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Objective To investigate the antitumor effect of apatinib on breast cancer cells in vitro and its mechanism. Methods CCK-8 assay was used to detect the inhibitory effect of apatinib on the proliferation of breast cancer cell line MDA-MB-231. Annexin V-FITC/PI apoptosis detection kit was used to detect the effect of apatinib on the apoptosis of MDA-MB-231 cells. The effect of apatinib on lactate production in MDA-MB-231 cells was detected by lactate content assay kit. The effect of apatinib on the extracellular acidification rate of MDA-MB-231 cells was detected by glycolysis stress test kit. Results Apatinib inhibited the proliferation of breast cancer MDA-MB-231 cells in vitro in a concentration-dependent manner (P < 0.05). The half maximal inhibitory concentration (IC50) of apatinib in MDA-MB-231 cells was 1.56μmol/L for 48h treatment. Apatinib also induced the apoptosis of MDA-MB-231 cells in a concentration-dependent manner (P < 0.05). Apatinib inhibited intracellular lactate content in MDA-MB-231 cells in a concentration-dependent manner (P < 0.05). Apatinib also decreased extracellular acidification rate of MDA-MB-231 cells, including glycolytic capacity and glycolytic reserve (P < 0.05). Conclusion Apatinib could induce the apoptosis of breast cancer cell line MDA-MB-231 by inhibiting aerobic glycolysis.

Nonglioblastomatous diffuse glioma (non‐GDG) is a heterogeneous neuroepithelial tumor that exhibits a varied survival range from 4 to 13 years based on the diverse subtypes. Recent studies demonstrated novel molecular markers can predict prognosis for non‐GDG patients; however, these findings as well as pathological classification strategies show obvious limitations on malignant transition due to the heterogeneity among non‐GDGs. Therefore, developing reliable prognostic biomarkers and therapeutic targets have become an urgent need for precisely distinguishing non‐GDG subtypes, illuminating the underlying mechanism. Nuclear factor κβ (NF‐κB) has been proved to be a significant nuclear transcriptional regulator with specific DNA‐binding sequences to participate in multiple pathophysiological processes. However, the underlying mechanism of NF‐κB activation still needs to be further investigated. Herein, our results indicated retinol‐binding protein 1 (RBP1) was significantly upregulated in the IDHWT and 1p19qNon co‐del non‐GDG subtypes and enriched RBP1 expression was markedly correlated with more severe outcomes. Additionally, malignant signatures of the non‐GDG cells including proliferation, migration, invasion, and self‐renewal were significantly suppressed by lentiviral knockdown of RBP1. To further explore the underlying molecular mechanism, bioinformatics analysis was performed using databases, and the results demonstrated RBP1 was strongly correlated with tumor necrosis factor α (TNFα)–NF‐κB signaling. Moreover, exogenous silencing of RBP1 reduced phosphorylation of IkB‐kinase α (IKKα) and thus decreased NF‐κB expression via decreasing the degradation of the IκBα protein. Altogether, these data suggested RBP1‐dependent activation of NF‐κB signaling promoted malignancy of non‐GDG, indicating that RBP1 could be a reliable prognostic biomarker and potential therapeutic target for non‐GDG. [ABSTRACT FROM AUTHOR]

This research was undertaken to investigate the influence of the sizing components, principally coupling agents and film formers, of glass fiber on the interface of reinforced polyurethane composites. The contents of film-forming agents and coupling agents were, respectively, checked by acetone extraction and heat treatment. The categories and chemical structures of the film-forming agents, which mainly exist in the extracting solutions, were investigated by nuclear magnetic resonance spectroscopy. The coupling agents, which mainly existed on the extracted glass fiber surfaces, were analyzed by X-ray photoelectron spectroscopy. Then, the interfacial adhesion properties between glass fibers of untreated, extracted and heat-treated and polyurethane resin were measured with micro-droplet test. The results show that the interfacial shear strength of the glass fiber-reinforced polyurethane composite mainly depends on the coupling agents, in which the N-containing groups play a dominant role. The film formers also take some effects, in which the hydroxyl groups have the greatest contribution. [ABSTRACT FROM AUTHOR]

Background: In patients with chronic hepatitis B (CHB), the relation of interkeukin-7 (IL-7) to either the T follicular helper cells (Tfh cells) or to a specific cellular immune response is not clear. Objectives: The present study aims to explore the possible relationship of IL-7 to Tfh cells and to hepatitis B virus (HBV)-specific cellular immune response in patients with CHB. Methods: Ninety-one adult patients with CHB were divided into groups A, B, and C, according to the patients' IL-7 levels (low, medium, and high). Tfh cells and HBV-specific cytotoxic T lymphocytes (CTLs) were detected with flow cytometry; IL-7 and IL-21 were determined with a double antibody sandwich enzyme-linked immunosorbent assay; and HBV DNA was determined by using a real-time fluorescent quantitative polymerase chain reaction. Results: The results showed that the levels of IL-7, Tfh cells, IL-21, and HBV-specific CTLs of patients in group C were significantly higher than those of patients in group B, (P < 0.01 for each comparison) and that the levels of these four parameters of patients in group B were significantly higher than those of the patients in group A (P < 0.01 for each comparison). Meanwhile, the level of HBV DNA of the patients in group C was significantly lower than that of the patients in group B (P < 0.01), and that of the patients in group B was significantly lower than that of the patients in group A (P < 0.05). Multiple linear regression analyses showed that IL-7, Tfh cells, IL-21, and HBV-specific CTL might have effects on HBV DNA and that only the HBV-specific CTL had an independent effect on HBV DNA (P < 0.01). IL-7, Tfh cells, and IL-21 showed independent effects on HBV-specific CTL (P < 0.05, P < 0.01, and P < 0.01). Conclusions: This study suggests that the IL-7 level of CHB patients may be related to Tfh cells. In CHB patients, IL-7 possibly increases the level of Tfh cells and HBV-specific cellular immune responses and thereby reduces the HBV DNA level. [ABSTRACT FROM AUTHOR]

Objective: To observe the short-term effect of sequentially combined multimodal artificial liver treatment (SCMALT) on HBV-related acute-on-chronic liver failure (HBV-ACLF)., Methods: HBV-ACLF patients 155 cases undergoing artificial liver treatment were analyzed, and they were sorted into the SCMALT group and the conventional-modal artificial liver treatment (CALT) group. The clinical data of all patients were recorded and the serum levels of interleukin-8 (IL-8), chemokine interferon-inducible protein-10 (IP-10), and interleukin-6 (IL-6) were detected. The changes in the 30-day survival rate, cytokine level, model for end-stage liver disease (MELD) score, and complications of artificial liver treatment were analyzed., Results: After being followed up for 30 days, 104 patients survived and 51 died. At the end of the whole-course treatment, the decreases in IL-6, IP-10, and IL-8 levels and MELD scores in the SCMALT group were greater than in the CALT group. Cox regression suggested WBC (OR=1.066, 95% CI 1.012-1.123, P=0.017), AT-III activity (OR=0.935, 95% CI 0.907-0.964, p=0.000) at baseline, artificial liver treatment mode (OR=0.362, 95% CI 0.164-0.800, p=0.012), number of artificial liver treatments (OR=0.656.95% CI 0.436-0.986, p=0.043), spontaneous peritonitis (OR=0.337, 95% CI 0.165-0.689, p=0.003), and hepatic encephalopathy (OR=0.104, 95% CI 0.028-0.388, p=0.001) were independent influencing factors of 30-day survival rate. SCMALT can significantly prolong the survival period of the patient. No obvious difference was shown in the proportions of bleeding and circulation instability between the two groups (p>0.05)., Conclusion: Compared with the CALT, SCMALT can more effectively remove inflammatory mediators and reduce the MELD score in HBV-ACLF patients, which can obviously ameliorate the prognosis, with less effect on the platelet count., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objectives: Aurora kinase B (AURKB) and Ubiquitin conjugating enzyme E2C (UBE2C) are involved in tumorigenesis of gliomas and other malignancies as well, but their clinicopathologic significance in gliomas is unknown and the prognostic value of combined expression of AURKB and UBE2C has not been explored. In this study, we investigate the correlation between glioma prognosis and combined expressions of AURKB and UBE2C thus to identify novel therapeutic targets and prognostic biomarkers for glioma patients., Methods: AURKB was identified as one of the key candidate kinase-encoding genes in three different databases by using kinome-wide bioinformatic analysis. Afterwards, UBE2C was chosen as the most closely relevant genes to AURKB according to Spearman correlation test. Then the expressions of AURKB and UBE2C at either transcriptome or protein levels were measured by quantitative Real-time PCR (qRT-PCR) or immunohistochemistry (IHC), respectively. Additionally, Kaplan-Meier analyses were conducted using data from TCGA, Rembrandt and our clinical center to investigate the clinical significance of AURKB and UBE2C. Furthermore, receiver operating characteristic (ROC) analysis was performed to evaluate the sensitivity and specificity of AURKB and UBE2C in predicting the outcomes of glioma patients. Moreover, survival data of patients who underwent post-surgical chemo/radio treatment were extracted and the Kaplan-Meier analyses were performed to investigate the correlation between treatment resistance and combined expressions of AURKB and UBE2C., Results: Both AURKB and UBE2C were significantly up-regulated in gliomas compared to normal brain tissues and the combined elevation of AURKB and UBE2C were strongly associated with histological classification in glioma. Moreover, overexpression of either AURKB or UBE2C strongly correlated to more severe overall survival. Notably, upregulation of these two genes revealed unfavorable outcomes (shorter overall survival and therapy resistance) in glioma patients with significant sensitivity and specificity., Conclusion: Simultaneously elevated expressions of AURKB and UBE2C was strongly correlated to poor prognosis and therapy resistance in glioma, furthermore, our data suggest for the first time that the combination of AURKB and UBE2C overexpression could be highly sensitive prognostic markers and potential therapeutic targets for glioma patients., (Copyright © 2019 Elsevier GmbH. All rights reserved.)