FRA-1 suppresses apoptosis of Helicobacter pylori infected MGC-803 cells.

Previous research has demonstrated a correlation between elevated expression of Fos-related antigen 1 (FRA-1) and malignancies. Nevertheless, the role of FRA-1 in Helicobacter pylori infected gastric cancer cells remains vague. Our study aims to investigate whether FRA-1 plays a role in the apoptosis of MGC-803 induced by H. pylori and possible mechanisms. MGC-803 cells were used in vitro to establish a cell model of H. pylori infection. After stimulation with H. pylori, the expression of FRA-1 was increased in MGC-803 cells. H. pylori infection promoted the apoptosis of MGC-803 cells, and led to cell cycle arrest and increased oxidative stress levels. Furthermore, the knockdown of FRA-1 reinforced these changes. H. pylori decreased the expression of Bcl2, Caspase3 and Caspase9, while increased the level of BAX, Cleaved-Caspase3 and Cleaved-Caspase9; in addition, it led to the decrease of major proteins in Ras/Erk and PI3K/AKT signaling pathway. As expected, these changes were augmented by FRA-1 knockdown. Our results demonstrated that high expression of FRA-1 induced by H. pylori suppresses apoptosis in MGC-803 cells which may be regulated by oxidative stress and cycle arrest through caspase family, Ras/Erk and PI3K/AKT signaling pathway.

Viral metagenomics reveals sapoviruses of different genogroups in stool samples from children with acute gastroenteritis in Jiangsu, China.

Sapoviruses (SAVs), including several genogroups (GI to GV), are one of the causes of acute gastroenteritis (AGE). In this study, viral metagenomics revealed the presence of sapoviruses of different genogroups in stool from children with AGE. Eight different complete SAV genomes were determined, of which five belonged to GI and the other three belonged to GII, GIV and GV, respectively. Although they were highly similar to published sequences, the GIV and GV were the first complete genome sequences of these SAVs found in China. In a prevalence investigation, 19% of subjects with AGE were positive for SAVs, while none of the control group was positive.

Summary of Turbocharging as a Waste Heat Recovery System for a Variable Altitude Internal Combustion Engine.

The increase in altitude causes the decrease in internal combustion engine power and the increase in pollutant emission. Converting waste heat into more useful forms of energy through the recovery of waste heat from internal combustion engines is the most promising mechanism for improving both of these goals. This paper comprehensively reviews the development and research of waste heat recovery technology of an internal combustion engine in a variable altitude environment. It is found that exhaust gas turbocharging is the most promising waste heat recovery technology to restore high-altitude internal combustion engine power. Turbochargers are affected by low temperature and low pressure at high altitudes, resulting in poor environmental adaptability, inadequate supercharging ratios, and decreased supercharging efficiency. Therefore, it is very important to select the high pressurization system facing the plateau area and its reasonable matching characteristics. The quality of exhaust energy determines how much waste heat a turbine can recover, and only the exergy part of exhaust energy can realize heat/work conversion. The main disadvantage of turbocharging technology applied in the plateau area is that the speed ratio deviates from the design value, leading to the increase of flow loss inside the supercharger. Therefore, optimizing the internal flow field of a high-altitude supercharger is a key problem to improve the efficiency of energy recovery. The conclusion drawn from this Review is that a two-stage turbocharging system will be a key technology to improve the thermal efficiency and reduce the fuel consumption of high-altitude internal combustion engines in the coming decades. In addition, the efficient utilization of the exhaust energy of the two-stage turbine and the influence of the variable compression process of the two-stage compressor on the working medium in the cylinder will be the focus of future research.

Aberrant Expression of Gastric Carcinoma High Expressed Transcript 1 is a Diagnostic and Prognostic Biomarker in Human Cancer.

BACKGROUND: Gastric carcinoma high expressed transcript 1 (GHET1), a long noncoding RNA (LncRNA), has been reported to be involved in tumor genesis and cancer progression. High GHET1 expression is correlated with a poor prognosis in cancer. In this meta-analysis, we investigated the association between GHET1 and lymph node metastasis, differentiation, vascular invasion and so on in human cancer. METHODS: We performed systematic search in PubMed, EMBASE, Wiley Online Library, Wiley Online Library, and Medline from January 1, 1996 to September 25, 2017. A total of 8 studies were selected for further research. RESULTS: The result showed that GHET1 expression was significantly associated with OS (hazard ratio [HR] = 2.23; 95% CI, 1.86-2.67; P < 0.0001), including digestive system tumor (HR = 2.17; 95% CI, 1.63-2.89; P < 0.0001). Moreover, high GHET1 expression was related to tumor size (odds ratio [OR] = 2.15, 95% CI: 1.57-2.94; P < 0.00001), TNM stage (Ⅲ+Ⅳ vs.Ⅰ+Ⅱ; OR = 4.02, 95% CI:3.06-5.28; P < 0.00001), lymph node metastasis (Yes vs. No; OR = 3.55, 95% CI:2.54-4.95; P < 0.00001), differentiation (poor vs. well or moderate; OR = 1.72, 95% CI:1.22-2.42; P = 0.002), vascular invasion (Yes vs. No; OR = 3.03, 95% CI:1.80-5.12; P = 0.00001). Also, we found that high expression of GHET1 has a significant relationship with analysis method and sample size. It almost higher in different human cancers. CONCLUSIONS: GHET1 may serve as a potential clinical biomarker and poor survival and high-risk recurrence in cancers.

DAB2 suppresses gastric cancer migration by regulating the Wnt/ß-catenin and Hippo-YAP signaling pathways.

BACKGROUND: Disabled-2 (DAB2), a potential tumor suppressor, plays an in important role in cancer development and cellular differentiation. Its lower expression levels have founded in many cancers. In addition, DAB2 is involved in multiple signaling pathways, including TGF-ß and Wnt signal pathways. Gastric cancer (GC) is a common gastrointestinal malignant tumor. Nonetheless, the role of DAB2 in GC remains unclear. METHODS: Thirty-seven clinical specimens of GC tissues and adjacent non-tumor tissues were examined by immunohistochemistry. Proteins were extracted from two of them to perform Western blot analysis. Then, CMV-MCS-3FLAG-SV40-DAB2 and si-DAB2 were transfected into MGC and SGC cell line, respectively. The migration of GC cells was evaluated by transwell migration assay. And, the expression of migration related proteins was detected by Western blot and immunofluorescence (IF). RESULTS: Eighty-six percent (32/37) of patients DAB2 staining was reduced in GC tissues compared to adjacent normal tissues. Further studies showed that in six human GC cell lines, the level of DAB2 expression was lower than normal gastric epithelial cells, and that DAB2 was closely related to cell migration in vitro. In DAB2 silenced cells, the Wnt/ß-catenin signaling was increased and the Hippo-YAP pathway was affected. In addition, lower DAB2 level led to nuclear translocation of ß-catenin and Yap. CONCLUSIONS: The lower expression of DAB2 regulates cell migration in GC via interfering with the Wnt and Hippo signaling pathway. Our findings suggested that DAB2 played an important role in the migration of GC.

[Cloning and expressing cagT gene of type IV secretion system in Helicobacter pylori and influence of cytokine secretion and cell proliferation on SGC-7901 cell].

OBJECTIVE: To detect the influence of the CagT protein on interleukin-8 secretion and proliferation in SGC-7901 cells. METHODS: Helicobacter pylori cagT gene was amplified by PCR with the genomic DNA of H. pylori NCTC 11637 as template, then it was inserted into an expression vector pQE30. The recombinant plasmid was transformed into E. coli M15. Recombinant protein was expressed by Isopropylthio-beta-D-Galacgoside (IPTG) induction and confirmed by Western blot. Fusion protein with 6xHis tag was purified using Ni(2+)-NTA agarose. Interleukin-8 mRNA expression of SGC7901 cells was determined by reverse transcriptase polymerase chain reaction (RT-PCR). Cell viability was determined by methyl thiazolyl tetrazolium assay (MTT). RESULTS: The GenBank accession number of the amplified sequence is EF114758. The sequence analysis for cagT showed that it shares 97%-99% homology with other strains of H. pylori in Gene bank. The molecular mass of the product is 32kDa, and its purity is 98% analyzed by SDS-PAGE. After the protein was dialyzed, it can stimulate SGC7901 cells to express interleukin-8 and the growth of cells was inhibited in a dose- and time-dependent manner. CONCLUSION: It is indicated that we have obtained the correct cagT gene and expressed in E. coli M15. The protein can stimulate the cells to express cytokine interleukin-8 and inhibit proliferation of cells, which posed a basis for further research on its biological function.

Type IV secretion system in Helicobacter pylori: a new insight into pathogenicity.

OBJECTIVE: To review the research progress on Type IV secretion system (T4SS) in Helicobacter pylori. DATA SOURCES: The data used in this review were identified by searching of PUBMED (1995 - 2007) online resources using the key terms 'Type IV secretion system' and 'Helicobacter pylori'. STUDY SELECTION: Mainly original articles and critical reviews written by major pioneer investigators of this field were selected. RESULTS: The research progress on T4SS in Helicobacter pylori was summarized. The structure and function was discussed. CONCLUSIONS: T4SS is not only involved in toxin secretion and injection of virulence factors into eukaryotic host target cells, but also involved in horizontal DNA transfer to other bacteria and eukaryotic cells, through DNA uptake from or release into the extracellular milieu. It provides a new insight into the pathogenicity of Helicobacter pylori and a novel target for antimicrobials development. However, many challenges remain for us in understanding the biological role of T4SS in Helicobacter pylori.