Removal of N-nitrosopyrrolidine from GAC by a three-dimensional electrochemical reactor: degradation mechanism and degradation path.

Nitrogen-containing disinfection by-products (N-DBPs) produced in the process of drinking water disinfection are widely concerning due to the high cytotoxicity and genotoxicity. It is due to the difficulty of natural degradation of N-DBPs in water and the fact that conventional treatment systems do not effectively treat N-DBPs in drinking water. In this study, N-nitrosopyrrolidine (NPYR) in water was electrocatalytically degraded by a three-dimensional electrode reactor (3DER). This system applied graphite plates as anode and cathode. The granular activated carbon (GAC) was used as third electrode. The degradation of NPYR using a continuous flow three-dimensional electrode reactor was investigated by examining the effects of flow rate, current density, electrolyte concentration, and pollutant concentration on the degradation efficiency, energy consumption, and reaction kinetics of GAC particle electrodes. The results showed that the optimal operating conditions were flow rate = 0.45 mL/min, current density = 6 mA/cm2, Na2SO4 concentration = 0.28 mol/L, and NPYR concentration = 20 mg/L. Under optimal conditions, the degradation of NPYR exceeded 58.84%. The main contributor of indirect oxidation was deduced from free radical quenching experiments. NPYR concentration was measured by GC-MS with DB-5 capillary column, operating in full scan monitoring mode for appropriate quantification of NPYR and intermediates. Based on the identification of reaction intermediates, a possible pathway for the electrochemical oxidation of NPYR on GAC particle electrodes was proposed.

Theoretical Investigation of Ru(II) Complexes with Long Lifetime and a Large Two-Photon Absorption Cross-Section in Photodynamic Therapy.

Two-photon photodynamic therapy (TP-PDT), as a new method for cancer, has shown unique advantages in tumors. A low two-photon absorption cross-section (δ) in the biologic spectral window and a short triplet state lifetime are the important issues faced by the current photosensitizers (PSs) in TP-PDT. In this paper, the photophysical properties of a series of Ru(II) complexes were studied by density functional theory and time-dependent density functional theory methods. The electronic structure, one- and two-photon absorption properties, type I/II mechanisms, triplet state lifetime, and solvation free energy were calculated. The results showed that the substitution of methoxyls by pyrene groups greatly improved the lifetime of the complex. Furthermore, the addition of acetylenyl groups subtly enhanced δ. Overall, complex 3b possess a large δ(1376 GM), a long lifetime (136 µs), and better solvation free energy. It is hoped that it can provide valuable theoretical guidance for the design and synthesis of efficient two-photon PSs in the experiment.

Aqueous rechargeable ammonium ion batteries based on MoS2/MXene with a ball-flower morphology as an anode and NH4V4O10 with a layered structure as a cathode.

Due to the small hydrated ionic radius and light molar mass of ammonium ions, aqueous ammonium ion batteries attract much attention, providing high security, environmental friendliness and low cost. However, the lack of suitable electrode materials with high specific capacity is a big challenge for practical application. Therefore, in view of this problem, we fabricated an anode applying a MoS2 material with a ball-flower morphology anchored to MXene nanoflakes, and it shows excellent rate capability in a novel aqueous ammonium ion battery. The corresponding charge capacities of composite electrodes are 279.2, 204.4, 173.2, 118.7, and 80.5 mA h g-1 at 20, 50, 100, 200, and 500 mA g-1, respectively. Meanwhile, polyvanadate was selected as a cathode material for a full aqueous ammonium ion battery, and interestingly it was discovered that the size of this material decreases with increasing synthesis temperature. The discharge capacities of NH4V4O10 electrodes fabricated at 140 °C, 160 °C, and 180 °C at 50 mA g-1 are 88.6, 125.1 and 155.5 mA h g-1, respectively. Furthermore, we also explore the corresponding electrochemical mechanism using XRD and XPS. A full aqueous ammonium ion battery based on both electrodes shows superior ammonium ion storage properties and provides new ideas for the development of this strategy.

Insight into micropollutant abatement during ultraviolet light-emitting diode combined electrochemical process: Reaction mechanism, contributions of reactive species and degradation routes.

Electrochemical process coupling with ultraviolet light-emitting diode for micropollutant abatement was evaluated in the treatment of wastewater containing Cl-. Four representative micropollutants, atrazine, primidone, ibuprofen and carbamazepine, were selected as target compounds. The impacts of operating conditions and water matrix on micropollutant degradation were investigated. Fluorescence excitation-emission matrix spectroscopy spectra and high performance size exclusion chromatography were employed to characterize the transformation of effluent organic matter in treatment. The degradation efficiencies of atrazine, primidone, ibuprofen and carbamazepine are 83.6 %, 80.6 %, 68.7 % and 99.8 % after 15 min treatment, respectively. The increment of current, Cl- concentration and ultraviolet irradiance promote the micropollutant degradation. However, the presence of bicarbonate and humic acid inhibit micropollutant degradation. The mechanism of micropollutant abatement was elaborated based on reactive species contributions, density functional theory calculation and degradation routes. Free radicals (HO•, Cl•, ClO• and Cl2•-) could be generated by chlorine photolysis and subsequent propagation reactions. The concentrations of HO• and Cl• are 1.14 × 10-13 M and 2.0 × 10-14 M in optimal condition, respectively, and the total contributions of HO• and Cl• for the degradation of atrazine, primidone, ibuprofen and carbamazepine are 24 %, 48 %, 70 % and 43 %, respectively. The degradation routes of four micropollutants are elucidated based on intermediate identification, Fukui function and frontier orbital theory. Micropollutants can be effectively degraded in actual wastewater effluent, and the small molecule compound proportion increases during effluent organic matter evolution. Compared with photolysis and electrolysis, the coupling of the two processes has potential for energy saving in micropollutant degradation, which shed light on the prospects of ultraviolet light-emitting diode coupling with electrochemical process for effluent treatment.

Circ_0001103 alleviates IL-1ß-induced chondrocyte cell injuries by upregulating SIRT1 via targeting miR-375.

BACKGROUND: Osteoarthritis (OA) is a common inflammatory disease characterized by articular cartilage degeneration and injury. Circular RNAs (circRNAs) are widely involved in the development of human diseases, including OA. The objective of this study was to investigate the function and functional mechanism of circ_0001103 in OA. METHODS: Cell model of OA was established by treating chondrocytes with interleukin-1ß (IL-1ß). The expression of circ_0001103, miR-375 and sirtuin 1 (SIRT1) mRNA was measured using quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was assessed using cell counting kit-8 (CCK-8) assay. Cell apoptosis was determined using flow cytometry assay. The expression levels of inflammatory factors were quantified by qRT-PCR. The expression of extracellular matrix (ECM) metabolism-related markers, including Collagen Type II Alpha 1 Chain (COL2A1) and A disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS4), was detected by western blot. Predicted target relationship between miR-375 and circ_0001103 or SIRT1 by the bioinformatics tools was validated by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: Circ_0001103 was downregulated in OA tissues and IL-1ß-induced chondrocytes. Overexpression of circ_0001103 attenuated IL-1ß-induced chondrocyte apoptosis, inflammatory responses and ECM degradation. MiR-375 was targeted by circ_0001103, and miR-375 could bind to SIRT1. Circ_0001103 overexpression increased the expression of SIRT1 by suppressing miR-375. Rescue experiments suggested that miR-375 restoration reversed the effects of circ_0001103 overexpression, and SIRT1 knockdown overturned the effects of miR-375 inhibition. CONCLUSION: Circ_0001103 governed the miR-375/SIRT1 axis to ameliorate IL-1ß-induced chondrocyte injuries, implying that circ_0001103 was a promising biomarker in OA pathogenesis.

Identification of microRNA­363­3p as an essential regulator of chondrocyte apoptosis in osteoarthritis by targeting NRF1 through the p53­signaling pathway.

Osteoarthritis (OA) is a degenerative joint disease that affects the physical, and mental health of middle­aged and elderly people. The aims of the present study were to determine the biological function and molecular mechanisms of miR­363­3p in chondrocyte apoptosis. Exploration of the molecular mechanisms of OA may be helpful in the understand of the causes, and facilitating the prevention and treatment of OA. In the present study, the expression of nuclear respiratory factor1 (NRF1) was downregulated in the articular cartilage of OA rats in vivo and lipopolysaccharide (LPS)­treated chondrocytes in vitro. MicroRNAs (miRNA) are regulators of gene expression in the progression of OA. TargetScan software was used to predict that NRF1 was a potential target for miRNA (miR)­363, and this was confirmed in subsequent experiments. The expression of miR­363­3p was negatively correlated with the expression of NRF1, and its expression was significantly upregulated in OA model rats and in LPS­induced chondrocytes compared with the expression in the respective controls. In addition, the overexpression of miR­363­3p increased the levels of interleukin (IL)­1ß, IL­6 and tumor necrosis factor­α in vivo, and was demonstrated to promote chondrocyte injury and apoptosis by Safranin O staining and TUNEL. Moreover, the inhibition of miR­363­3p expression increased the expression of NRF1 and protected chondrocytes from apoptosis in vitro and in vivo, whereas the overexpression of miR­363­3p downregulated NRF1 expression and promoted LPS­induced chondrocyte apoptosis through the p53 pathway in vitro. The results of this study suggested that miR­363­3p­mediated inhibition of NRF1may be associated with chondrocyte apoptosis in OA.

Artifact correction in low-dose dental CT imaging using Wasserstein generative adversarial networks.

PURPOSE: In recent years, health risks concerning high-dose x-ray radiation have become a major concern in dental computed tomography (CT) examinations. Therefore, adopting low-dose computed tomography (LDCT) technology has become a major focus in the CT imaging field. One of these LDCT technologies is downsampling data acquisition during low-dose x-ray imaging processes. However, reducing the radiation dose can adversely affect CT image quality by introducing noise and artifacts in the resultant image that can compromise diagnostic information. In this paper, we propose an artifact correction method for downsampling CT reconstruction based on deep learning. METHOD: We used clinical dental CT data with low-dose artifacts reconstructed by conventional filtered back projection (FBP) as inputs to a deep neural network and corresponding high-quality labeled normal-dose CT data during training. We trained a generative adversarial network (GAN) with Wasserstein distance (WGAN) and mean squared error (MSE) loss, called m-WGAN, to remove artifacts and obtain high-quality CT dental images in a clinical dental CT examination environment. RESULTS: The experimental results confirmed that the proposed algorithm effectively removes low-dose artifacts from dental CT scans. In addition, we showed that the proposed method is efficient for removing noise from low-dose CT scan images compared to existing approaches. We compared the performances of the general GAN, convolutional neural networks, and m-WGAN. Through quantitative and qualitative analysis of the results, we concluded that the proposed m-WGAN method resulted in better artifact correction performance preserving the texture in dental CT scanning. CONCLUSIONS: The image quality evaluation metrics indicated that the proposed method effectively improves image quality when used as a postprocessing technique for dental CT images. To the best of our knowledge, this work is the first deep learning architecture used with a commercial cone-beam dental CT scanner. The artifact correction performance was rigorously evaluated and demonstrated to be effective. Therefore, we believe that the proposed algorithm represents a new direction in the research area of low-dose dental CT artifact correction.

CXCL12/CXCR4 axis induces proliferation and invasion in human endometrial cancer.

OBJECTIVE: Since that we have previously found CXCL12/CXCR4, an important biological axis is highly transcribed in several cancer cells. We aim to investigate whether CXCL12/CXCR4 axis regulates critical processes in neoplastic transformation that affects endometrial cancer cell biology. METHODS: The expression levels of CXCR4 were analyzed in human normal endometrial tissue, simple hyperplasia, atypical hyperplasia and endometrial cancer cells by immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR). Serum CXCL12 was measured by Enzyme-Linked Immunosorbent Assay (ELISA) in Ishikawa endometrial cancer cell line. To study the biological function of CXCL12/CXCR4 in endometrial cancer, short interfering RNA silencing of CXCR4 was established to analyze the roles of CXCL12/CXCR4 in proliferation, migration, invasion and apoptosis of Ishikawa cells in vitro. RESULTS: The expression level of CXCR4 in endometrial cancer tissue was higher as compared to atypical hyperplasia, simple hyperplasia and normal cycling endometrium cells. Ishikawa cells secreted CXCL12 spontaneously and continuously for 96 hrs in culture. The proliferation, migration and invasion of Ishikawa cells was significantly induced, and the apoptosis was significantly reduced by CXCL12 in combination with CXCR4. Moreover, CXCR4 silencing could significantly antagonize all these functions. CONCLUSIONS: CXCL12/CXCR4 axis plays an important role in the proliferation, invasion and metastasis of endometrial cancer, indicating that CXCR4 could be the target for the treatment of endometrial cancer.

Inhibition of CXCR4 and CXCR7 for reduction of cell proliferation and invasion in human endometrial cancer.

As one of the most common malignant cancers in female reproductive tract, endometrial cancer accounts for 20-30 % of the most frequent gynecological malignancy, which is originated from endometrial epithelial. The molecular mechanisms for the generation of endometrial cancer are up to now unclear, hindering the development of corresponding therapy. CXCR4 and CXCR7 were receptors of CXCL12 chemokine ligand, which could regulate critical procedures of neoplastic transformation, including proliferation, invasion, and apoptosis of the cells. The messenger RNA (mRNA) and protein expression levels of CXCR4 and CXCR7 in human endometrial adenocarcinoma cancer, as well as in Ishikawa and HEC-1-A cell line, were analyzed by using reverse-transcription polymerase chain reaction (RT-PCR) and Western blotting. In order to explore the biological function of CXCR4 and CXCR7 in endometrial tumor, small interference RNAs of CXCR4 and CXCR7 fragments were designed, synthesized, and transfected into Ishikawa and HEC-1-A by using Lipofectamine2000. The influence of RNA interference (RNAi)-mediated silencing CXCR4 and CXCR7 on the cell proliferation was investigated under CCK-8. The invasion assay was performed transwell, and cell apoptosis was tested by FCM. Higher mRNA and protein expression levels of CXCR4 and CXCR7 were investigated in endometrial adenocarcinomas. The expression levels of CXCR4 and CXCR7 could be inhibited by RNA interference, reducing the cell proliferation, invasion in Ishikawa and HEC-1-A cells. In this study, we also observed that treated with CXCR4 and CXCR7 small interfering RNA (siRNA) arrested cells in S phase. CXCL12/CXCR4 and CXCL12/CXCR7 receptor ligand systems affect the invasion of endometrial carcinoma cell line into Ishikawa and HEC-1-A. CXCR4 and CXCR7 were silenced by RNAi, which can inhibit the invasion of Ishikawa and HEC-1-A cell lines. Hence, CXCR4 and CXCR7 are expected to become two target genes for the treatment of endometrial carcinoma.