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[Advances associated with allergen portion discovery from the elimination and control of allergic diseases].
Background Long noncoding RNA (lncRNA) MORT is silenced in many malignancies, but its role in cancer remains hardly known. Methods The expression of MORT and NOTCH1 was determined by real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Correlation between MORT and NOTCH1 was analyzed by Pearson's correlation analysis. To further investigate the interaction between MORT and NOTCH1, overexpression experiments were performed. Results In our study, MORT expression was downregulated in hepatocellular carcinoma (HCC), while NOTCH1 expression was upregulated in HCC patients. Hepatitis B virus and hepatitis C virus infection and tumor size did not significantly affect MORT expression, but MORT expression was lower in metastatic HCC patients compared with nonmetastatic HCC patients. MORT and NOTCH1 were inversely correlated across HCC tissues. MORT overexpression decreased NOTCH1 expression, while NOTCH1 overexpression did not significantly affect MORT. MORT overexpression inhibited the migration and invasion of HCC cells, while NOTCH1 overexpression promoted the migration and invasion of HCC cells. learn more In addition, NOTCH1 overexpression attenuated the effects of MORT overexpression on cell migration and invasion. Conclusion Therefore, MORT overexpression may inhibit HCC by downregulating NOTCH1.Background Recent investigations have suggested that long noncoding RNA (lncRNA) MIR22HG is commonly dysregulated in multiple types of malignancies. Nevertheless, the roles of MIR22HG in human colorectal carcinoma (CRC) are not well explored. Materials and Methods Quantitative real-time polymerase chain reaction (qPCR) and in situ hybridization (ISH) assay were used to measure the expression of MIR22HG. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and migration, as well as invasion assays, were utilized to determine the roles of MIR22HG on growth, apoptosis, migration, and invasiveness of CRC cell. The expression of E-cadherin and N-cadherin was measured using western blotting and immunohistochemistry staining assay. CRC cell growth in vivo was analyzed using nude mice xenograft. Results The qPCR and ISH assay revealed that MIR22HG was downregulated in CRC sample compared with in normal tissue. MIR22HG was also significantly downexpressed in CRC cells compared with that in normal colonic epithelial cell line. Overexpression of MIR22HG inhibited the growth, migration ability, and invasiveness of CRC cell in vitro. In addition, MIR22HG suppressed the epithelial-mesenchymal transition (EMT) and induced the apoptosis of human CRC cell. Moreover, the authors demonstrated that MIR22HG inhibited the tumor growth of CRC cell and regulated the expression of EMT markers (E-cadherin and N-cadherin) in vivo. Conclusion Altogether, these results implied that lncRNA MIR22HG restrained the aggressive phenotypes of CRC cell.Background Both TEK and miR-19a-3p have been reported to regulate lung adenocarcinoma (LUAD) progression. However, the association between TEK and miR-19a-3p in LUAD remained unknown. This research aimed to investigate a novel miR-19a-3p/TEK interactome in LUAD cells. Methods The mRNA expression and protein expression in the cell lines were determined using qPCR and Western blot assay, respectively. CCK-8 assay, EDU assay, flow cytometry cell apoptosis assay, scratch assay, and cell-to-extracellular matrix adhesion assay were performed to detect the proliferation, apoptosis, migration, and adhesion ability of A549 and H1975 cell lines. Results Findings revealed that both mRNA and protein levels of TEK were downregulated in the LUAD tumor tissues and cell lines. It was also found that compared with the control group, the transfection of TEK overexpression plasmids into H1975 and A549 cell lines significantly inhibited cancerous phenotypes. However, experimental results indicated that by downregulating TEK, miR-19a-3p promoted LUAD cell phenotypes. Conclusion This research demonstrated that an interactome existed between miR-19a-3p and TEK and that miR-19a-3p could suppress LUAD tumors by inhibiting TEK. This novel interactome could be used as a novel therapy target for LUAD.Background To investigate morphology, physical property, loadability, stability, and release profiles of a novel drug-eluting microsphere, CalliSpheres, in vitro and explore its embolic efficacy and safety in vivo. Materials and Methods CalliSpheres (50-150 μm, 100-300 μm, and 300-500 μm) and doxorubicin at different amounts (20, 40, 80, and 100 mg) and concentrations (5 and 10 mg/mL) were prepared for experiments. Dynamic light scattering and an Agilent 1260 high-performance liquid chromatography system were used to quantify bead diameters and the efficiency of drug loading and release, respectively. Twelve New Zealand rabbits were treated with catheter-aided hepatic embolization using CalliSpheres. Results CalliSpheres displayed a red color after loading with doxorubicin, and the mean diameters were decreased by 20.7-25.8%. Almost 100% of the drug was incorporated with CalliSpheres in different sizes immersed with doxorubicin 20 mg, while loading efficiency ranged from 75.8% to 100.0% with doxorubicin at 40, 80, and 100 mg dependent on CalliSpheres sizes (smaller sizes, higher loading efficiency). Besides, elevated loading efficiency was observed at higher concentration of doxorubicin solutions. As for release profiles, doxorubicin was released from CalliSpheres quickly at the very beginning, and doxorubicin release percentage was increased in the 50-150 μm group (39.2% ± 1.2%) compared with the 100-300 μm group (31.3% ± 1.3%) and 300-500 μm group (31.7% ± 2.5%). Digital subtraction angiography, computed tomography, and histopathologic emanation results proved in vivo safety and embolic efficacy of CalliSpheres. Conclusions CalliSpheres present with good physical characteristics and satisfactory loading and releasing profiles in vitro and are well tolerated and efficient in embolization in vivo.Rationale Health outcomes of people with coronavirus disease (COVID-19) range from no symptoms to severe illness and death. Asthma, a common chronic lung disease, has been considered likely to increase the severity of COVID-19, although data addressing this hypothesis have been scarce until very recently.Objectives To review the epidemiologic literature related to asthma's potential role in COVID-19 severity.Methods Studies were identified through the PubMed (MEDLINE) and medRxiv (preprint) databases using the search terms "asthma," "SARS-CoV-2" (severe acute respiratory syndrome coronavirus 2), and "COVID-19," and by cross-referencing citations in identified studies that were available in print or online before December 22, 2020.Measurements and Main Results Asthma prevalence data were obtained from studies of people with COVID-19 and regional health statistics. We identified 150 studies worldwide that allowed us to compare the prevalence of asthma in patients with COVID-19 by region, disease severity, and mortality.
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