The role of miRNA and lncRNA in gastric cancer.

Gastric cancer is one of the most common cancers and has the highest mortality rate worldwide. It is worthwhile to explore the mechanism of gastric cancer progression. An increasing number of studies have found that non-coding RNAs including miRNA and lncRNA play important roles in gastric cancer progression. This review summarized the role of ectopic miRNA in gastric cancer proliferation, growth, migration, invasion and apoptosis. Meantime, aberrantly expressed miRNA also received a great deal of attention as potential biomarker for gastric cancer diagnosis and therapy. Over the last decade, lncRNA was considered to regulate gastric cancer progression at the transcript and post-transcript level. At the transcript level, lncRNA induced gastric cancer progression by changing chromatin modification and mRNA stabilization to regulate mRNA and miRNA expression. Furthermore, lncRNA regulated gastric cancer progression by completely combining with miRNA to produce ceRNA or promote protein stabilization at the post-transcript level. Greater attention of miRNA and lncRNA in gastric cancer can provide new insight of mechanism of cancer development and may be acted as a new anticancer target.

[Optimization of Promoter and Support for Co-based/zeolites Catalysts in Catalytic Reduction of NOx by CH4].

Catalytic behavior of Co-based/zeolites catalysts was investigated in NOx reduction by CH4. Optimization of promoter and support was investigated by catalytic tests, and the relationship between catalytic activity and catalyst structure was illustrated by catalyst characterization. Co-Fe/SAPO-34 exhibited the highest activity among various Co-base/zeolites catalysts. The maximum conversion of NOx with 52.7% was obtained on Co-Fe/SAPO-34 at 450℃. The inhibition of activity of Fe/zeolites became severe in the presence of SO2, CO2, and H2O. CO2 exerted virtually no effect on the SCR activity of Co-Fe/zeolites. The inhibition of NOx conversion by H2O was reversible for Co-Fe/zeolites catalysts. Cobalt species were mainly present in CoO and Co(OH)2 states in Co-Fe/SAPO-34. Co3O4and Co(OH)2 were the main cobalt species of Co-Fe/ZSM-5, while CoO, CoAl2O4 and Co3O4 might be present in Co-Fe/Beta. The ratio of Fe2+/Fe3+ in the surface layer of Co-Fe/zeolites decreased in the order of Co-Fe/ZSM-5(3.98) > Co-Fe/SAPO-34(0.52) > Co-Fe/Beta(0.43). The active states of cobalt species and suitable ratio of Fe2+/Fe3+ were important for the activity of Co-Fe/zeolites in CH4-SCR. CH4-SCR over Co-Fe/zeolite catalysts started with the adsorption of NO and CH4 on Brønsted acid sites of the zeolite to produce NO+and carbon-containing species(-C=O and -COO) in the presence of oxygen, respectively. Subsequently, the important intermediates of nitrate species were generated from NO+ at the active sites. Finally, nitrate species reacted with carbon-containing species to form N2 and CO2.

[Clinical analysis and autoimmune regulator gene mutation of autoimmune polyendocrinopathy syndrome type I in a family: a report of one case].

The clinical data of one patient with autoimmune polyendocrinopathy syndrome type I were collected. PCR-DNA direct bidirectional sequencing was applied for mutation screening of 14 exons in autoimmune regulator (AIRE) gene in the patient and her parents. A total of 50 unrelated healthy controls were selected and tested. The bioinformatic methods were used to predict the possible impact of the mutations on the structure and function of the AIRE protein. The results of sequencing showed that heterozygous mutation c.622G>T (p.G208W) in exon 5 of the AIRE gene was detected in the patient and was a novel mutation, which had not been reported in the HGMD database and latest articles. This mutation was not detected in the 50 unrelated normal controls. The novel mutation of c.622G>T (p.G208W) in AIRE gene might play an important role in the pathogenesis of this case of autoimmune polyendocrinopathy syndrome type I.

Small Bowel Endoscopy Diagnostic Yield and Reasons of Obscure GI Bleeding in Chinese Patients.

Aim. To investigate the diagnostic yield and etiologies of patients with obscure gastrointestinal bleeding (OGIB) using capsule endoscopy (CE) or double-balloon enteroscopy (DBE). Method. We studied the data of 532 consecutive patients with OGIB that were referred to Xinqiao Hospital in Chongqing from December 2005 to January 2012. A lesion that was believed to be the source of the bleeding (ulceration, mass lesion, vascular lesion, visible blood, inflammation, or others) was considered to be a positive finding. We analyzed the diagnostic yield of CE and SBE and the etiologies of OGIB. Result. CE and SBE have similar diagnostic yields, at 71.9% (196/231) and 71.8% (251/304), respectively. The most common etiology was erosions/ulceration (27.1%) followed by mass lesion (19.4%) and angiodysplastic/vascular lesions (13.9%). By stratified analysis, we found that erosions/ulceration (27.1%) was the most common etiology for the 21-40-year age group. Mass lesion was the most common etiology in the 41-60-year age group. However, in the >60 years age group, angiodysplastic/vascular lesions were significantly increased compared with the other groups, even though erosions/ulceration was most common. Conclusion. In this study, we found that CE and SBE have similar diagnostic yields and erosions/ulceration was the most common reason for OGIB, followed by mass lesion and angiodysplasias.

Fine-mapping of immunodominant linear B-cell epitopes of the Staphylococcus aureus SEB antigen using short overlapping peptides.

Staphylococcal enterotoxin B (SEB) is one of the most potent Staphylococcus aureus exotoxins (SEs). Due to its conserved sequence and stable structure, SEB might be a good candidate antigen for MRSA vaccines. Although cellular immune responses to SEB are well-characterized, much less is known regarding SEB-specific humoral immune responses, particularly regarding detailed epitope mapping. In this study, we utilized a recombinant nontoxic mutant of SEB (rSEB) and an AlPO4 adjuvant to immunize BALB/c mice and confirmed that rSEB can induce a high antibody level and effective immune protection against MRSA infection. Next, the antisera of immunized mice were collected, and linear B cell epitopes within SEB were finely mapped using a series of overlapping synthetic peptides. Three immunodominant B cell epitopes of SEB were screened by ELISA, including a novel epitope, SEB205-222, and two known epitopes, SEB97-114 and SEB247-261. Using truncated peptides, an ELISA was performed with peptide-KLH antisera, and the core sequence of the three immunodominant B cell epitopes were verified as SEB97-112, SEB207-222, and SEB247-257. In vitro, all of the immunodominant epitope-specific antisera (anti-SEB97-112, anti-SEB207-222 and anti-SEB247-257) were observed to inhibit SEB-induced T cell mitogenesis and cytokine production from splenic lymphocytes of BALB/c mice. The homology analysis indicated that SEB97-112 and SEB207-222 were well-conserved among different Staphylococcus aureus strains. The 3D crystal structure of SEB indicated that SEB97-112 was in the loop region inside SEB, whereas SEB207-222 and SEB247-257 were in the ß-slice region outside SEB. In summary, the fine-mapping of linear B-cell epitopes of the SEB antigen in this study will be useful to understand anti-SEB immunity against MRSA infection further and will be helpful to optimize MRSA vaccine designs that are based on the SEB antigen.

Macrophage migration inhibitory factor polymorphism and the risk of ulcerative colitis and Crohn's disease in Asian and European populations: a meta-analysis.

OBJECTIVE: To determine whether macrophage migration inhibitory factor (MIF) gene polymorphism is associated with the risk of inflammatory bowel disease (IBD). DESIGN: System review and meta-analysis. METHODS: MEDLINE, EMBASE, Web of Science databases, Cochrane Library and the Chinese Biomedical Literature database (CBM) were searched for the case-control trails for MIF and IBD. All the studies included in this manuscript met the inclusion and exclusion criteria. An OR analysis using a 95% CI was employed to assess the association of the MIF-173 G/C polymorphism with IBD susceptibility. RESULTS: There was a significant association between the MIF-173 G/C gene polymorphism and IBD in the total population under the recessive model (CC vs GC+GG; OR=1.75, CI 1.04 to 2.95, p=0.04 for heterogeneity) and the codominant model (CC vs GG; OR=1.74, CI 1.02 to 2.97, p=0.04 for heterogeneity). In the stratified analysis by ethnicity, significantly increased risks were observed for Asians using the recessive (OR=1.75, CI 1.04 to 2.95, p=0.04 for heterogeneity) and codominant models (OR=1.74, CI 1.02 to 2.97, p=0.04 for heterogeneity). Within the subgroups of UC and CD, significant differences were observed regarding UC using the recessive (OR=1.60, CI 1.09 to 2.35, p=0.02 for heterogeneity) and codominant models (OR=1.64, CI 1.12 to 2.41, p=0.01 for heterogeneity). In the stratified analysis by ethnicity for UC, significant differences were observed regarding CC in Asians vs GC+GG (OR=1.73, CI 1.02 to 2.94, p=0.04 for heterogeneity). CONCLUSIONS: The meta-analysis suggested that the MIF-173 G/C polymorphism contributed to the susceptibility of IBD. When considering the subgroups of ethnicity and UC and CD, the results suggested that the polymorphism is more significant for UC in Asians.

PLCE1 polymorphism and upper gastrointestinal cancer risk: a meta-analysis.

BACKGROUND: In recent years, the PLCE1 rs2274223 polymorphism has been extensively investigated as a potential risk factor for upper gastrointestinal cancers, including squamous cell carcinoma (ESCC) and gastric cancer. However, the results of these studies have been inconsistent. METHODS: A meta-analysis of 13 case-control studies was performed including more than 11,000 subjects with genotyped PLCE1 rs2274223 polymorphisms. Odds ratios (OR) with 95% confidence intervals (CI) were employed to assess the association of the PLCE1 rs2274223 polymorphism with a susceptibility to ESCC or gastric cancer. RESULTS: A statistically significant increase in the risk of ESCC was associated with the PLCE1 rs2274223 polymorphism. This included the homozygous genetic model (OR = 1.46), heterozygous genetic model (OR = 1.25) and allelic genetic model (OR = 1.23). Similar results were consistently found for gastric cancer. In a subgroup analysis, the PLCE1 rs2274223 polymorphism was found to be a very sensitive marker for gastric cardia cancer as shown by the homozygous genetic model (OR = 2.23), heterozygous genetic model(OR = 1.59) and allelic genetic model (OR = 1.47). The risk associations of all of the gastric cardia cancer models were statistically significant. In contrast, none of the genetic models for non-cardia gastric cancer were significant. CONCLUSIONS: In this meta-analysis, the PLCE1 rs2274223 polymorphism was confirmed to have a statistically significant association with an increasing risk of ESCC and gastric cancer. The increase risk was especially observed for gastric cardia cancer.

A dominant CD4(+) T-cell response to Helicobacter pylori reduces risk for gastric disease in humans.

BACKGROUND & AIMS: Immunodominance is an important feature of antiviral, antitumor, and antibacterial cellular immune responses, but it is not well demonstrated in the immune responses against Helicobacter pylori. Antigen-specific CD4(+) T cells protect mice against infection with H pylori. We investigated the immunodominant CD4(+) T-cell response to neuraminyllactose-binding hemagglutinin (HpaA), which is a conserved, H pylori-specific colonization factor that is being investigated as an antigen for vaccination strategies. METHODS: HpaA-specific CD4(+) T cells were expanded with autologous peripheral blood mononuclear cells that had been incubated with recombinant HpaA and characterized using overlapping synthetic peptides. We compared the percentage of CD4(+) T cells with specificity for HpaA(88-100), restricted to HLA-DRB1*1501, among 59 H pylori-infected subjects with different gastric diseases. RESULTS: We identified and characterized several immunodominant CD4(+) T-cell epitopes derived from HpaA. The immunodominant CD4(+) T-cell responses specific to HpaA(88-100) were observed in most H pylori-infected individuals who expressed HLA-DRB1*1501 and were significantly more abundant in patients with less severe diseases (P < .05). CONCLUSIONS: The HLA-DRB1*1501-restricted immunodominant CD4(+) T-cell response to HpaA(88-100) is associated with reduced risk of severe gastric diseases. Further study of these and other immunodominant CD4(+) T-cell responses to H pylori will provide insight into mechanisms of protective immunity and aid in vaccine design.

Systemic immunization with an epitope-based vaccine elicits a Th1-biased response and provides protection against Helicobacter pylori in mice.

Vaccine-mediated Th1-biased CD4+ T cell responses have been shown to be crucial for protection against Helicobacter pylori (H. pylori). In this study, we investigated whether a vaccine composed of CD4+ T cell epitopes together with Th1 adjuvants could confer protection against H. pylori in a mouse model. We constructed an epitope-based vaccine, designated Epivac, which was composed of predicted immunodominant CD4+ T cell epitopes from H. pylori adhesin A (HpaA), urease B (UreB) and cytotoxin-associated gene A product (CagA). Together with four different Th1 adjuvants, Epivac was administered subcutaneously and the prophylactic potential was examined. Compared to non-immunized mice, immunization with Epivac alone or with a Th1 adjuvant significantly reduced H. pylori colonization, and better protection was observed when an adjuvant was used. Immunized mice exhibited a strong local and systemic Th1-biased immune response, which may contribute to the inhibition of H. pylori colonization. Though a significant specific antibody response was induced by the vaccine, no correlation was found between the intensity of the humoral response and the protective effect. Our results suggest that a vaccine containing CD4+ T cell epitopes is a promising candidate for protection against H. pylori infection.