Visible Light Photoactivity of g-C3N4/MoS2 Nanocomposites for Water Remediation of Hexavalent Chromium.

Water pollution has becoming an increasingly serious issue, and it has attracted a significant amount of attention from scholars. Here, in order remove heavy metal hexavalent chromium (Cr (VI)) from wastewater, graphitic carbon nitride (g-C3N4) was modified with molybdenum disulfide (MoS2) at different mass ratios via an ultrasonic method to synthesize g-C3N4/MoS2 (CNM) nanocomposites as photocatalysts. The nanocomposites displayed efficient photocatalytic removal of toxic hexavalent chromium (Cr (VI)) from water under UV, solar, and visible light irradiation. The CNM composite with a 1:2 g-C3N4 to MoS2 ratio achieved optimal 91% Cr (VI) removal efficiency at an initial 20 mg/L Cr (VI) concentration and pH 3 after 120 min visible light irradiation. The results showed a high pH range and good recycling stability. The g-C3N4/MoS2 nanocomposites exhibited higher performance compared to pure g-C3N4 due to the narrowed band gap of the Z-scheme heterojunction structure and effective separation of photo-generated electron-hole pairs, as evidenced by structural and optical characterization. Overall, the ultrasonic synthesis of g-C3N4/MoS2 photocatalysts shows promise as an efficient technique for enhancing heavy metal wastewater remediation under solar and visible light.

Simultaneous catalytic oxidation of elemental mercury and arsine over CeO2(111) surface: a density functional theory study.

Ceria (CeO2)-based materials are potential catalysts for the removal of the Hg0 and AsH3 present in reducing atmospheres. However, theoretical studies investigating the Hg0 and AsH3 removal capacity of ceria remain limited. In this study, the adsorption behavior and mechanistic pathways for the catalytic oxidation of Hg0 and AsH3 on the CeO2(111) surface, including the calculation of optimized adsorption configurations and energies, were investigated using density functional theory calculations. The results suggest that Hg0 and AsH3 are favorably adsorbed on the CeO2(111) surface, whereas CO is not, which is crucial for selective removal when CO is a desirable gas component. Furthermore, AsH3 is adsorbed more favorably than Hg0. In addition, the calculations revealed that the Hg atom is initially adsorbed on the surface and then oxidized by lattice oxygen to form HgO. Concerning AsH3 decomposition, the stepwise dehydrogenation of AsH3 followed by bonding with lattice O atoms to form the As-O bond seems the most plausible. Finally, the adsorbed As-O bond is further forms elemental As and As2O3. Therefore, CeO2 can adsorb and remove Hg0 and AsH3, making it a promising catalyst for the simultaneous catalytic oxidation of Hg0 and AsH3 in strongly reducing off-gas.

MiRNA-29a serves as a promising diagnostic biomarker in children with temporal lobe epilepsy and regulates seizure-induced cell death and inflammation in hippocampal neurons.

Temporal lobe epilepsy (TLE) in children is one of the most common refractory epilepsies. MicroRNAs (miRNAs) show abnormal expression in neurological disorders. The objective of this study was to determine changes in expression and the role of miR-29a in children with TLE. Sixty-five TLE patients and 70 normal controls were recruited. The levels of miR-29a were quantified using qRT-PCR. An in vitro TLE cell model was established using primary hippocampal cells cultured in magnesium-free medium. Cell viability, cell apoptosis and inflammatory cytokine concentrations were evaluated. The luciferase reporter assay was applied to confirm the target gene, HMGB1. A low level of MiR-29a expression was observed in the serum of children with TLE, which demonstrated a negative association with the concentration of serum TNF-α, IL-6, and IFN-γ. The level of MiR-29a demonstrated high specificity and sensitivity in children with TLE. A low level of expression of miR-29a was also detected in the TLE cell model. MiR-29a over-expression reversed the decreased cell viability induced by TLE, and alleviated cell apoptosis. Release of TNF-α, IL-6, and IFN-γ induced by TLE was also inhibited by miR-29a over-expression. HMGB1, which was downregulated in the serum of TLE patients, was shown to be a target gene of miR-29a, and negatively correlated with miR-29a level. The downregulation of serum miR-29a may serve as a non-invasive diagnostic biomarker for children with TLE. MiR-29a may be involved in the pathogenesis of TLE through regulation of neuronal apoptosis and neuroinflammation via targeting HMGB1.

Low miR-192 expression predicts poor prognosis in pediatric acute myeloid leukemia.

BACKGROUND: Abnormal expression of miR-192 has been observed in a variety of human cancers, but the expression pattern of miR-192 and its prognostic value in pediatric acute myeloid leukemia (AML) is poorly known. OBJECTIVE: This study was to explore the expression status of miR-192 and its clinical significance in pediatric patients with AML. METHODS: Quantitative RT-PCR was carried out to detect miR-192 expression level in the serum from 97 AML cases and 50 healthy controls. RESULTS: The results showed that downregulation of serum miR-192 was observed in pediatric AML patients and strongly correlated with aggressive clinical features. Increased serum miR-192 expression occurred more frequently in the AML subjects with favorable risk cytogenetics. Moreover, serum miR-192 expression showed good performance to screen pediatric AML subjects from normal controls. Furthermore, serum miR-192 was identified as a independent prognostic indicator for both overall survival and event free survival. In addition, low serum miR-192 expression significantly contributed to poor prognosis in the whole cohort of AML patients or the AML patients with intermediate-risk cytogenetics. CONCLUSIONS: Collectively, serum miR-192 potentially can be a reliable biomarker for the diagnosis and prognosis in pediatric AML.

Knockdown of Annexin A1 Enhances Radioresistance and Inhibits Apoptosis in Nasopharyngeal Carcinoma.

Radiotherapy is the primary treatment for nasopharyngeal carcinoma while radioresistance can hinder efficient treatment. To explore the role of annexin A1 and its potential mechanisms in radioresistance of nasopharyngeal carcinoma, human nasopharyngeal carcinoma cell line CNE2-sh annexin A1 (knockdown of annexin A1) and the control cell line CNE2-pLKO.1 were constituted and CNE2-sh annexin A1 xenograft mouse model was generated. The effect of annexin A1 knockdown on the growth of xenograft tumor after irradiation and radiation-induced DNA damage and repair was analyzed. The results of immunohistochemistry assays and Western blotting showed that the level of annexin A1 was significantly downregulated in the radioresistant nasopharyngeal carcinoma tissues or cell line compared to the radiosensitive nasopharyngeal carcinoma tissues or cell line. Knockdown of annexin A1 significantly promoted CNE2-sh annexin A1 xenograft tumor growth compared to the control groups after irradiation. Moreover, the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assays revealed that knockdown of annexin A1 significantly inhibited apoptosis in vivo compared to the control groups. We assessed the intracellular reactive oxygen species levels and the extent of radiation-induced DNA damage and repair using reactive oxygen species assay, comet assays, and immunohistochemistry assay. The results showed that knockdown of annexin A1 remarkedly reduced the intracellular reactive oxygen species levels, level of DNA double-strand breaks, and the phosphorylation level of H2AX and increased the accumulation of DNA-dependent protein kinase in nasopharyngeal carcinoma cells after irradiation. The findings suggest that knockdown of annexin A1 inhibits DNA damage via decreasing the generation of intracellular reactive oxygen species and the formation of γ-H2AX and promotes DNA repair via increasing DNA-dependent protein kinase activity and therefore improves the radioresistance in nasopharyngeal carcinoma cells. Together, our findings suggest that knockdown of annexin A1 promotes radioresistance in nasopharyngeal carcinoma and provides insights into therapeutic targets for nasopharyngeal carcinoma radiotherapy.

Comparative study of image quality between axial T2-weighted BLADE and turbo spin-echo MRI of the upper abdomen on 3.0 T.

OBJECTIVE: To compare image quality of turbo spin-echo (TSE) with BLADE [which is also named periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER)] on magnetic resonance imaging (MRI) for upper abdomen. MATERIALS AND METHODS: This study involved the retrospective evaluation of 103 patients (63 males, 40 females; age range 19-76 years; median age 53.8 years) who underwent 3.0 T MRI with both conventional TSE T2-weighted imaging (T2WI) and BLADE TSE T2WI. Two radiologists assessed respiratory motion, gastrointestinal peristalsis, and vascular pulsation artifacts, as well as the sharpness of the liver and pancreas edges. Scores for all magnetic resonance (MR) images were recorded. Wilcoxon's rank test was used to compare hierarchical data. Cohen's kappa coefficient was adopted to analyze interobserver consistency. RESULTS: Compared to TSE T2WI, BLADE TSE T2WI reduced all of the examined motion artifacts and increased the sharpness of the liver and pancreas edges (all P < 0.05). Medium to good interobserver consistency was obtained for evaluating these indicators. The scanning time of BLADE TSE T2WI was 4-16 s shorter than that of conventional TSE T2WI. CONCLUSION: Compared to TSE sequence, the BLADE technique can reduce the respiratory motion, gastrointestinal peristalsis, and vascular pulsation artifacts, while decreasing the scanning time and improving the anatomic detail and image quality.

Effect of keratinocyte growth factor on growth and transdifferentiation of primary alveolar epithelial type II cells.

BACKGROUND/AIM: To investigate the effects of keratinocyte growth factor (KGF) on the growth and transdifferentiation of primary alveolar epithelial type II cells (AECIIs). MATERIALS AND METHODS: The number of primary AECIIs, their viability, and cell cycle and apoptosis were studied under KGF treatment using a hemocytometer, trypan blue exclusion, and flow cytometry, respectively. Positive expressions of surfactant protein C (SP-C), aquaporin 5 (AQP5), and thyroid transcription factor 1(TTF-1) were examined with indirect immunofluorescence; mRNA levels of SP-C, AQP5, and TTF-1 were determined by polymerase chain reaction. RESULTS: In response to KGF treatment, cell numbers were significantly increased, more cells were blocked in the S phase, and fewer cells were apoptotic or necrotic on days 2 and 4, but there was little effect on cell viability. In addition, KGF treatment resulted in higher levels of SP-C on days 2 and 8 while lowering them on day 4, higher levels of AQP5 on day 4 while lowering them on day 8, and higher levels of TTF-1 on days 2, 6, and 8. CONCLUSION: KGF treatment promoted proliferation of AECIIs, inhibited cell apoptosis, promoted transdifferentiation of AECIIs, and induced alveolar epithelial type I cells to revert to AECIIs.