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Ultraviolet (UV)/chlorine draws increasing attention for the abatement of recalcitrant organic pollutants. Herein, it was found that TiO2 would significantly promote the degradation of dimethyl phthalate (DMP) in the UV/chlorine system (from 19 to 84%). Hydroxyl radicals (HO•) and chlorine radicals (Cl•) were the dominant reactive species for DMP degradation in the UV/chlorine/TiO2 system. Chlorine decayed much faster in UV/chlorine/TiO2 compared with UV/chlorine, which is possibly because photogenerated electrons (ecb-) and superoxide radicals (O2•-) have high reactivity with chlorine. As a result, the recombination of photogenerated holes (hvb+) and ecb- was inhibited and the accumulation of HO• and Cl• was facilitated. A kinetic model was established to simulate the reaction process, and it was found that the concentrations of HO• and Cl• were several times to dozens of times higher in UV/chlorine/TiO2 than that in UV/chlorine. The contributions of HO• and Cl• to DMP degradation were 70.3 and 29.7% by model simulation, respectively, and were close to the probe experiment result. In the UV/chlorine/TiO2 system, the degradation of DMP did not follow pseudo-first-order kinetics but the degradation of benzoate fitted well with pseudo-first-order kinetics. This phenomenon was elucidated by the structure of the pollutant and TiO2 and further tested by calculating the adsorption energy (Eads)/binding energy (Eb) with density functional theory. Due to faster decay of chlorine, lower amounts of disinfection byproducts formed in UV/chlorine/TiO2 compared with UV/chlorine. Adding TiO2 into the UV/chlorine system can promote the degradation of recalcitrant organic pollutants in an aqueous environment.

Colorectal cancer has high morbidity and mortality worldwide, especially in western countries; the incidence of colorectal cancer has been high, which is closely related to the high intake of red meat; and the N-glycolylneuraminic acid (Neu5Gc) is responsible for red meat-induced colorectal cancer. A large number of previous studies have suggested that exogenous Neu5Gc-activated inflammation induced the occurrence of colorectal cancer. However, it has not been known whether the Neu5Gc has a direct inducing effect on colorectal cancer. In this study, we found that Neu5Gc promoted the proliferation of colorectal cancer cells and normal intestinal epithelial cells, and further screened out 98 Neu5Gc targets related to the occurrence and development of colorectal cancer by network pharmacology. Subsequently, GO and KEGG enrichment analyses of these targets revealed that mainly enriched in the PI3K-Akt signaling pathway. Then, we selected SRC, HRAS, CDK2, CCNA2, and AKT2 as core targets based on the phenomena of the previous experiments and the available literature reports, and then we used AutoDock for molecular docking with Neu5Gc; the results found that these five genes could bind to Neu5Gc stably. In vitro experiments showed that the mRNA levels of SRC, HRAS, AKT2, CDK2, and CCNA2 were upregulated and the protein levels of HRAS, AKT2, and CCNA2 were enhanced in FHC and SW620 cells after Neu5Gc (100 ng/mL) treatment. In conclusion, this study revealed that Neu5Gc probably acted as a carcinogen that stimulates the expression of proto-oncogene HRAS and the PI3K-Akt pathway and accelerated cell cycle progression. These findings revealed a novel mechanism that Neu5Gc promoted the occurrence and development of colorectal cancer.

Hydroxylamine (NH

Ultraviolet (UV)/chlorine draws increasing attention for the abatement of recalcitrant organic pollutants. Herein, it was found that TiO

Though hydroxylamine (NH

Co-existing of arsenate (As(V)) and arsenite (As(III)) in aquatic environment have posed a great threat to humans due to the high mobility and toxicity. Developing practical methods for the removal of arsenic contamination in water source is vital for improving human wellbeing. Here, a novel nanostructured Fe-Ti-Mn composite oxide (FTMO) for the efficient removal of arsenic was synthesized using a simultaneous oxidation and co-precipitation method. The adsorbent was amorphous or poorly crystallized and was aggregated from heterogeneous nano-sized particles, with a high specific surface area of 434.3 m2/g. Batch experimental results showed that the FTMO effectively removed both As(V) and As(III), and the maximal adsorption capacities of arsenic species at 25 °C were 74.4 mg/g (As(V)) and 122.3 mg/g (As(III)), respectively. The arsenic removal process was endothermic and spontaneous, and the uptake of arsenic was highly pH-dependent. The inhibitive influence of competitive substances on the adsorption behavior followed by the order of: SO42−

Hydroxylamine is commonly known to enhance the performance of Fe(II)-based advanced oxidation processes (AOPs) by promoting Fe(II) regeneration from Fe(III). Recently, ferryl ion (Fe(IV)) was found as an important reactive specie in Fe(II)/peroxydisulfate (PDS) system, while the interaction between hydroxylamine and Fe(IV) in Fe(II)/hydroxylamine/PDS system was still ambiguous. Therefore, the role of hydroxylamine, especially in interaction with reactive species, was systematically studied therein. With methyl phenyl sulfoxide (PMSO) as a probe compound, an original function of hydroxylamine to transform the major reactive species from Fe(IV) to radicals (SO4 - and OH) for potential pollutants oxidation was clarified. Experimental results combined with Density Functional Theory (DFT) calculations showed that SO4 -, OH and Fe(IV) all contributed to PMSO oxidation. Hydroxylamine showed the greatest promotional effect on the production of SO4 -, while the production of Fe(IV) was inhibited with concentrations of hydroxylamine increasing from 0.2 to 1.4 mM. Compared with PMSO, hydroxylamine showed stronger scavenging ability towards Fe(IV) than SO4 - and OH. Thus, more than 50% of radicals was consumed by PMSO and Fe(IV) mainly reacted with hydroxylamine to regenerate Fe(II). In a word, hydroxylamine played a dual role during potential pollutants oxidation in Fe(II)/hydroxylamine/PDS system, namely (1) transforming the major reactive species from Fe(IV) to radials (SO4 - and OH) and (2) regenerating Fe(II) from both Fe(IV) and Fe(III). This study provides an insight into the role of hydroxylamine and its interactions with Fe(IV), which advances our understanding on similar Fe(II)/reductants/PDS systems.

Hydroxylamine showed an outstanding performance on enhancing the oxidation of pollutants in Fe(II) involved advanced oxidation processes, while the detailed reaction schemes have not been fully revealed. Specific functions of hydroxylamine in the oxidation of benzoic acid with Fe(II)/persulfate (PDS) system were explored. With the addition of hydroxylamine, degradation kinetics of benzoic acid deviated from both two-stage kinetics and pseudo first order kinetics, but could be interpreted well with binomial regression analysis. Degradation rate constant (kobs) of benzoic acid was calculated and showed the same variation trend with [hydroxylamine][Fe(III)]2/([Fe(II)][H+])2, the value of which was changed during reaction processes. A detailed kinetic model for simulating the degradation profile of benzoic acid with hydroxylamine acceleration was proposed for the first time and indicated that interactions of hydroxylamine and Fe(III) were fast equilibrium reactions, which was a dominant factor influencing the oxidation kinetics of benzoic acid in Fe(II)/hydroxylamine/PDS system. Comparative study showed that when 1.4 mM of ascorbic acid was added into Fe(II)/PDS system, degradation kinetics of benzoic acid was similar to that enhanced by hydroxylamine. However, when 0.6 mM or 1.0 mM of ascorbic acid was added, oxidation kinetics still presented as the two-stage profile. Kinetic simulations indicated that Fe(II) was produced slower from Fe(III)-ascorbic acid complexes than that with hydroxylamine, which caused the difference in oxidation kinetics. This study could improve our understanding about the effect of hydroxylamine and other reductants in promoting pollutants elimination in Fe(II)/PDS system.

Though hydroxylamine (NH2OH) is effective for accelerating pollutants degradation in Fenton and Fenton-like systems, the effect of anions simultaneously introduced by the hydroxylamine salts have always been ignored. Herein, effect of two commonly used hydroxylamine salts, hydroxylamine hydrochloride (NH2OH·HCl) and hydroxylamine sulfate [(NH2OH)2·H2SO4], for the degradation of dimethyl phthalate (DMP) in peroxymonosulfate (PMS)/Fe(II) system was comparatively investigated. Degradation efficiency of DMP with NH2OH·HCl was 1.6 times of that with same dosages of (NH2OH)2·H2SO4. SO4·−, Fe(IV) and ·OH formed in the PMS/Fe(II)/NH2OH system, but ·OH was the major species for DMP degradation. Addition of Cl− significantly improved the production of ·OH and Cl·, and the exposure dose of ·OH (CT·OH) was more than 10 times that of CTCl· as the concentration of Cl− increased to 1 mM. Calculations based on branching ratios of Cl· and ·OH indicated that the reactions of Cl− with SO4·− and Cl· with H2O were not the only production sources of ·OH in the system. Further experiments with methyl phenyl sulfoxide (PMSO) as the probe indicated that Cl− would facilitate the shift of reactive species from Fe(IV) to radicals (SO4·− or ·OH) in the system. Both hydroxylation and nitration intermediate products were detected in the oxidation of DMP. Cl− promoted the formation of hydroxylation intermediates and reduced the formation of nitration intermediates. This study revealed for the first time that Cl− could shift reactive species from Fe(IV) to radicals in PMS/Fe(II) system, raising attention to the influence of the coexisting anions (especially Cl−) for pollutants oxidation in iron-related oxidation processes.

There are a series problems that are caused by the complex geological and various types of foundation soil of the canal during the excavation process in the first stage of the South-to-North Water Transfer Project, such as the different strength of the same rock, especially the undulating boundary of the rocks and the varying buried depth. The author made a detail research on the spatial distribution of the basic rocks and the calculation for the volume of the excavation to save the problems and calculate the excavation volume of the rocks with different strength, also the cross and vertical method were used to provide the necessary technology data and a technology support for planning and programming of project construction.

The gene of human neurotrophin-3 (hNT3), a 380 bp fragment corresponding to a 14 kDa protein, was amplified by PCR with genome DNA of human whole blood as the template and cloned into a vector pTXB1. The recombinant including the hNT3 gene was expressed in E. coli and the target product was in the form of inclusion bodies. After denaturation and renaturation, the hNT3 was purified on an affinity column by a self-cleaving intein. The bioactivity assay showed that the purified hNT3 induced profuse neurite outgrowth from the dorsal root ganglia (DRG) explants.

Bone marrow-derived mesenchymal stem cells (MSCs) have emerged as attractive candidates for cellular therapies for heart and other organ-system disorders. However, a major dilemma in stem cell therapy for ischemic heart diseases is the low survival of transplanted cells in the ischemic and peri-infarcted region. In this study, MSCs were treated by hypoxia and serum deprivation (H/SD) to mimic the ischemic microenvironment of infarcted hearts where MSCs were transplanted. The effects of proteasome inhibitor MG-132 on H/SD-induced apoptosis and paracrine effects were investigated. Apoptosis of MSCs was detected by Annexin V-FITC flow cytometric analysis. Transcriptional levels of IL-1β, TNF-α and IL-10 were examined by real-time PCR. The nuclear translocation of NF-κBp65 was assessed by immunocytochemical staining. Translational changes of IL-1β and TNF-α were detected by Western blot. The secretion of IL-10 from MSCs was examined by ELISA assay. The results showed that MG-132 could effectively suppress H/SD-induced MSCs apoptosis. Furthermore, the induced IL-1β and TNF-α transcription was also inhibited by MG-132 treatment, which may be due to the inhibition of NF-κBp65 nuclear translocation by MG-132. Importantly, MG-132 effectively enhanced H/SD-induced transcription and secretion of IL-10, which is an important paracrine factor from MSCs. Our findings suggest that pretreatment of MSCs by MG-132 before cell transplantation may be an effective strategy to improve cell survival and enhance paracrine effects of MSCs.

Autotaxin (ATX), a member of nucleotide pyrophosphatase/phosphodiesterase (NPP) family, is also named as phosphodiesterase Iα (PD-Iα) or NPP2. ATX is the unique member among the NPPs that can function as a lysophospholipase D (lysoPLD), converting lysophosphatidylcholine into lysophosphatidic acid (LPA). LPA acts on specific G-protein-coupled receptors to elicit a wide range of cellular response, including cell proliferation, cell migration and cell contraction, etc. As the major LPA-producing phospholipase, many ATX's features and functions are dependent on the production of LPA. ATX and LPA together form the ATX-LPA functional axis. The present review summarizes the current progress in function and biological activities of ATX-LPA axis.