Abstract Objective The paper investigated the effect and molecular mechanism of Houttuynin on breast cancer in vitro, so as to provide clinical basis for the treatment of breast cancer with Houttuynin. Methods: Cell survival rate was measured by MTT assay. Cell apoptosis was detected by flow cytometry and AO/EB double staining method. The expressions of PI3K, AKT, and mTOR proteins and their phosphorylation levels were determined by WB experiment. Results: Houttuynin can significantly inhibit the growth of breast cancer cells and arrest cell cycle in the G2/M phase. Houttuynin induced apoptosis of breast cancer cells through two pathways, namely, mitochondria and death receptors. It was verified by WB experiment that Houttuynin could induce autophagy in breast cancer cells and reduce the expressions of PI3K, AKT, mTOR and other proteins. Conclusion: Houttuynin induced breast cancer cell apoptosis by inhibiting PI3K/AKT signaling pathway, thereby inhibiting the proliferation of breast cancer cells.

Abstract Transfection efficiency was estimated to optimize the conditions for RNA interference (RNAi), including transfection time, validity, and nucleic acid concentration and type, using the EZ Trans Cell Reagent, a cationic polymer. An shRNA against GFP was designed and transfected into cells using the EZ transfection reagent. The shRNA significantly decreased the expression of GFP. In addition, pre-diluted transfection reagent at room temperature and small nucleic acids increased the transfection efficiency, which peaked at 24 h. Compared with circular nucleic acids, linear nucleic acids showed higher transfection efficiency and a higher genome integration rate. We optimized cationic polymer-mediated RNAi conditions, and our data will be useful for future RNAi studies.

OBJECTIVES: To evaluate the efficacy of autologous platelet-rich plasma (PRP) gel in the treatment of refractory pressure injuries and its effect on wound healing time and quality of life of patients. METHODS: A random number table method was used to group 102 patients with refractory pressure injuries into either a control group (CG) (51 cases) receiving negative pressure wound therapy (NPWT) or a study group (SG) (51 cases) receiving NPWT+PRP gel. RESULTS: The total efficacy rate in the SG (92.16%) was higher than that in the CG (76.47%) (p<0.05). The SG exhibited lower visual analog scale (VAS) scores and pressure ulcer scale for healing (PUSH) scores, smaller wound sizes and depths, and shorter wound healing times than the CG after 21 days of treatment (p<0.05). After 6 months of treatment, the SG scored higher than the CG on the psychological, physiological, social functions, and daily activity domains on the World Health Organization Quality of Life (WHOQOL-BREF) scale (p<0.05). The incidence of postoperative complications in the SG (13.73%) was not significantly different from that of the CG (7.84%) (p>0.05). CONCLUSION: In the treatment of refractory pressure injuries, PRP gel can accelerate wound healing, reduce wound pain, shorten the treatment cycle, regulate tissue inhibitor matrix metalloproteinase-1 (TIMP-1) and matrix metalloproteinase-9 (MMP-9) levels and the expression of specific proteins in granulation tissue, reduce the levels of the inflammatory factors interleukin-1β (IL-1β), IL-8, and tumor necrosis factor-α (TNF-α), and improve the quality of life of patients without increasing complications.

In this study, we replaced 30% of the cement with steel slag to prepare binding material; additionally, small amounts of CaCO3 and CaSO4·2H2O were added. This was done to study the compound effect of CaCO3 and CaSO4·2H2O on the strength of steel slag-cement binding materials. The hydration degree of the steel slag cementitious material was analyzed by XRD, TG and SEM. The results showed that the optimum proportions of CaCO3 and CaSO4·2H2O were 3% and 2%, respectively. Compared with the steel slag-cement binders without adding CaCO3 and CaSO4·2H2O, the compressive strength increased by 59.9% at 3 days and by 17.8% at 28 days. Acting as the nucleation matrix, CaCO3 could accelerate the hydration of C3S. In addition, CaCO3 was involved in the hydration reaction, generating a new hydration product, which could stably exist in a slurry. Meanwhile, CaSO4·2H2O could increase the number of AFt. The compound effect of CaCO3 and CaSO4·2H2O enhanced the intensity of steel slag-cement binding materials and improved the whole hydration behavior.

The central carbon metabolic system is the upstream energy source for microbial fermentation. In addition, it is a master switch for increasing the production of metabolites and an important part of the microbial metabolic network. Investigation into the relationship between genes, environmental factors, and metabolic networks is a main focus of systems biology, which significantly impacts research in biochemistry, metabolic engineering, and synthetic biology. To this end, the central carbon metabolic flux under a variety of growth conditions or using strains with various genetic modifications was previously measured in Saccharomyces cerevisiae using 13C tracer technology. However, the measured values were not integrated and investigated further. In this study, we collected and analyzed the metabolic flux rates of the central carbon metabolic system in S. cerevisiae measured in recent studies. We carried out preliminary analyses of flux values of each pathway, performed regression analyses on relationship between different fluxes, and extracted principal component factors of the flux variables. Based on the results, the general characteristics of pathway flux distribution were clustered and explored, and the effects of environmental and genetic factors on the flux distribution were analyzed. Furthermore, this study explored the relationship between similarity in the enzyme's transcriptional regulation and the correlations in the enzyme's reaction flux. Our results provide a foundation for further studies on the control of the central carbon metabolic flux and facilitate the search for targets in metabolic engineering research.