Superimposed OER and UOR performances by the interaction of each component in an Fe-Mn electrocatalyst.

The oxygen evolution reaction (OER) and alternative urea oxidation reaction (UOR) are both important half reactions correlated with hydrogen production. Transition metal based catalysts with double metal composition exhibit excellent electrocatalytic performance for the OER or UOR due to their synergetic effect and coupling of different active sites. However, the development of OER/UOR bifunctional electrocatalysts is unsatisfying and the role of each metallic active site in the OER and UOR is still unclear. Herein, we report a Fe-Mn based OER and UOR bifunctional catalyst through a simple one-step electrodeposition method. For the OER, the introduction of Mn improves the conductivity of the catalysts and fine-tunes the electron density of the Fe active sites. For the UOR, both Fe and Mn act as active sites and their coupling effect further improves the UOR activity. The catalyst with the optimal Mn/Fe ratio achieved an overpotential of 237 mV for the OER and a potential of 1.35 V for the UOR at 100 mA cm-2. This study provides a simple synthesis protocol for constructing bifunctional catalysts for green hydrogen production.

C1QTNF6 is overexpressed in gastric carcinoma and contributes to the proliferation and migration of gastric carcinoma cells.

In the present study, proteins differentially expressed between gastric cancer tissue and para­tumoral normal gastric tissues were screened, and the function of the highly expressed protein C1QTNF6 in gastric carcinoma was investigated. The differential expression of mRNAs extracted from the tumor and adjacent tissues was analyzed using GeneChip assay. An AGS si­C1QTNF6 cell line was constructed using shRNA­C1QTNF6 lentivirus. The cell invasion and migration ability of C1QTNF6­knockdown cells were determined by Transwell chamber migration and wound healing assays, respectively. The effects of C1QTNF6 on AGS cell cycle distribution and apoptosis were detected using a FACScan flow cytometer. The results demonstrated that the expression of 109 genes was increased and the expression of 129 was decreased in tumor tissues. Among these genes, the C1QTNF6 gene was highly expressed in tumor tissues and the AGS7901 cell line. C1QTNF6­knockdown decreased the cell growth, and the proliferative and migration ability, as well as increasing the apoptosis of gastric carcinoma cells. In addition, the number of AGS cells in the G2/M phase was significantly increased after 5 days of C1QTNF6­shRNA lentivirus infection. The results of the present study indicated that C1QTNF6 serves an important role in the development of gastric carcinoma. C1QTNF6 is involved in promoting the proliferation and migration, and in reducing the apoptosis of gastric carcinoma cells. These results provided a potential therapeutic target for the treatment of gastric carcinoma.

Expression of interleukin-17 and its clinical significance in gastric cancer patients.

To investigate the expression of interleukin 17 (IL-17) in serum and tumor tissues, and evaluate the correlation between IL-17 and clinical characteristics from patients with gastric cancer. From January 2009 to January 2010, total 50 patients with gastric cancer and 50 healthy controls were enrolled. The patients included 32 males and 18 females with average age of (62.05 ± 11.98) years. The concentration of serum IL-17 was detected by ELISA. Intratumoral IL-17 expression and microvessel density (MVD) were examined by immunohistochemical staining. Compared with healthy controls, patients with gastric cancer had higher levels of IL-17 in serum (p < 0.01) and cancer tissues. High expression of IL-17 was associated with high MVD (p < 0.01). IL-17 in cancer tissues was associated with the clinical stage of the tumors (p < 0.01) and lymph node metastasis (p < 0.05). No statistically significant correlation between the serum IL-17 and the clinical pathological features was found. Increased expression of IL-17 was seen in patient with gastric cancer. IL-17 may be involved in the progression of gastric cancer by promoting angiogenesis in tumor microenvironment.

Promoter methylation regulates cigarette smoke-stimulated cyclooxygenase-2 expression in esophageal squamous cell carcinoma.

OBJECTIVE: Cigarette smoke extracts (CSE) could promote esophageal squamous cell carcinoma (ESCC) through upregulation of cyclooxygenase-2 (COX-2) expression. Promoter methylation mediates the transcriptional modulation of the COX-2 gene. The aim of the study was to explore whether COX-2 promoter methylation regulated COX-2 expression and functional activity in ESCC exposed to CSE. METHODS: The methylation status of COX-2 promoter in two human ESCC cell lines, EC109 and TE-1, was examined using bisulfite sequencing analysis. COX-2 mRNA and protein expression were detected by reverse-transcription polymerase chain reaction and Western blot. Prostaglandin E2 (PGE2) was examined by enzyme linked immunosorbent assay (ELISA). RESULTS: The promoter was hypermethylated in TE-1 which had a low level of COX-2 expression and was hypomethylated in EC109 with a relatively high level of COX-2 expression. Stimulation by cigarette smoke ethanol extract (EE) resulted in increased COX-2 expression in EC109, but not in TE-1. Treatment with 5-aza-2'-deoxycytidine (5-aza-DC) demethylated the promoter and upregulated COX-2 expression as well as PGE(2) production in TE-1, especially followed by EE stimulation. No significant effect was observed in EC109. CONCLUSION: These findings suggest that promoter methylation may be one of the mechanisms regulating COX-2 expression in ESCC in response to stimulation of CSE.