An Improved BERT and Syntactic Dependency Representation Model for Sentiment Analysis.

Text representation of social media is an important task for users' sentiment analysis. Utilizing the better representation, we can accurately acquire the real semantic information expressed by online users. However, existing works cannot achieve the best results. In this paper, we construct and implement a sentiment analysis model based on the improved BERT and syntactic dependency. Firstly, by studying the word embeddings of BERT, we have ameliorated the embeddings representation. Attention mechanism is added to the word embeddings, sentence embeddings, and position embeddings. Secondly, we have exploited the dependency syntax analysis of the text, and the dependency relationship of different syntactic components will be obtained. For different syntactic components, the hierarchical attention mechanism is used to construct the phrase embeddings or block embeddings. Finally, we splice the syntactic blocks for sentiment analysis. Extensive experiments show that the proposed model has a stronger ability than the baselines on two standard data sets.

Circular RNA circ_0074027 indicates a poor prognosis for NSCLC patients and modulates cell proliferation, apoptosis, and invasion via miR-185-3p mediated BRD4/MADD activation.

Circular RNAs play an imperative role in cancer development and metastasis by regulating oncogenic and tumor-suppressive pathways. However, the role and mechanism of circ_0074027 in non-small-cell lung cancer (NSCLC) have not been elucidated. The expression levels of circ_0074027 were detected by qRT-PCR. The link between circ_0074027 expression and clinicopathologic parameters was analyzed by Fisher's exact test. The prognostic role of circ_0074027 was investigated by Kaplan-Meier and Cox regression analysis. Cell counting kit-8 and flow cytometric assays were utilized to evaluate NSCLC cell proliferation and apoptosis, respectively. Wound scratch and Transwell tests were applied to detect cell migratory and invasive capacities. The interaction potential of circ_0074027 and miR-185-3p was analyzed by the circBank database, and verified by dual-luciferase reporter assay. The downstream gene of miR-185-3p was also investigated. Circ_0074027 was elevated in NSCLC specimens and cell lines. Overexpressed circ_0074027 was related to more advanced TNM stages, poorer differentiation grade, and worse overall survival. Upregulated circ_0074027 increased the proliferation of H1299 cells by inhibiting cell apoptosis. Cell migration and invasion were enhanced after circ_0074027 overexpression. Silenced circ_0074027 caused the opposite effects in the A549 cell line. For mechanism investigation, circ_0074027 directly sponges miR-185-3p to enhance bromodomain-containing protein 4 (BRD4) and MAPK-activating death domain-containing protein (MADD) expression levels at the posttranscriptional level. Furthermore, we found the oncogenic function of circ_0074027 is attributed to its modulation of BRD4 and MADD. Collectively, upregulated circ_0074027 in NSCLC accelerates cell progression via miR-185-3p/BRD4/MADD pathway as a competing endogenous RNA.

Elevation of circular RNA circ_0005230 facilitates cell growth and metastasis via sponging miR-1238 and miR-1299 in cholangiocarcinoma.

Cholangiocarcinoma (CCA) is a highly malignant carcinoma with high mortality rate worldwide. Emerging evidence indicates that aberrantly expressed circular RNAs (circRNAs) functions crucial roles in tumor progression. In this work, we focused on a novel circRNA, circ_0005230, in carcinogenesis and development of CCA. Circ_0005230 levels in CCA specimens and cells were measured by qRT-PCR. The clinical implication of circ_0005230 was analyzed by fisher's exact test. Gain/loss of-function assays were conducted to reveal the effects of circ_0005230 on the cell proliferation, apoptosis, migration and invasion of CCA cells. Xenograft and lung metastatic models were constructed to confirm the in vitro data. Dual luciferase reporter and rescue assays were carried out to illuminate the mechanism behind the regulatory actions. As data showed, circ_0005230 was elevated in tumors and CCA cells. Its expression in tumor samples was related to clinical severity. Functionally, circ_0005230 significantly facilitated cell growth, clone-forming ability and metastatic properties and inhibit cell apoptosis in CCA cells. The in vivo study further validated the in vitro results. However, knockdown of circ_0005230 did not affect normal biliary epithelial (HIBEC) cell growth and apoptosis. For the mechanism investigation, circ_0005230 could directly sponge miR-1238 and miR-1299 to exert its oncogenic functions. Overall, this work showed that circ_0005230 might act as an effective therapeutic target for CCA.

GPC1 regulated by miR-96-5p, rather than miR-182-5p, in inhibition of pancreatic carcinoma cell proliferation.

To determine the relationships between miR-96-5p/-182-5p and GPC1 in pancreatic cancer (PC), we conducted the population and in vitro studies. We followed 38 pancreatic cancer patients, measured and compared the expression of miR-96-5p/-182-5p, GPC1, characteristics and patients' survival time of different miR-96-5p/-182-5p expression levels in PC tissues. In an in vitro study, we investigated the proliferation, cycle and apotosis in cells transfected with mimics/inhibitors of the two miRNAs, and determine their effects on GPC1 by dual-luciferase assay. In the follow-up study, we found that the expressions of miR-96-5p/-182-5p were lower/higher in PC tissues; patients with lower/higher levels of miR-96-5p/-182-5p suffered poorer characteristics and decreased survival time. In the in vitro study, the expressions of miR-96-5p/-182-5p were different in cells. Proliferation of cells transfected with miR-96-5p mimics/inhibitors was lower/higher in Panc-1/BxPC-3; when transfected with miR-182-5p mimics/inhibitors, proliferation of cells were higher/lower in AsPC-1/Panc-1. In a cell cycle study, panc-1 cells transfected with miR-96-5p mimics was arrested at G0/G1; BxPC-3 cells transfected with miR-96-5p inhibitors showed a significantly decrease at G0/G1; AsPC-1 cells transfected with miR-182-5p mimics was arrested at S; Panc-1 cells transfected with miR-182-5p inhibitors showed a decrease at S. MiR-96-5p mimics increased the apoptosis rate in Panc-1 cells, and its inhibitors decreased the apoptosis rate in BxPC-3. Dual luciferase assay revealed that GPC1 was regulated by miR-96-5p, not -182-5p. We found that miR-96-5p/-182-5p as good markers for PC; miR-96-5p, rather than -182-5p, inhibits GPC1 to suppress proliferation of PC cells.

The Wnt antagonist sFRP1 as a favorable prognosticator in human biliary tract carcinoma.

Inactivation of Secreted Frizzled-Related Protein-1 (SFRP1) and overexpression of ß-catenin play important roles in the development and progression of a wide range of malignancies. We sought to determine whether the expression of SFRP1 and ß-catenin correlates with clinicopathologic parameters in human biliary tract cancer (BTC) and to evaluate the potential roles of these proteins as prognostic indicators. The expression of SFRP1 and ß-catenin in 78 patients with BTC and 36 control patients as investigated by immunohistochemistry. A wide variety of statistical parameters were assessed to determine the association between these proteins and the occurrence, clinical features, and overall survival rate in BTC.SFRP1 and ß-catenin had an inverse correlation (r = -0.636, P<0.0001) as assessed by Spearman rank analysis, with 52 (66.7%) of the BTC samples negative for SFRP1 expression and 53 (68.0%) positive for ß-catenin expression. Expression of each protein was associated with the histological type and lymph node invasion of BTC. A significantly poorer overall survival rate was observed for patients with low SFRP1 expression (P<0.0001) or high ß-catenin expression (P = 0.007). SFRP1 expression (P<0.0001), ß-catenin expression (P<0.01) and histological type (P<0.01) were correlated with overall survival rate as assessed by univariate analysis; while multivariate analysis suggested that SFRP1 (hazard ratio, 10.514; 95% confidence intervals, 2.381-39.048; P<0.0001) may serve as an independent prognostic factor for BTC. Collectively, these results demonstrate that SFRP1 is a favorable prognostic factor for human BTC and that its expression inversely correlates with that of ß-catenin.

Insulin and hypertonic glucose in the management of aseptic fat liquefaction of post-surgical incision: a meta-analysis and systematic review.

A meta-analysis and systematic review assessing randomised controlled trials (RCTs) was sought to determine whether subcutaneous injection of insulin with hypertonic glucose promotes healing in postoperative incisions with aseptic fat liquefaction. We searched the Cochrane library, Pubmed, EMBASE, National Science Digital Library (NSDL) and China Biological Medicine Database (CBMdisc) for literature published from 1 January 1990 to 30 September 2011. RCTs that evaluated subcutaneous injection of insulin with hypertonic glucose as a treatment for postoperative wound with fat liquefaction were sought. Wound healing was the primary endpoint. Jadad score and Cochrane Collaboration's tool were used for assessing quality of studies and risk of bias. We abstracted data regarding time to wound healing, cost and adverse effects. The random-effects inverse variance model was used for all analyses using weighted mean difference and 95% confidence interval. Eight trials (414 participants) were identified that met the inclusion criteria. Subcutaneous injection of insulin with hypertonic glucose significantly reduces time to healing by 6·33 days compared with conventional drainage, with less cost. There was no report concerning adverse effects. Subcutaneous injection of insulin with hypertonic glucose may improve the healing process in postoperative wounds with aseptic fat liquefaction.

Arsenic trioxide and promyelocytic leukemia protein-adenovirus synergistically inhibit in vitro and in vivo growth of a hepatoma cell line.

The present study investigated the in vitro and in vivo growth-inhibitory effects of combination therapy with arsenic trioxide (As2O3) and an adenovirus expressing promyelocytic leukemia protein (Ad-PML). Growth of HepG2 cells in culture was not inhibited by As2O3 at concentrations below 5 micromol/L (p > 0.05). However, growth was inhibited by Ad-PML alone and synergistic growth inhibition was observed following combined treatments (p < 0.05). Flow cytometry analyses demonstrated an increase in apoptosis following combined treatment with As2O3 and Ad-PML for 24 h, which was correlated with increased p53 and decreased Bcl-2 expression. To examine treatment effects on in vivo cell growth, control HepG2 cells and cells treated with As2O3, Ad-PML, or both therapies were subcutaneously injected in nude mice. After 6 weeks, tumor volumes were 0.097 +/- 0.031 and 0.083 +/- 0.005 cm3 in the control and As2O3 alone groups, respectively (p > 0.05), but were undetectable in the Ad-PML alone or Ad-PML plus As2O3 groups. Finally, established HepG2 tumors in nude mice were injected with PBS, Ad-PML, As2O3, or Ad-PML plus As2O3, the tumor volumes were measured by ultrasound, and the therapeutic effects were compared. As2O3 alone had no effect at concentrations below 5 micromol/L (p > 0.05), while Ad-PML alone at a multiplicity of infection of 20 or As2O3 plus Ad-PML significantly decreased tumor volumes (p < 0.05). Thus, the combination of As2O3 and Ad-PML has synergistic inhibitory effects on hepatocellular carcinoma (HCC), possibly resulting from regulation of apoptotic gene expression enhanced HCC apoptosis.

Prevention of central cell damage to isolated islets of Langerhans in hamsters by low temperature preconditioning.

BACKGROUND: The efficacy of clinical islet transplantation has been demonstrated with autografts, and although islet allografts have established insulin independence in a small number of IDDM patients, the treatment is confounded by the necessity of central cell damage immunosuppression, the lack of donor tissue, and recurring islet immunogenicity. These limitations underscore a need to develop therapies to serve the large population of diabetic patients. This study was designed to document central cell damage to isolated islets of Langerhans in hamsters and its prevention. METHODS: Islets were cultured at 37 degree centigrade for 7-14 days after isolation, and then at 26 degree centigrade for 2,4 and 7 days before additional culture at 37 degree centigrade for an additional 7 days. Central cell damage in the isolated islets was monitored by video-microscopy and analyzed quantitatively by a computer-assisted image analysis system. The analysis included daily measurement of the diameter and the area of the isolated islets and the area of the central cell damage that developed in those islets over time during culture. Histological examination and TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay were used to characterize cell damage and to monitor islet function. RESULTS: Microscopic analysis showed that during the 7 to 14 days of culture at 37 degree centigrade, central cell damage appeared in the larger islets with diameters greater than 200 microm, which included both necrotic and apoptotic cell death. Low temperature (26 degree centigrade) culture prevented central cell damage of isolated islets. The 7-day culture procedure at 26 degree centigrade could inhibit most of the central cell (excluding diameters greater than 300 microm) damage when the islets were rewarmed to 37 degree centigrade. CONCLUSIONS: Our results indicate that central cell damage to isolated islets of Langerhans correlates with the size of the islets. Low temperature (26 degree centigrade) culture can prevent central cell damage to the isolated islets, and is capable to successfully precondition these islets for 37 degree centigrade culture. These novel findings may help to understand the pathophysiology of early loss of islet tissue after transplantation, and may provide a new strategy to improve graft function in the clinical setting of islet transplantation.