The Study of the Effects of Yunnan Yuxi Dialect on Received Pronunciation

In A Brief Analysis of Yuxi Dialect, Fu Chang makes a detailed explanation on dialects’ features and the value of its study. In The General Received Pronunciation of British English by Fengtong Chang, the author dealt with reasons why London English became standard English, and also elaborated on consonants and vowels in British English. Up to today no one has ever made a contrast between the two languages and further diminished the interference from dialect in English pronunciation learning of the Yuxi students. This paper is designed to make a contrast between the two languages: Yuxi dialect in Zhoucheng and Received Pronunciation; as well as the differences between their consonants and vowels respectively can be achieved to rectify the pronunciations’ deviation in English learning. It is intended to improve English teaching quality of Yuxi dialect speakers and enhance the pronunciation standardization of English there

A Study of Equivalent Translation from the Perspective of Narrative Stylistics: The Case of Tao’s The Color Purple

The author’s narrative strategy is the soul of the novel, and the words are the medium to express this soul. The issue of faithfulness in novel translation involves not only the faithfulness of the content, but also the form of expression - narrative strategy. This paper takes Tao Jie’s translation of Alice Walker’s the Color Purple as the research object, and probes into the formal equivalence of the translation from the perspective of narrative stylistics, that is, personal narrative voice, character discourse expression and the stylistic features of black American English. This paper explores the guiding role of narrative stylistics in literary translation practice, hoping to provide reverse translation experience for Chinese literary translation.

Cell surface-specific N-glycan profiling in breast cancer

Aberrant changes in specific glycans have been shown to be associated with immunosurveillance, tumorigenesis, tumor progression and metastasis. In this study, the N-glycan profiling of membrane proteins from human breast cancer cell lines and tissues was detected using modified DNA sequencer-assisted fluorophore-assisted carbohydrate electrophoresis (DSA-FACE). The N-glycan profiles of membrane proteins were analyzed from 7 breast cancer cell lines and MCF 10A, as well as from 100 pairs of breast cancer and corresponding adjacent tissues. The results showed that, compared with the matched adjacent normal tissue samples, two biantennary N-glycans (NA2 and NA2FB) were significantly decreased (p <0.0001) in the breast cancer tissue samples, while the triantennary glycan (NA3FB) and a high-mannose glycan (M8) were dramatically increased (p = 0.001 and p <0.0001, respectively). Moreover, the alterations in these specific N-glycans occurred through the oncogenesis and progression of breast cancer. These results suggested that the modified method based on DSA-FACE is a high-throughput detection technology that is suited for analyzing cell surface N-glycans. These cell surface-specific N-glycans may be helpful in recognizing the mechanisms of tumor cell immunologic escape and could be potential targets for new breast cancer drugs

Specific N-glycans of Hepatocellular Carcinoma Cell Surface and the Abnormal Increase of Core-α-1, 6-fucosylated Triantennary Glycan via N-acetylglucosaminyltransferases-IVa Regulation

Glycosylation alterations of cell surface proteins are often observed during the progression of malignancies. The specific cell surface N-glycans were profiled in hepatocellular carcinoma (HCC) with clinical tissues (88 tumor and adjacent normal tissues) and the corresponding serum samples of HCC patients. The level of core-α-1,6-fucosylated triantennary glycan (NA3Fb) increased both on the cell surface and in the serum samples of HCC patients (p \u3c 0.01). Additionally, the change of NA3Fb was not influenced by Hepatitis B virus (HBV)and cirrhosis. Furthermore, the mRNA and protein expression of N-acetylglucosaminyltransferase IVa (GnT-IVa), which was related to the synthesis of the NA3Fb, was substantially increased in HCC tissues. Knockdown of GnT-IVa leads to a decreased level of NA3Fb and decreased ability of invasion and migration in HCC cells. NA3Fb can be regarded as a specific cell surface N-glycan of HCC. The high expression of GnT-IVa is the cause of the abnormal increase of NA3Fb on the HCC cell surface, which regulates cell migration. This study demonstrated the specific N-glycans of the cell surface and the mechanisms of altered glycoform related with HCC. These findings lead to better understanding of the function of glycan and glycosyltransferase in the tumorigenesis, progression and metastasis of HCC

Specific N-glycans of Hepatocellular Carcinoma Cell Surface and the Abnormal Increase of Core-α-1, 6-fucosylated Triantennary Glycan via N-acetylglucosaminyltransferases-IVa Regulation

Glycosylation alterations of cell surface proteins are often observed during the progression of malignancies. The specific cell surface N-glycans were profiled in hepatocellular carcinoma (HCC) with clinical tissues (88 tumor and adjacent normal tissues) and the corresponding serum samples of HCC patients. The level of core-α-1,6-fucosylated triantennary glycan (NA3Fb) increased both on the cell surface and in the serum samples of HCC patients (p \u3c 0.01). Additionally, the change of NA3Fb was not influenced by Hepatitis B virus (HBV)and cirrhosis. Furthermore, the mRNA and protein expression of N-acetylglucosaminyltransferase IVa (GnT-IVa), which was related to the synthesis of the NA3Fb, was substantially increased in HCC tissues. Knockdown of GnT-IVa leads to a decreased level of NA3Fb and decreased ability of invasion and migration in HCC cells. NA3Fb can be regarded as a specific cell surface N-glycan of HCC. The high expression of GnT-IVa is the cause of the abnormal increase of NA3Fb on the HCC cell surface, which regulates cell migration. This study demonstrated the specific N-glycans of the cell surface and the mechanisms of altered glycoform related with HCC. These findings lead to better understanding of the function of glycan and glycosyltransferase in the tumorigenesis, progression and metastasis of HCC

Psychometric properties of the Chinese version of the preoperative assessment of readiness tool among surgical patients

BackgroundThe evaluation of the surgical readiness of patients plays an important role in clinical care. Preoperative readiness assessment is needed to identify the inadequacy among surgical patients, which provides guide for interventions to improve patients’ preoperative readiness. However, there is a paucity of high-level, quality tool that evaluate surgical readiness of patients in China. The purpose of this study is to translate the Preoperative Assessment of Readiness Tool (PART) into Chinese and determine the reliability and validity of the Chinese version in the population of surgical patients.MethodsUsing a standard translation-backward method, the original English version of PART was translated into Chinese. A convenient sampling of 210 surgical patients was recruited from 6 hospitals in Zhejiang Province to test the psychometric properties of this scale including internal consistency, split-half reliability, content validity, structure validity, and floor/ceiling effect.ResultsA total of 194 patients (92%) completed questionnaires. The Chinese version of PART achieved Cronbach’s alphas 0.948 and McDonald’s omega coefficient 0.947, respectively, for the full scale. The estimated odd-even split-half reliability was 0.959. The scale-level content validity index was 0.867, and the items content validity index ranged from 0.83 to 1.0.The output of confirmatory factor analysis (CFA) revealed a two-factor model (χ2 = 510.96; df = 86; p &lt; 0.001; root mean square error approximation = 0.08) with no floor/ceiling effect.ConclusionThe Chinese version of PART demonstrated acceptable reliability and validity among surgical patients. It can be used to evaluate patients’ preoperative preparation and help health professionals provide proper preoperative support

FOXO1 Inhibits Tumor Cell Migration via Regulating Cell Surface Morphology in Non-Small Cell Lung Cancer Cells

Background/Aims: Cell surface morphology plays pivotal roles in malignant progression and epithelial-mesenchymal transition (EMT). Previous research demonstrated that microvilli play a key role in cell migration of non-small cell lung cancer (NSCLC). In this study, we report that Forkhead box class O1 (FOXO1) is downregulated in human NSCLC and that silencing of FOXO1 is associated with the invasive stage of tumor progression. Methods: The cell proliferation, migration, and invasion were characterized in vitro, and we tested the expression of the Epithelial-mesenchymal transition (EMT) marker by immunofluorescence staining and also identified the effect of FOXO1 on the microvilli by scanning electron microscopy (SEM). Results: Functional analyses revealed that silencing of FOXO1 resulted in an increase in NSCLC cell proliferation, migration, and invasion; whereas overexpression of FOXO1 significantly inhibited the migration and invasive capability of NSCLC cells in vitro. Furthermore, cell morphology imaging showed that FOXO1 maintained the characteristics of epithelial cells. Immunofluorescence staining and western blotting showed that the E-cadherin level was elevated and Vimentin was reduced by FOXO1 overexpression. Conversely, the E-cadherin level was reduced and Vimentin was elevated in cells silenced for FOXO1. Furthermore, scanning electron microscopy (SEM) showed that FOXO1 overexpression increased the length of the microvilli on the cell surface, whereas FOXO1 silencing significantly reduced their length. Conclusions: FOXO1 is involved in human lung carcinogenesis and may serve as a potential therapeutic target in the migration of human lung cancer

MAP1S Controls Breast Cancer Cell TLR5 Signaling Pathway and Promotes TLR5 Signaling-based Tumor Suppression

<div><p>Targeting TLR5 signaling in breast cancer represents a novel strategy in cancer immunotherapy. However, the underlying mechanism by which TLR5 signaling inhibits cancer cell proliferation and tumor growth has not been elucidated. In this study, we found TLR5 agonist flagellin inhibited the cell state of activation and induced autophagy, and reported that autophagy protein MAP1S regulated the flagellin/TLR5 signaling pathway in breast cancer cells through enhancement of NF-κB activity and cytokine secretion. Remarkably, MAP1S played a critical role in tumor suppression induced by flagellin, and knockdown of MAP1S almost completely abrogated the suppression of tumor growth and migration by flagellin treatment. In addition, elevated expression of MAP1S in response to flagellin feed-back regulated tumor inflammatory microenvironment in the late stages of TLR5 signaling through degradation of MyD88 in autophagy process. These results indicate a mechanism of antitumor activity that involves MAP1S-controlled TLR5 signaling in breast cancer.</p></div