Objective To evaluate the changes of function of right ventricular using echocardiography after transcatheter closure of atrial septal defect(ASD)and to study the feasibility and superiority of echocardiographic evaluation of right ventricular function. Methods In 70 patients with transcatheter closure of ASD,echocardio?graphic examinations were made different time intervals after the closure to calculate right cardiac morpnology and function. Results After closure ASD in different time intervals, the size of RAEDd1, RAEDd2, RVEDd1, RVEDd2, RVEDd3, Inferior Vena Cava and RIMP, RVEF, TAPSE and FAC were obviously decreased(P<0.01)between two groups. All events were obviously decreased compared precious function(P < 0.01)and the interaction of the time (P < 0.01). Conclusion The construction of right ventricular narrows gradually and the function recovers after transcatheter closure of ASD in a year and those who did not become worse.

Objective:To investigate the expression of long non-coding RNA (lncRNA) CALCOCO1 in bladder cancer tissue and its effect on the proliferation and migration of bladder cancer cells by regulating miR-200a-3p.Methods:The relative expression levels of CALCOCO1 in bladder cancer tissues and adjacent tissues were analyzed by TCGA database. Human bladder cancer cells UM-UC-3 were selected, and the cells were divided into negative control group and CALCOCO1 group, and NC plasmid and CALCOCO1 plasmid were transfected into UM-UC-3 cells respectively. The expression level of CALCOCO1 in each group was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation and migration ability of UM-UC-3 cells were detected by MTT assay and Transwell migration assay. Bioinformatics technology was used to predict and dual-luciferase reporter gene experiments to verify the targeting relationship between CALCOCO1 and miR-200a-3p. The expression levels of miR-200a-3p in UM-UC-3 cells in each group were detected by qRT-PCR. Western blotting was used to detect the expression of UM-UC-3 cells proliferation and migration phenotype in each group. Measurement data were expressed as mean ± standard deviation ( ± s), t-test was used for comparison between two groups, and repeated measurement analysis of variance was used for comparison at different time. Results:Compared with adjacent tissues, the relative expression level of CALCOCO1 in bladder cancer tissues was significantly lower, the difference was statistically significant( P<0.01). The relative expression of CALCOCO1 in UM-UC-3 cells in CALCOCO1 group and negative control group was 9.66±2.51 and 1.07±0.59, respectively. The relative expression level of CALCOCO1 in CALCOCO1 group was significantly higher than that in negative control group, the difference was statistically significant ( P<0.01). Compared with the negative control group, the proliferation activity of UM-UC-3 cells in the CALCOCO1 group was decreased ( P<0.05), and the migration number of UM-UC-3 cells was significantly decreased ( P<0.01). CALCOCO1 had a binding site with miR-200a-3p ( P<0.01). The relative expression of miR-200a-3p in UM-UC-3 cells in CALCOCO1 group and negative control group was 1.02 ± 0.31 and 5.79 ± 1.68, respectively, the difference was statistically significant ( P<0.01). Compared with the negative control group, the expression levels of proliferation phenotype proteins CCNB1, CCNE1 and CCND2 in UM-UC-3 cells in CALCOCO1 group decreased, and the expression levels of migration phenotype proteins FOXC2 and Fibronectin decreased. Conclusion:The expression of CALCOCO1 is down-regulated in bladder cancer tissue, promoting the expression of CALCOCO1 can inhibit the proliferation and migration of bladder cancer UM-UC-3 cells through targeted down-regulation of miR-200a-3p expression.

Influenza B virus (IBV) is a segmented negative-strand RNA virus, which often causes local outbreak or seasonal epidemic along with influenza A virus (IAV) in the world. It is pathogenic to children, teenagers and elderly people and has a higher mortality rate in children and adolescents, so it poses a serious threat to public health and health. IBV is more likely to cause complications than IAV and the disease burden of IBV even exceeds IAV in the epidemic season. Recently, especially after winter of 2017, IBV has become the dominant strain in many areas of our country and seriously affects people's health. In view of this, this article reviews the structure, epidemiology, immunology and prevention of IBV, aiming at enhancing public's perceptions of the virus and providing reference for making strategies for prevention and control of influenza B.

The CRISPR/Cas9 gene editing technology directs Cas9 protein to recognize, bind and cleave the target site specifically by using artificial single-guide RNA (sgRNA), through non-homologous end joining or homologous end-recombinant repair mechanisms of cells, which can be engineered to knockout or knock-in of genomes. RIG-I is a pattern recognition receptor that recognizes the 5'-triphosphate-containing RNA in the cytoplasm and activates IRF3/7 and NF-κB by interacting with the downstream signaling molecule MAVS, thus initiating the expression of type I interferons and inflammatory factors. Previous studies found that influenza B virus (IBV) can up-regulate the expression of RIG-I. In the present study, to explore whether RIG-I is the major receptor for IBV to active the antiviral innate immune response and its effect on IBV replication, RIG-I gene in 293T cells was knocked out by CRISPR-Cas9 system, and a stable RIG-I knockout 293T (RIG-I(-/-) 293T) cell line was screened by puromycin pressure. The results of Western blotting showed that RIG-I was not expressed in this cell line after IBV or Sendai virus (SeV) infection, indicating that the RIG-I(-/-) 293T cell line was successfully constructed. The transcription levels of interferons, inflammatory factors and interferon-stimulated genes in RIG-I(-/-) 293T cells which were infected by IBV decreased significantly compared with those in wild-type 293T cells. Moreover, the phosphorylation of p65 and IRF3 were not detected in IBV or SeV infected RIG-I(-/-) 293T cells. It is indicated that the expression of cytokines mainly depends on the RIG-I-mediated signaling pathway at the early stage of IBV infection. Furthermore, the multi-step growth curves of IBV in the wild type and RIG-I(-/-) 293T cells showed that RIG-I inhibited the replication of IBV. Collectively, the RIG-I knockout 293T cell line was successfully constructed. We found that RIG-I is the main receptor for IBV to active the antiviral innate immune response and is critical for inhibiting IBV replication, which lays the foundation for further study of IBV infection mechanism.

This paper aims to explore the effects of chicken interferon-γ (ChIFN-γ) and interleukin-2 (ChIL-2) on type 1 helper (Th1) T lymphocyte differentiation. To be specific, ChIFN-γ and ChIL-2 were first expressed in Escherichia coli competent cells and then purified by Ni-NTA affinity chromatography. Different concentration of ChIFN-γ and ChIL-2 were employed to stimulate the lymphocytes in chicken peripheral blood which had been activated by concanavalin A (Con A), and the mRNA levels of cytokines related to Th1 cell differentiation were detected by real-time quantitative PCR (RT-qPCR). The results showed that both ChIFN-γ and ChIL-2 can significantly up-regulate mRNA levels of cytokines related to Th1 cell differentiation and the optimal concentration was 12.5 μg/mL and 25.0 μg/mL, respectively. In addition, specific-pathogen-free (SPF) chickens were immunized with ChIL-2 or ChIFN-γ together with H9N2 vaccine, or H9N2 vaccine alone by oral administration or intramuscular injection, respectively. The mRNA levels of cytokines related to Th1 cell differentiation were detected after immunization. The results showed that ChIFN-γ and ChIL-2 significantly up-regulated the mRNA levels of cytokines related to Th1 cell differentiation induced by H9N2 vaccine compared with H9N2 vaccine alone, and that the intramuscular injection was better than oral administration. In this study, we verified that ChIFN-γ and ChIL-2 can significantly enhance mRNA levels of cytokines related to Th1 cell differentiation induced by ConA or H9N2 vaccine in vitro and in vivo. The results of this study can lay a theoretical basis for using ChIFN-γ and ChIL-2 as vaccine adjuvants.
Animals ; Cell Differentiation ; Chickens ; Concanavalin A ; Cytokines/genetics* ; Influenza A Virus, H9N2 Subtype/genetics* ; Interferon-gamma/metabolism* ; Interleukin-2/genetics* ; RNA, Messenger

Influenza B virus (IBV) is more likely to cause complications than influenza A virus (IAV) and even causes higher disease burden than IAV in a certain season, but IBV has received less attention. In order to analyze the genetic evolution characteristics of the clinical strain IBV (B/Guangxi-Jiangzhou/1352/2018), we constructed genetic evolution trees and analyzed the homology and different amino acids of hemagglutinin and neuraminidase referring to the vaccine strains recommended by World Health Organization (WHO). We found that strain B/Guangxi-Jiangzhou/1352/2018 was free of interlineage reassortment and poorly matched with the vaccine strain B/Colorado/06/2017 of the same year. We also determined the median lethal dose (LD₅₀) and the pathogenicity of strain B/Guangxi-Jiangzhou/1352/2018 in mice. The results showed that the LD₅₀ was 10^5.9 TCID₅₀ (median tissue culture infective dose), the IBV titer in the lungs reached peak 1 d post infection and the mRNA level of the most of inflammatory cytokines in the lungs reached peak 12 h post infection. The alveoli in the lungs were severely damaged and a large number of inflammatory cells were infiltrated post infection. The study demonstrated that the clinical strain IBV (B/Guangxi-Jiangzhou/1352/2018) could infect mice and induce typical lung inflammation. This will facilitate the research on the pathogenesis and transmission mechanism of IBV, and provide an ideal animal model for evaluation of new vaccines, antiviral and anti-inflammatory drug.
Amino Acids/genetics* ; Animals ; Antiviral Agents/pharmacology* ; China ; Cytokines/metabolism* ; Hemagglutinins/metabolism* ; Humans ; Influenza B virus/pathogenicity* ; Influenza, Human/virology* ; Mice ; Neuraminidase/genetics* ; Orthomyxoviridae Infections/virology* ; Phylogeny ; RNA, Messenger/metabolism* ; Virulence/genetics*

This study aimed to explore the mechanism of how African swine fever virus (ASFV) I226R protein inhibits the cGAS-STING signaling pathway. We observed that I226R protein (pI226R) significantly inhibited the cGAS-STING-mediated type Ⅰ interferons and the interferon-stimulated genes production by dual-luciferase reporter assay system and real-time quantitative PCR. The results of co-immunoprecipitation assay and confocal microscopy showed that pI226R interacted with cGAS. Furthermore, pI226R promoted cGAS degradation through autophagy-lysosome pathway. Moreover, we found that pI226R decreased the binding of cGAS to E3 ligase tripartite motif protein 56 (TRIM56), resulting in the weakened monoubiquitination of cGAS, thus inhibiting the activation of cGAS and cGAS-STING signaling. In conclusion, ASFV pI226R suppresses the antiviral innate immune response by antagonizing cGAS, which contributes to an in-depth understanding of the immune escape mechanism of ASFV and provides a theoretical basis for the development of vaccines.
Animals ; Swine ; African Swine Fever Virus/metabolism* ; Membrane Proteins/metabolism* ; Immunity, Innate ; Nucleotidyltransferases/metabolism* ; Signal Transduction/genetics*

Objective: To systematically review the quality and reporting quality of colorectal cancer screening guidelines, and to provide reference for the update of colorectal cancer screening guidelines and colorectal cancer screening in China. Methods: "Colorectal cancer", "colorectal tumor", "screening", "screening", "guide", "consensus", "Colorectal cancer", "Colorectal neoplasms", "Screening", "Early Detection of Cancer", "Guideline" and "recommendation" were used as search keywords. The literature retrieval for all the Chinese and English guidelines published before April 2018 was conducted by using PubMed, Embase, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang Data, China Biology Medicine disc (CBMdisc), Cochrane Library, Guideline International Network, China Guidelines Clearinghouse (CGC) and the official website of the US Preventive Services Task Force (USPSTF), the American Cancer Society (ACS), International Agency for Research on Cancer (IARC), Australia Cancer Council (ACC) and Association of Coloproctology of Great Britain & Ireland (ACPGBI). The inclusion criteria were independent guidance documents for colorectal cancer screening. The language is limited to Chinese and English. The exclusion criteria were literature on interpretation, evaluation, introduction, etc., as well as the translated version of the guide and old guides. The quality and reporting norms of colorectal cancer screening guidelines were compared and evaluated using the European Guideline Research and Assessment Tool (AGREE Ⅱ) and the Practice Guideline Reporting Standard (RIGHT). Results: A total of 15 guides were included. The results of the AGREE Ⅱ quality evaluation showed that the overall quality of 15 guides was high. Among them, there were 9 guides with an overall score of 50 or more, 10 with a recommendation level of "A", and 2 with a rating of "B". There were 3 guides for "C"; each guide scores higher in scope and purpose, and clarity, and scores vary greatly in the areas of participants, rigor, applicability, and independence. The results of the RIGHT evaluation showed that 15 guides were insufficient in six areas except for background information, evidence, recommendations, reviews and quality assurance, funding and conflict of interest statements and management, and other aspects. Conclusion The overall quality of included guidelines for colorectal cancer screening is high, but the normative nature needs to be strengthened.