[Effect of band ligation or combined with tissue adhesive in the treatment of gastroesophageal varices and portal vein blood flow situational changes].

42 cases with gastroesophageal varices were prospectively included. The groups were treated with endoscopic band ligation or combined with tissue adhesive. The results showed that the left gastric vein internal diameter, average blood flow velocity and blood flow volume after the treatment of band ligation combined with tissue adhesive were significantly lower than that of the treatment of band ligation alone, and the differences were statistically significant (P < 0.05). Spleen and portal vein internal diameter, blood flow and average velocity, the liver and spleen size, shear wave velocity and liver function grade of the two groups after treatment did not change significantly (P > 0.05). The effective rate of band ligation combined with tissue adhesive in the treatment of esophageal and gastric varices (66.67%, 52.38%) were higher than that of band ligation alone (42.85%, 23.81%) (P > 0.05), and the re-bleeding rate of the latter was higher (9.52% and 19.05%, P > 0.05). Hence, it is suggested that the combined therapy is safe and more effective, and has no apparent effect on liver function and portal hypertension.

MiR-150 alleviates EMT and cell invasion of colorectal cancer through targeting Gli1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiR-150 alleviates EMT and cell invasion of colorectal cancer through targeting Gli1, by H. Fan, X. Liu, W.-W. Zheng, Z.-H. Zhuang, C.-D. Wang, published in Eur Rev Med Pharmacol Sci 2017; 21 (21): 4853-4859-PMID: 29164577" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/13726.

MiR-150 alleviates EMT and cell invasion of colorectal cancer through targeting Gli1.

OBJECTIVE: Epithelial-mesenchymal transition (EMT) is related to colorectal cancer invasion and metastasis. Glioma-associated oncogene homolog 1 (Gli1) abnormal expression is associated with EMT, invasion, and metastasis in various cancers. MiR-150 is found downregulated in colorectal cancer pathogenesis. Bioinformatics analysis shows the complementary targeted relationship between miR-150 and the 3'-UTR of Gli1 mRNA. This study explores the role of miR-150 in regulating Gli1 expression, colorectal cancer cell EMT, and invasion. MATERIALS AND METHODS: Dual luciferase assay confirmed the targeted relationship between miR-150 and Gli1 predicted by bioinformatics analysis. MiR-150 and Gli1 expressions were compared in NCM460, SW480, and SW620 cells. Cell colony formation and invasion were tested in SW480 and SW620 cells. Anip973 and AGYZ83-a cells were treated by 10 ng/mL TGF-ß1 to detect miR-150 and Gli1 expressions. SW620 cells were cultured in vitro and divided into five groups, including miR-NC, miR-150 mimic, si-NC, si-Gli1, and miR-150 mimic + si-Gli1 groups. RESULTS: MiR-150 specifically inhibited Gli1 expression. The level of miR-150 was significantly downregulated, while Gli1 was elevated in SW480 and SW620 cells compared with that in NCM460 cells. SW620 exhibited markedly stronger invasive and colony formation abilities than SW480. The level of miR-150 was apparently reduced, whereas Gli1 was increased in SW620 than that in SW480 cells after the treatment of TGFß1. MiR-150 mimic and/or si-Gli1 transfection markedly reduced Gli1 and Snail levels, upregulated E-cadherin expression, and attenuated cell colony formation and invasion. CONCLUSIONS: Downregulation of miR-150 and elevation of Gli1 promote the development and invasion of colorectal cancer cell EMT. MiR-150 attenuated the progression of colorectal cancer cell EMT via inhibiting Gli1.

Review article: 'true' re-infection of Helicobacter pylori after successful eradication--worldwide annual rates, risk factors and clinical implications.

BACKGROUND: The incidence of 'true' re-infection with Helicobacter pylori after successful eradication remains uncertain. AIM: To determine the worldwide rates, risk factors and clinical implications of 'true' re-infection of Helicobacter pylori. 'True' re-infection of H. pylori is defined as the situation where tests for H. pylori infection, which were negative for 12 months after eradication, become positive again at a later stage. RESULTS: Thirty six studies were identified through a literature search to be able to produce annual rates of 'true' re-infection, and data from 33 original articles were considered reliable and adequate in the further review. Generally, the reported rates varied from 0% to 23.4% in adults and from 1.9% to 9.6% in children. Most studies from developed countries reported rates of less than 1%, whereas relatively higher rates were reported in most of the developing countries. Small sample sizes included in the studies appeared to be associated with increased re-infection rates. Interfamilial transmission is the major cause of re-infection, although iatrogenic re-infection through contaminated endoscopic equipment has been reported. CONCLUSION: Helicobacter pylori re-infection is not a concern in a clinical setting, especially in the developed world; however, caution must be exercised in most developing countries.

Epstein-Barr virus latent membrane protein 1 (LMP1) upregulates Id1 expression in nasopharyngeal epithelial cells.

Nasopharyngeal carcinoma is closely associated with Epstein-Barr virus (EBV) infection. The EBV-encoded LMP1 has cell transformation property. It suppresses cellular senescence and enhances cell survival in various cell types. Many of the downstream events of LMP1 expression are mediated through its ability to activate NF-kappaB. In this study, we report a novel function of LMP1 to induce Id1 expression in nasopharyngeal epithelial cells (NP69) and human embryonal kidney cells (HEK293). The Id1 is a basic helix-loop-helix (bHLH) protein and a negative transcriptional regulator of p16(INK4a). Expression of Id1 facilitates cellular immortalization and stimulates cell proliferation. With the combination of both specific chemical inhibitors and genetic inhibitors of cell signaling, we showed that induction of Id1 by LMP1 was dependent on its NF-kappaB activation domain at the carboxy-terminal region, CTAR1 and CTAR2. Induction of Id1 by LMP1 may facilitate clonal expansion of premalignant nasopharyngeal epithelial cells infected with EBV and may promote their malignant transformation.

[Analysis of group composit of crude oil by on-line coupling of capillary HPLC-HTGC].

The group composition of crude oil was analyzed by on-line coupled capillary HPLC-HTGC. After removal of asphaltenes, the oil sample was separated by capillary HPLC into aliphatics, aromatics and resins. The interface cut and stored each fraction, and transfered them into GC sequentially. The group contents of oil were determined by FID. The error of reproducibility(RSD) was less than 3%. The method is accurate, time saving, and easy for operation. It is very important for quality control and development of new and better products in crude oil.

[Cloning and expression of Streptomyces lividans promoters].

BamHI restriction fragments from Streptomyces lividans TK24 chromosome DNA have been cloned into BamHI site of promoter probe plasmid pIJ486. Transformants were selected on the medium containing 5 micrograms/ml of neomycin. Four recombinant plasmids pMG1(10.6 kb), pMG40(7.6 kb), pMG50(10.8 kb) and pMG88(7.92 kb), were found and designated respectively. The inserted fragments in pMG40 and pMG50 were reduced to 0.78kb and 2.2 kb by BglII digestion and rejoining. The different levels of neomycin and kanamycin resistance of these recombinant plasmids were determined. The results revealed that pMG50-25 showed a high level of neomycin resistance (90 micrograms/ml) and kanamycin resistance (500 micrograms/ml).

[Cloning and expression of E. coli glucose isomerase gene in Streptomyces lividans].

E. coli glucose isomerase gene was cloned into Streptomyces lividans using shuttle plasmid vector pSE-3. First plasmid pXI203 was constructed in E. coli using plasmids pXI200 (containing 1.6 kb glucose isomerase gene) and pGEM-3 digested with EcoR1. Then, recombinant plasmid pSEX100 was also constructed in E. coli using plasmids pXI203 and pSE-3 digested with HindIII. When the pSEX100 was transformed into Streptomyces lividans protoplasts, recombinants were obtained on R5YE medium containing 50 micrograms/ml neomycin and 50 micrograms/ml thiostrepton. The results showed that the E. coli glucose isomerase gene cloned and expressed in Streptomyces lividans via the analysis of restriction enzyme digestion as well as the detection of the glucose isomerase activity.