Search

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]

The interface microzone characteristics determine the thermophysical properties of diamond/Cu composites, while the mechanisms of interface formation and heat transport still need to be revealed. Here, diamond/Cu-B composites with different boron content were prepared by vacuum pressure infiltration. Diamond/Cu-B composites up to 694 W/(mK) were obtained. The interfacial carbides formation process and the enhancement mechanisms of interfacial heat conduction in diamond/Cu-B composites were studied by HRTEM and first-principles calculations. It is demonstrated that boron can diffuse toward the interface region with an energy barrier of 0.87 eV, and these elements are energetically favorable to form the B4C phase. The calculation of the phonon spectrum proves that the B4C phonon spectrum is distributed in the range of the copper and diamond phonon spectrum. The overlapping of phonon spectra and the dentate structure together enhance the interface phononic transport efficiency, thereby improving the interface thermal conductance. [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]

Increasing evidence suggests that intestinal dysbiosis, intestinal barrier dysfunction, and activated Toll-like receptor 4 (TLR4) signaling play key roles in the pathogenesis of NAFLD. Dahuang Zexie Decoction (DZD) has been verified to be effective for treating NAFLD, but the mechanisms remain unclear. In this study, we investigated the effects of DZD on NAFLD rats and determined whether such effects were associated with change of the gut microbiota, downregulated activity of the TLR4 signaling pathway, and increased expressions of tight junction (TJ) proteins in the gut. Male Sprague Dawley rats were fed high-fat diet (HFD) for 16 weeks to induce NAFLD and then given DZD intervention for 4 weeks. We found that DZD reduced body and liver weights of NAFLD rats, improved serum lipid levels and liver function parameters, and relieved NAFLD. We further found that DZD changed intestinal bacterial communities, inhibited the intestinal TLR4 signaling pathway, and restored the expressions of TJ proteins in the gut. Meanwhile ten potential components of DZD had been identified. These findings suggest that DZD may protects against NAFLD by modulating gut microbiota-mediated TLR4 signaling activation and loss of intestinal barrier. However, further studies are needed to clarify the mechanism by which DZD treats NAFLD. [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]