Abstract. Gastric cancer is one of the most common malignant tumors and one of the leading causes of cancer-related mortality. Recent studies have revealed that there is a difference in microRNA (miR/miRNA) profiles between cancerous and normal tissues. To find a potentially useful prognostic predictor and a promising therapeutic tool for gastric cancer, the present study investigated the expression and clinical significance of the miR-200 family in gastric cancer. The miR-200 family has five members: hsa-miR-200a, hsa-miR-200b, hsa-miR-200c, hsa-miR-141 and hsa-miR-429. In 46 clinical samples of gastric cancer and paired non-cancerous tissues, the present study observed that the expression levels of the miR-200 family in the cancer tissues were significantly lower than those in the non-cancerous tissues (P<0.001). Lower levels of the five family members were associated with histological grade and the presence of an intravascular cancer embolus (P<0.05). The results revealed that the miR-200 family is downregulated in gastric cancer, and that there are significant differences in the expression of the miR-200 family between normal and cancer tissues. The miR-200 family may therefore become a potentially useful prognostic predictor of the aggressiveness of gastric cancer and a possible therapeutic tool in affected patients.

Gastric cancer remains a worldwide burden as the second leading cause of cancer-related death. Drug resistance of chemotherapy looms as a major clinical obstacle to successful treatment. Recent evidence indicated that miRNA-200c can restore the sensitivity of NSCLC cells to cisplatin and cetuximab. The expression of miRNA-200c and RhoE were investigated in gastric cancer tissues and cells (SGC7901 and SGC7901/DDP) by qRT-PCR. A luciferase reporter assay was done to understand the potential correlation between miRNA-200c and RhoE. Pre-miR-200c was transfected in SGC7901/DDP cells to confirm whether miRNA-200c could regulate RhoE expression. RhoE was knocked down to explore the role of RhoE on sensitivity of chemotherapy in gastric cancer by MTT. Western blot analysis was performed to further explore the mechanism of RhoE in regulating drug resistance. The results showed that miRNA-200c was significantly lower in cancerous tissues than those in the paired normal tissues, whereas the expression of RhoE was just the opposite. The significant difference of miRNA-200c and RhoE were observed between SGC7901 cells and SGC7901/DDP cells. miRNA-200c has target sites in the 3'-UTR of RhoE mRNA by luciferase reporter assay. Transfection of pre-miR-200c reduces RhoE expression. Meanwhile, the knockdown of RhoE enhanced the sensitivity of SGC7901/DDP cells and changed expression of some genes. These suggested that miRNA-200c regulated the sensitivity of chemotherapy to cisplatin (DDP) in gastric cancer by possibly targeting RhoE.

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Coal seam with low permeability is widely distributed in China. Injection of flue gas (N2:CO2 = 0.85:0.15) is an effective approach to improve coal seam gas drainage efficiency. This process relates complex responses among ternary gases (CH4, CO2, and N2) competitive sorption on coals, gas diffusion, gas‐water migration by means of two‐phase flow, and coal deformation. In this paper, an improved hydraulic‐mechanical model coupling above interactions is established for flue gas injection enhanced gas drainage. This model is used to simulate flue gas enhanced drainage by finite element method. The sensitivity analyses of key factors are made to recovery a better understanding on the processes controlling flue gas enhanced drainage. Results show that the flue gas enhanced drainage can indeed improve the efficiency of gas extraction and reduce the gas pressure to the required value in a shorter duration. Due to the competitive adsorption and gas sweeping effect of injected flue gas, CH4 is driven toward drainage borehole, and CH4 pressure and content near the injection borehole decrease faster than that near the drainage borehole. The peak CH4 pressure laterally moves from the injection borehole to the drainage borehole. Higher injection pressure, initial permeability, and smaller sorption affinity ratios may lead to greater CH4 production rate at early drainage stage, but smaller CH4 production rate at late stage. The factors controlling the behavior of flue gas enhanced drainage are initial permeability, injection pressure, and sorption affinity ratios in order. This work offers useful framework to investigate important technical challenges associated with enhanced mine gas drainage, as well as unconventional gas development.

Abstract. The present study was conducted in order to investigate the inhibitory effects of ginsenoside Rg3 combined with chemotherapy on Eca-109 esophageal squamous cell carcinoma (ESCC) in mice. Tumor xenograft models were established in the right forelimb of 20 BALB/c nude mice by subcutaneous injection. The tumor-bearing mice were randomly assigned to 4 treatment groups (n=5 per group) as follows: the control group (saline), the ginsenoside Rg3 alone group (6 mg/kg/day, once a day for 3 weeks), the chemotherapy alone group (paclitaxel 10 mg/kg/day + cisplatin 5 mg/kg/day on days 1, 7, 14 and 21) and the chemotherapy + Rg3 group (combined treatment). The length and width of the tumor were directly measured with calipers at different time points and the tumor volume (cm 3 ) was calculated using the formula 0.52 x length x width 2 every other day. The mice were sacrificed by cervical dislocation following completion of therapy, the tumors were removed and weighed and the expression levels of Ki-67 were determined by immunohistochemistry. The results indicated that the coadministration of ginsenoside Rg3 significantly enhanced the inhibitory effects of chemotherapy on tumor growth. In addition, the expression levels of Ki-67 in the chemotherapy + Rg3 group were significantly lower compared to those in the other 3 groups. The chemotherapy + Rg3 group also exhibited the lowest microvascular density among all four groups. These findings suggested that ginsenoside Rg3 may improve the antitumor efficacy of chemotherapy in Eca-109 ESCC in mice.