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To investigate the comprehensive effects of the Al and Zr element contents on the microstructure evolution of the AlNbTiVZr series light-weight refractory high entropy alloys (HEAs), five samples were studied. Samples with different compositions were designated Al1.5NbTiVZr, Al1.5NbTiVZr0.5, AlNbTiVZr, AlNbTiVZr0.5, and Al0.5NbTiVZr0.5. The results demonstrated that the actual density of the studied HEA samples ranged from 5.291 to 5.826 g·cm−3. The microstructure of these HEAs contains a solid solution phase with a BCC structure and a Laves phase. The Laves phase was further identified as the ZrAlV intermetallic compound by TEM observations. The microstructure of the AlNbTiVZr series HEAs was affected by both the Al and Zr element contents, whereas the Zr element showed a more dominant effect due to Zr atoms occupying the core position of the ZrAlV Laves phase (C14 structure). Therefore, the as-cast Al0.5NbTiVZr0.5 sample exhibits the best room temperature compression property with a compression strength (σp) of 1783 MPa and an engineering strain of 28.8% due to having the lowest ZrAlV intermetallic compound area fraction (0.7%), as characterized by the EBSD technique. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is a major malignant tumor type with a high incidence and mortality. Infection with hepatitis virus is a high‑risk factor. Previous studies have demonstrated that microRNA (miR)‑223 was downregulated in HCC tissues. NOD‑like receptor family, pyrin domain containing 3 (NLRP3)‑is a potential target of miR‑223 and has a vital role in hepatitis infection. The present study was performed to investigate the role of miR‑223 in the proliferation and apoptosis of HCC cells through regulating NLRP3. A dual luciferase reporter assay was performed to confirm the direct interaction between miR‑223‑3p and the 3' untranslated region of NLRP3 mRNA. Hep3B cells were then transfected with miR‑223 mimics and the proliferation and apoptosis were determined by an MTT and a flow cytometric assay, respectively. The expression of NLRP3 and caspase‑1 was analyzed at the mRNA as well as at the protein level by reverse transcription‑quantitative polymerase chain reaction and western blot analysis, respectively. The secretion of interleukin (IL)‑1β and IL‑18 in the culture supernatants was measured by ELISA. The dual luciferase assay confirmed NLRP3 as a direct target of miR‑223. Overexpression of miR‑223 in hep3B cells significantly suppressed cell proliferation and promoted apoptosis. Furthermore, the expression of NLRP3 was downregulated by miR‑223 transfection. Certain downstream factors of the NLRP3 pathway were also downregulated following overexpression of miR‑223. Caspase‑1 was decreased at the transcriptional level and the cleaved caspase‑1 was decreased at the protein level. Secretion of IL‑1β and IL‑18 into the culture medium by cells transfected with miR‑223 was lower than that by the control cells. In conclusion, the tumor suppressor role of miR‑223 was associated with the regulation of NLRP3 inflammasome components. miR‑223 inhibited HCC cell proliferation and promoted apoptosis by directly targeting NLRP3. Downstream production of caspase‑1, IL‑1β and IL‑18 were also repressed by miR‑223. These results provided insight into the association between the innate immune system and the genesis of HCC. [ABSTRACT FROM AUTHOR]

Persistent infection with hepatitis B virus (HBV) is associated with host immune response. CD4+ T cells play an important role in HBV - specific immune response. The restoration of HBV - specific T - cell response after antiviral therapy using nucleoside and nucleotide analogues is also associated with CD4+ T cells. In recent years, two new subsets of CD4+ T cells, namely regulatory T cells (Tregs) and T helper 17 cells (Th17 cells), have been identified and shown to be related to disease progression and liver damage in patients with persistent HBV infection. Here we primarily summarized the differentiation and function of Tregs and Th17 cells and reviewed the interaction between the two types of cells in persistent infection and their changes after clinical antiviral therapy. We hope it wiil be helpful to clinical immunotherapy and prognostic assessment. [ABSTRACT FROM AUTHOR]

Traditional Chinese medicine has made some progress in the study of liver fibrosis, and provides valuable experience for clinical treatment of liver fibrosis. The aim of this study was to investigate the rationality of compatibility use of Salvia miltiorrhiza and Radix astragali on liver fibrosis in rats. For this purpose, the rat model of liver fibrosis was treated with single or different compatibilities of herbals extracts for 4 weeks. Saline and colchicine were set as a negative and positive control, respectively. Liver histopathology, liver function, and expressions of key proteins in the TGF-β/Smad/Wnt pathway were assessed. Results showed that compared with colchicine, herbal extracts showed better ability to reduce deposition of α-SMA and type I collagen, and improve liver function. The effect of R. astragali extracts and 1:1 compound on improving liver fibrosis and liver function was relatively better than other treatment options. The compound groups showed a particularly significant effect on reducing Cyclin D1 expression. It was concluded that the 1:1 compatibility use of S. miltiorrhiza extracts and R. astragali extracts can preferably attenuate liver fibrosis by regulating the expression of TGF-β1 and Cyclin D1.