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A translation system is made up of a source text subsystem and a target text subsystem. The elements in the system are interrelated and exert influence on each other. Translation studies from a systems-theoretic perspective focus primarily on literary texts, while business discourses are seldom explored. In order to assess the translation quality of company profiles, a three-level model from the systems theory perspective has been proposed. The three levels are the preliminary data level, the discourse level, and the contextual level. The results show that the translator should attach great importance to improving and restructuring the source text and reconstructing experiential meaning, interpersonal meaning, and textual meaning. The translation should be reader-oriented and adapt to the cultural context of the target language.

Qualitative Systematic Review (QSR) is the second-generation literature review that aims to synthesize primary qualitative studies. Its use is growing rather rapidly in medicine, nursing, education and other fields, but it remains underutilized in applied linguistics. In order to invite more qualitative systematic reviews in applied linguistics, this paper first provides the definition of QSR, outlines the key steps for its conduct, elaborates on the core procedure, i.e., synthesis methods, then illustrates with published examples of qualitative systematic reviews in applied linguistics, and finally explores the future directions.

The CXC chemokines belong to a family which includes 17 different CXC members. Accumulating evidence suggests that CXC chemokines regulate tumor cell proliferation, invasion, and metastasis in various types of cancers by influencing the tumor microenvironment. The different expression profiles and specific function of each CXC chemokine in head and neck squamous cell carcinoma (HNSCC) are not yet clarified. In our work, we analyzed the altered expression, interaction network, and clinical data of CXC chemokines in patients with HNSCC by using the following: the Oncomine dataset, cBioPortal, Metascape, String analysis, GEPIA, and the Kaplan–Meier plotter. The transcriptional level analysis suggested that the mRNA levels of CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL8, CXCL9, CXCL10, CXCL11, and CXCL13 increased in HNSCC tissue samples when compared to the control tissue samples. The expression levels of CXCL9, CXCL10, CXCL11, CXCL12, and CXCL14 were associated with various tumor stages in HNSCC. Clinical data analysis showed that high transcription levels of CXCL2, CXCL3, and CXCL12, were linked with low relapse-free survival (RFS) in HNSCC patients. On the other hand, high CXCL14 levels predicted high RFS outcomes in HNSCC patients. Meanwhile, increased gene transcription levels of CXCL9, CXCL10, CXCL13, CXCL14, and CXCL17 were associated with a higher overall survival (OS) advantage in HNSCC patients, while high levels of CXCL1, and CXCL8 were associated with poor OS in all HNSCC patients. This study implied that CXCL1, CXCL2, CXCL3, CXCL8, and CXCL12 could be used as prognosis markers to identify low survival rate subgroups of patients with HNSCC as well as be potential suitable therapeutic targets for HNSCC patients. Additionally, CXCL9, CXCL10, CXCL13, CXCL14, and CXCL17 could be used as functional prognosis biomarkers to identify better survival rate subgroups of patients with HNSCC.

Recent researches have reported that long noncoding RNA (lncRNA) five prime to Xist (FTX) plays a crucial role in the initiation and progression of cancers. In the current study, the clinical significance and functional roles of lncRNA FTX in colorectal cancer (CRC) progression were investigated. A significant increase of lncRNA FTX expression in CRC tissue and cell lines was observed. Overexpression of lncRNA FTX was significantly associated with the bigger tumor diameter, the advanced TNM stage, the lymph node, and distant metastasis, and also predicted poor prognosis of patients with CRC. Functional analyses demonstrated that knockdown of lncRNA FTX markedly inhibited CRC cell proliferation, migration, and invasion in vitro. Mechanistically, FTX directly interacted with miR-215 and suppressed miR-215 expression. FTX also bind to vimentin and reduced its phosphorylation level on Ser83 in CRC cells. Finally, using siRNAs against lncRNA FTX could dramatically inhibit CRC growth and distant metastasis in vivo. Taken together, our data demonstrated an oncogenic role of lncRNA FTX in CRC tumorigenesis and progression via interaction with miR-215 and vimentin. Then, a promising therapeutic target for CRC was provided.

Tumor cells switch from an epithelial to a mesenchymal-like phenotype, which represents a key hallmark of human cancer metastasis, including gallbladder cancer (GBC). A large set of microRNAs (miRNAs/miRs) have been studied to elucidate their functions in initiating or inhibiting this phenotypic switching in GBC cells. In this paper, we attempted to identify the expression pattern of the miR-214/-3120 cluster and its mode of action in the context of GBC, with a specific focus being placed on their effects on EMT and autophagy in GBC cells. Human GBC cells GBC-SD were assayed for their migration, invasion, and autophagy using the Transwell chamber system, MDC staining, and transmission electron microscopy. The tumorigenicity and metastatic behavior of GBC-SD cells were tested in nude mice. The expression of EMT- and autophagy-specific markers (E-cadherin, N-cadherin, vimentin, ATG5, LC3II/LC3I, and Beclin1) was analyzed in cultured GBC-SD cells and in human GBC-SD xenografts. The E2F3 luciferase reporter activity in the presence of miR-214/-3120 was evaluated by a dual luciferase assay. The miR-214/-3120 was downregulated in GBC. Exogenous miR-214/-3120 inhibited the phenotypic switching of GBC cells from epithelial to mesenchymal, prevented autophagy, and suppressed the tumorigenicity and metastatic behavior of GBC-SD cells in vitro and in vivo. E2F3 was demonstrated to be the target gene of miR-214/-3120, and its knockdown in part mimicked the effect of miR-214/-3120 on the EMT, autophagy, tumorigenicity, and metastatic behavior of GBC-SD cells. These results demonstrated that the miR-214/-3120 cluster blocks the process of EMT and autophagy to limit GBC metastasis by repressing E2F3 expression.

Complex kinship identification such as half-sibling identification is a difficult task in forensic biology Here we represented an approach in dealing with half-sisters from different mothers, with the combination of autosomal and X chromosomal short-tandem repeats (STRs) data. X chromosomal STRs can offer additional information, especially in some cases where autosomal STRs alone may not provide enough information for an accurate opinion. In this case, half-sister or unrelated relationship between two women (S1 and S2) with different mothers were distinguished. 23 autosomal and 31 X chromosomal STRs of S1, S2, S1's mother (M1), S2's mother (M2) and S1's grandmother (G1) were profiled with three different commercial kits. As to X-chromosome STRs, likelihood ratios (LRs) were calculated by FamLinkX with consideration of linkage, linkage disequilibrium, and mutations. When only the profiles of the two individuals (S1 and S2) were available, LRs between S1 and S2 were 1.1110 × 102 based on 23 autosomal STRs and 3.2257 om107 based on 31 X chromosomal STRs. When the maternal genotypes were taken into consideration, LRs increased to 2.5297 × 103 and 3.0563 × 1018. Therefore, both the DNA profiles of each mothers and X chromosomal STRs are important in dealing with the identification of half-sisters from different mothers.

The present study was conducted to investigate the molecular mechanism of urotensin II (UII) and its receptor, G protein‑coupled receptor 14 (GPR14), in colonic inflammation. Urantide, a special antagonist of GPR14, and GPR14-siRNA were used to inhibit GPR14 signaling in dextran sulfate sodium (DSS)‑induced inflammation in mice and Caco-2 cells. The results showed that urantide alleviated rectal bleeding, histological injury and production of interleukin (IL)-17 and tumor necrosis factor‑α (TNF‑α) caused by DSS in mice. GPR14-siRNA transfection subsequent with GPR14 inhibition reduced DSS-induced interferon-γ (IFN)-γ production in Caco-2 cells. Meanwhile, both in vivo and in vitro data demonstrated that inhibition of UII/GPR14 alleviated nuclear factor-κB (NF-κB) activation caused by DSS. In conclusion, UII/GPR14 signaling was involved in the DSS-induced colonic inflammation and its inhibition may serve as a potential therapeutic target, which may be associated with the NF-κB signaling pathway.

Histone deacetylases (HDACs) can regulate cell-cycle, differentiation, and apoptosis of hepatocarcinoma (HCC) cells, while their roles in drug sensitivity remain unclear. Our results showed that the expression of HDAC2 was significantly increased in HCC doxorubicin (Dox) resistant cells as compared with their corresponding control cells. Over expression of HDAC2 can increase the cell viability and decrease the Dox sensitivity. Kaplan-Meier Plotter assay revealed that HCC patients with higher levels of HDAC2 had significantly poor prognosis than that of the lower expression patients. Mechanistically studies revealed that HDAC2 can regulate the transcription of ABCB1 via directly binding with its promoter and increasing its expression in Dox resistant HCC cells. Knockdown of HDAC2 significantly inhibited the expression of ABCB1. Co-immunoprecipitation revealed that HDAC2 can bind with c-fos, an important transcription factor of ABCB1, in HCC/Dox cells. Knockdown of c-Fos decreased the binding between HDAC2 and promoter of ABCB1 in HCC/Dox cells. Collectively, our data revealed that HDAC2 can regulate Dox sensitivity of HCC cells and the transcription of ABCB1.

Atom-Centered Multilayer Code (ACMC) is a novel coding algorithm by characterizing the sphere environment of a non-hydrogen atom, called center atom. This algorithm starts from the center atom and then develops to its environment layer by layer automatically without predefining specific fragments, and the number of layers is determined on the structure of the coded compound without limit. Fast searching strategy at the atomic level is obtained by using this code. The coding process and the global structure and substructure searching are discussed with examples.

Background The 3D structure and functions of ENPP4, a protein expressed on the surface of Bacillus Calmette–Guerin (BCG)-activated macrophages, are unknown. In this study, we analyzed the 3D structure of ENPP4 and determined its tumoricidal effects on MCA207 cells. Results Homology modeling showed that Arg305, Tyr341, Asn291, and Asn295 are important residues in substrate, adenosine triphosphate (ATP), binding. A molecular dynamics study was also carried out to study the stability of ENPP4 (including zinc atoms) as well as its ligand–enzyme complex. BCG increased ENPP4 expression in macrophages, and specific blocking of ENPP4 in BCG-activated macrophages (BAMs) significantly reduced their cytotoxicity against MCA207 cells. Conclusions These results indicate that zinc remains inside the ENPP4 protein, a BCG activated tumoricidal macrophage protein, throughout the simulation. Important information for the design of new inhibitors was obtained. Electronic supplementary material The online version of this article (doi:10.1186/s12944-016-0189-4) contains supplementary material, which is available to authorized users.