This paper studied the synergistic effects of turmeric extract, cartilage extract, Pueraria lobata and Coix (Coix lacryma-jobi) seed extract alone and the combination on the improvement of cartilage damage of rats with knee osteoarthritis. The synergistic effects of the three extracts in rat knee osteoarthritis were evaluated mainly by reducing knee swelling (inflammation), protecting chondrocyte and repairing joint cartilage. The results show that the turmeric extract has a more obvious effect in inhibiting joint swelling and improving cartilage damage, which is specifically manifested in the ability to better improve the levels of Collagen Ⅱ, matrix metalloproteinase 3 (MMP3), cartilage oligomeric matrix protein (COMP), tumor necrosis factor-alpha (TNF-α) and superoxide dismutase (SOD). The cartilage extract significantly improves the arthritic lesions by improving the levels of MMP3, COMP, TNF-α, prostaglandin E2 (PGE2) and SOD. Pueraria lobata and Coix seed extract improves the levels of Collagen Ⅱ and SOD, inhibits the elevation of MMP3, COMP, TNF-α and interleukin 1β (IL-1β), and improves cartilage damage of rats with knee osteoarthritis. The combined use of the three extracts exhibits better effects on the repair of rat knee cartilage. These data imply that by optimizing the ratio of turmeric extract, cartilage extract and Pueraria lobata and Coix seed extract, functional foods can be developed with significant anti-inflammatory and cartilage repairing effects and contribute to the realization of “Healthy China 2030”.

As the key component of quantitative real-time polymerase chain reaction （qPCR） technology, Taq DNA polymerase’s performance directly affects the further development of qPCR technology. However, the wild-type Taq DNA polymerase has inadequate properties in inhibitor tolerance and elongation performance. To obtain Taq DNA polymerase with high performance, this study fused the double-stranded DNA-binding protein Sso7d or Sto7d to the N-terminal or C-terminal of wild-type Taq DNA polymerase by genetic engineering technology, which four soluble expression transformants were constructed, and then the better transformant was screened by tolerance test. The results show that the better transformant Taq-Sto has the highest tolerance, with no impact on its thermal stability, and the target can be successfully amplified by Taq-Sto under the extension condition of 1 s/kbp, indicating that Taq-Sto has enhanced extension performance. It also shows good tolerance to humic acid, tannic acid and whole blood in TaqMan qPCR system. EMSA experiment shows that the binding affinity of Taq-Sto to DNA template is improved, which is beneficial to enhancing the competitiveness of Taq-Sto to DNA template. Taq-Sto was applied to the TaqMan qPCR detection of African swine fever virus (ASFV). Compared with commercial reagents, Taq-Sto has lower detection limit of ASFV, and the detection sensitivity in 2%~6% (volume fraction) pig fecal samples or pork samples is 100.0% and 85.4%, respectively, indicating that Taq-Sto has more advantages in the field of direct qPCR detection. The results provide a reference for the development of DNA polymerase with better performance, which is conducive to further promoting the practical application of qPCR technology.

Cell cycle dysregulation is one of the most important hallmarks of cancer. Bioinformatics studies have suggested that trigger transposable element-derived 1 (TIGD1) is expressed at higher levels in the tumor tissues from the clinical hepatocellular carcinoma (HCC) samples and may be related to the cell cycle. However, the underlying mechanism is unclear. To explore the specific mechanism of TIGD1 regulating the growth of hepatocellular carcinoma cells, this paper first analyzed the growth of HCC cell line Hep3B with TIGD1 knockdown by using shRNA plasmid. The results show that cell growth is inhibited. Then, cell cycle analysis by flow cytometry was used to investigate the effect of TIGD1 knockdown on cell cycle of HCC. The results show that the cell cycle progression of the Hep3B cell line is mainly blocked in the G2/M phase. Next, Immunoprecipitation (IP) experiments were used to verify the protein molecules with which TIGD1 might interact. And the results show that TIGD1 may be bound to Aurora kinase interacting protein 1 (AURKAIP1). Further, the Co-IP experiment confirmed the interaction between TIGD1 and AURKAIP1. AURKAIP1 is known to regulate the proteasomal degradation pathway of Aurora kinase A (AURKA), and AURKA is a mitotic regulatory protein that is closely associated with cell cycle progression. The paper further explored the effect of TIGD1 on AURKA protein levels, and the results show that TIGD1 knockdown obviously decreases the protein level of AURKA without affecting its mRNA level in Hep3B cells. In conclusion, TIGD 1 may affect cell cycle progression by regulating the post-transcriptional levels of AURKA in HCC cells, thus affecting the development of HCC.