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Hispidin (1) is a polyphenolic compound with a wide range of pharmacological activities that is distributed in both plants and fungi. In addition to natural extraction, hispidin can be obtained by chemical or enzymatic synthesis. In this study, the identification and characterization of an undescribed enzyme, PheG, from Phellinus igniarius (P. igniarius), which catalyzes the construction of a key C─C bond in the enzymatic synthesis of hispidin are reported. It is demonstrated in vitro that PheG generates hispidin by catalyzing C─C bond formation in the aldol condensation reaction. Based on these results, a plausible pathway for hispidin biosynthesis is proposed by utilizing the primary triacetic acid lactone (TAL, 2) and 3,4‐dihydroxybenzaldehyde (3). The mechanisms for the aldol condensation reaction of PheG are investigated using molecular dynamics (MD) simulations, molecular mechanics/generalized Born surface area (MM/GBSA) binding free energy calculations, density functional theory, and site‐specific mutations. The locations of the key amino acid residues that catalyze the conversion of substrates 2 and 3 to hispidin at the active site of PheG‐1 are identified. This study provides a new method for preparing hispidin with high efficiency and low cost. Hispidin is a polyphenolic compound with a variety of biological activities. Herein, a new aldol condensase PheG from Phellinus igniarius (P. igniarius) can catalyze tricetolatone and 3, 4‐dihydroxybenzaldehyde to hispidin. The catalytic mechanism of nucleophilic addition of PheG is determined by MM/GBSA, density functional theory calculation, and site‐directed mutation.

An activated carbon aerogel (ACA-500) with high surface area (1765 m 2  g −1 ), pore volume (2.04 cm 3  g −1 ), and hierarchical porous nanonetwork structure is prepared through direct activation of organic aerogel (RC-500) with a low potassium hydroxide ratio (1:1). Based on this substrate, a polyaniline (PANi)-coated activated carbon aerogel/sulfur (ACA-500-S@PANi) composite is prepared via a simple two-step procedure, including melt-infiltration of sublimed sulfur into ACA-500, followed by an in situ polymerization of aniline on the surface of ACA-500-S composite. The obtained ACA-500-S@PANi composite delivers a high reversible capacity up to 1208 mAh g −1 at 0.2C and maintains 542 mAh g −1 even at a high rate (3C). Furthermore, this composite exhibits a discharge capacity of 926 mAh g −1 at the initial cycle and 615 mAh g −1 after 700 cycles at 1C rate, revealing an extremely low capacity decay rate (0.48‰ per cycle). The excellent electrochemical performance of ACA-500-S@PANi can be attributed to the synergistic effect of hierarchical porous nanonetwork structure and PANi coating. Activated carbon aerogels with high surface area and unique three-dimensional (3D) interconnected hierarchical porous structure offer an efficient conductive network for sulfur, and a highly conductive PANi-coating layer further enhances conductivity of the electrode and prevents the dissolution of polysulfide species.

Background MicroRNAs (miRNAs) are a large group of post-transcriptional gene regulators that potentially play a critical role in tumorigenesis. Increasing evidences indicate that miR-744 deregulated in numerous human cancers including hepatocellular carcinoma (HCC). However, its role in HCC carcinogenesis remains poorly defined. In this study, we investigated the roles of miR-744 in tumor growth of HCC. Methods Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was conducted to detect the expression of miR-744 and Immunohistochemistry was performed to detect expression of c-Myc in HCC specimens and adjacent normal tissues. The biological functions of miR-744 were determined by cell proliferation and cell cycle assay. Furthermore, cell lines transfected with miR-744 mimics were analyzed in vitro . Luciferase reporter assays was performed to confirm whether miR-744 regulated the expression of c-Myc. Results Our results showed that the expression of miR-744 was frequently down-regulated in both HCC tissues and cells. Furthermore, restoration of miR-744 in HCC cells was statistically correlated with decrease of cell growth and restored G1 accumulation. Luciferase assay and Western blot analysis revealed that c-Myc is a direct target of miR-744. Down-regulation of miR-744 and up-regulation of c-Myc were detected in HCC specimens compared with adjacent normal tissues. Moreover, restoration of miR-744 rescues c-Myc induced HCC proliferation. Conclusions Our data suggest that miR-744 exerts its tumor suppressor function by targeting c-Myc, leading to the inhibition of HCC cell growth. miR-744 may serve as a potentially useful target for the miRNA-based therapies of HCC in the future.