Search

The characteristics of partially premixed methane/air combustion in aconfined geometry are experimentally investigated in two types of swirling flows introduced by using avane swirl (VS) and tangential jet swirl (TJS), respectively. To make acomparison, acoaxial jet (CJ) burner is also employed. The fuel and air are individually injected through their own inlets, partially premixed in amixing chamber, and then burned in aconfined cylindrical combustor. In VS and CJ combustors, the fuel is axially injected from the center; while in the TJS combustor the fuel is injected through either acentral inlet or tangential inlet. The geometry swirl number varies from 0 to 3.38. The flame structures, extinction limits, temperature distribution, NOx, CO concentrations and flow velocities are systematically examined to compare the flame characteristics. The detailed observations show that the swirl plays asignificant role in the fuel mixing, flame stabilization, and flame structures. As fuel is axially injected, ayellow flame is established at low airflow rate regardless of the swirl number values. As the airflow rate increases, ablue flame is obtained; the flame extinguishes at avery low global equivalence ratio of 0.25 in the VS and TJS combustors. When fuel and air are tangentially injected, ablue flame similar to premixed one is established; asteady flame is obtained from lean to rich limits (equivalence ratio of 0.5 to 1.68). The temperature is distributed more uniformly in the high swirl TJS combustor, particularly for the one adopts pure tangential jets of fuel and air, in which the measured NOx and CO concentrations are the lowest. The differences were mainly attributed to different mixing modes. [ABSTRACT FROM AUTHOR]

Background and Purpose Experimental Approach Key Results Conclusion and Implications As a highly heterogeneous cancer, hepatocellular carcinoma (HCC) shows different response rates to the multi‐kinase inhibitor lenvatinib. Thus, it is important to explore genetic biomarkers for precision lenvatinib therapy in HCC.The effect and mechanism of AXIN1 mutation on HCC were revealed by cell proliferation assay, long‐term clone formation assay, sphere formation assay and small molecule inhibitor library screening. A new therapeutic strategy targeting HCC with AXIN1 mutation was evaluated in humanized models (patient‐derived xenograft [PDX] and patient‐derived organoid [PDO]).Based on The Cancer Genome Atlas (TCGA) data, we screened 6 most frequently lost tumour suppressor genes in HCC (TP53, ARID1A, AXIN1, CDKN2A, ARID2 and PTEN) and identified AXIN1 as the most crucial gene for lenvatinib sensitivity. Further study showed that AXIN1‐knockout HCC cells had a more malignant phenotype and lower sensitivity to lenvatinib in vitro and in vivo. Mechanistically, the WNT pathway and its target gene c‐Myc were activated when AXIN1 was missing, and the expression of tumour suppressor p15 was inhibited by transcription co‐repressors c‐Myc and Miz‐1, resulting in the exacerbation of the resistant phenotype. Screening of a library of epigenetic‐related enzyme inhibitors showed that a KDM5B inhibitor up‐regulated p15 expression, leading to increased sensitivity to lenvatinib in vitro and in vivo.AXIN1‐deficient patients have a lower response to lenvatinib, which may be associated with suppression of p15 mediated by WNT pathway activation. KDM5B inhibitors can restore p15 levels, resulting in efficient killing of resistant cells in HCC. [ABSTRACT FROM AUTHOR]

Tumor associated macrophages (TAMs) are the main infiltrating component in the tumor microenvironment and play an important role in cancer progression. Baicalein has a wide range of pharmacological properties. This study explores the potential effect of baicalein on macrophages polarization and epithelial-mesenchymal transition (EMT) of breast cancer. Co-culture system was established to evaluate the interaction between TAMs and breast cancer cells. Then the role of baicalein in modulating TAMs function was assessed. Finally, breast cancer mouse model was established to study the underlying mechanism. In vitro experiments showed that co-culture with M2 macrophages significantly enhanced EMT of both MDA-MB-231 and MCF-7 breast cancer cells. Baicalein could regulate polarization of M2 and attenuate TGF-β1 secretion. In vivo experiments showed that compared with the MDA-MB-231 + M2 group, tumor growth and metastasis of baicalein + MDA-MB-231 + M2 group was significantly inhibited, with smaller tumor size and decreased lung metastasis lesions. Our findings suggest that the regulation of TAMs may be a novel mechanism underlying the anti-tumor effects of baicalein in breast cancer., Competing Interests: None.