Methods to synthesize crystalline covalent triazine frameworks (CTFs) are limited and little attention has been paid to development of hydrophilic CTFs and photocatalytic overall water splitting. A route to synthesize crystalline and hydrophilic CTF‐HUST‐A1 with a benzylamine‐functionalized monomer is presented. The base reagent used plays an important role in the enhancement of crystallinity and hydrophilicity. CTF‐HUST‐A1 exhibits good crystallinity, excellent hydrophilicity, and excellent photocatalytic activity in sacrificial photocatalytic hydrogen evolution (hydrogen evolution rate up to 9200 μmol g−1 h−1). Photocatalytic overall water splitting is achieved by depositing dual co‐catalysts in CTF‐HUST‐A1, with H2 evolution and O2 evolution rates of 25.4 μmol g−1 h−1 and 12.9 μmol g−1 h−1 in pure water without using sacrificial agent.

Methods to synthesize crystalline covalent triazine frameworks (CTFs) are limited and little attention has been paid to development of hydrophilic CTFs and photocatalytic overall water splitting. A route to synthesize crystalline and hydrophilic CTF‐HUST‐A1 with a benzylamine‐functionalized monomer is presented. The base reagent used plays an important role in the enhancement of crystallinity and hydrophilicity. CTF‐HUST‐A1 exhibits good crystallinity, excellent hydrophilicity, and excellent photocatalytic activity in sacrificial photocatalytic hydrogen evolution (hydrogen evolution rate up to 9200 μmol g−1 h−1). Photocatalytic overall water splitting is achieved by depositing dual co‐catalysts in CTF‐HUST‐A1, with H2 evolution and O2 evolution rates of 25.4 μmol g−1 h−1 and 12.9 μmol g−1 h−1 in pure water without using sacrificial agent.

Decellularization techniques have been widely used as an alternative strategy to produce matrices for organ reconstruction. This study investigated the impact of a detergent-enzymatic decellularization protocol on the extracellular matrix integrity, mechanical properties, and biocompatibility of decellularized tracheal matrices from rabbits. The tracheas of New Zealand white rabbits were decellularized using a modified detergent-enzymatic method (DEM). Antigenicity, cellularity, glycosaminoglycan content, DNA content, histoarchitecture, and mechanical properties were monitored during processing. The surface ultrastructure of the matrix was examined by scanning electron microscopy (SEM). Bioengineered and control tracheas were then implanted in major histocompatibility complex-unmatched rats (xenograft) heterotopically for 7, 15, and 30 days. Structural and functional analysis was performed after transplantation. The results showed that seven cycles of decellularization removed most of the cells and eliminated antigenicity. Histological and molecular biology analysis demonstrated that most of the cellular components and nuclear material were removed. SEM analysis revealed that the decellularized matrices retained the hierarchical structure of the native trachea, and biomechanical tests showed that decellularization did not significantly influence the mechanical properties. Seven, 15 and 30 days after implantation, decreased (p < 0.01) inflammatory reactions were observed in the xenograft models for decellularized matrices compared with control tracheas. No increases in IgM or IgG content were observed in rats that received bioengineered tracheas. In conclusion, this work suggests that seven cycles of the DEM generates a bioengineered rabbit tracheal matrix that is structurally and mechanically similar to native trachea.

A ternary electron transfer relay photocatalytic system for CO2 reduction was fabricated by decorating a porphyrin-based covalent triazine framework with α-Fe2O3 nanoparticles, and then further coupled with a Ru complex photosensitizer.

Decellularization techniques have been widely used as an alternative strategy for organ reconstruction. This study investigated the mechanical, pro-angiogenic and in vivo biocompatibility properties of decellularized airway matrices cross-linked with genipin. New Zealand rabbit tracheae were decellularized and cross-linked with genipin, a naturally derived agent. The results demonstrated that, a significant (p < 0.05) increase in the secant modulus was computed for the cross-linked tracheae, compared to the decellularized samples. Angiogenic assays demonstrated that decellularized tracheal scaffolds and cross-linked tracheae treated with 1% genipin induce strong in vivo angiogenic responses (CAM analysis). Seven, 15 and 30 days after implantation, decreased (p < 0.01) inflammatory reactions were observed in the xenograft models for the genipin cross-linked tracheae matrices compared with control tracheae, and no increase in the IgM or IgG content was observed in rats. In conclusion, treatment with genipin improves the mechanical properties of decellularized airway matrices without altering the pro-angiogenic properties or eliciting an in vivo inflammatory response.

Chirality is a ubiquitous phenomenon in nature, serving as a foundation for a variety of life activities on earth. Separation-free methods that rapidly and accurately distinguish chiral analytes in complex systems are highly demanded in fields ranging from drug quality control to the screening of privileged chiral catalysts. However, in situ enantidifferentiation methods possessing resolution and tunability that are comparable to those achieved by chiral high-performance liquid chromatography are rare. Herein, we report a Lewis pair−based system for enantioanalysis via recognition-enabled "chromatographic" 19 F NMR spectroscopy. The construction of Lewis pairs renders the detecting system not only enhanced affinity to chiral analytes but also superior and tunable resolving capability. Using this strategy, as many as 16 chiral analytes are simultaneously resolved without need for separation, thus opening new avenues for the development of precise and real-time detection methods that are robust enough for dealing with complex real-world samples.

SOX genes play an important role in a number of developmental processes. SOXs have been demonstrated to have potential roles as either tumor suppressors or promoters in various neoplastic tissues depending on the tumor status and type. The aim of this study was to investigate the functional role of SOXs in human cancers. Gene expression changes of SOXs in human hepatocellular carcinoma (HCC) tissues were detected using real-time quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) analysis and immunohistochemistry and compared with those in non-cancerous hepatic tissues. We found by qRT-PCR analysis and immunohistochemistry that the gene SOX8 was significantly upregulated in HCC. Furthermore, we discovered that SOX8 promoted cancer cell proliferation in vitro and that its expression was correlated with elevated β-catenin levels in HCC, whose function was required for the oncogenic effects of SOX8.

The present study aimed to investigate the inhibitory ability of β-hydroxyisovaleryl-shikonin (β-HIVS) on the proliferation of human cervical cancer HeLa cells and to identify the mechanism of this effect. The HeLa cells were treated with β-HIVS and the inhibition of cell growth was detected by an MTT assay. Flow cytometry was performed to analyze the apoptosis rate and cell cycle distribution of HeLa cells. Reverse transcription-polymerase chain reaction and western blot analysis were used to examine the expression of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway proteins. The results revealed that β-HIVS inhibited HeLa cell proliferation in a dose- and time-dependent manner. With the administration of increasing concentrations of β-HIVS, the apoptotic rate of HeLa cells was also increased. The cell cycle was slightly arrested at the S phase, with ~6% of cells in this phase, subsequent to treatment with 10 µM β-HIVS. In addition, β-HIVS markedly reduced the expression levels of PI3K, AKT, mTOR and 70-kDa ribosomal protein S6 kinase in HeLa cells. β-HIVS promoted cervical cancer cell apoptosis by inhibiting the PI3K/AKT/mTOR signaling pathway and suppressing downstream gene expression. The present study is expected to lead to the development of molecular targeted therapy for this signaling pathway as a novel method of cervical cancer treatment.