mesenchymal stem cells into neural cells

<p>Abstract</p> <p>Background</p> <p>Neural tissue has limited potential to self-renew after neurological damage. Cell therapy using BM-MSCs (bone marrow mesenchymal stromal cells) seems like a promising approach for the treatment of neurological diseases. However, the neural differentiation of stem cells influenced by massive factors and interactions is not well studied at present.</p> <p>Results</p> <p>In this work, we isolated and identified MSCs from mouse bone marrow. Co-cultured with CART (0.4 nM) for six days, BM-MSCs were differentiated into neuron-like cells by the observation of optical microscopy. Immunofluorescence demonstrated that the differentiated BM-MSCs expressed neural specific markers including MAP-2, Nestin, NeuN and GFAP. In addition, NeuN positive cells could co-localize with TH or ChAT by double-labled immunofluorescence and Nissl bodies were found in several differentiated cells by Nissl stain. Furthermore, BDNF and NGF were increased by CART using RT-PCR.</p> <p>Conclusion</p> <p>This study demonstrated that CART could promote the differentiation of BM-MSCs into neural cells through increasing neurofactors, including BNDF and NGF. Combined application of CART and BM-MSCs may be a promising cell-based therapy for neurological diseases.</p