Multi-Template-Guided Synthesis of High-Dimensional Molecular Assemblies for Humidity Gradient-Based Power Generators.

Systematically orchestrating fundamental building blocks into intricate high-dimensional molecular assemblies at molecular level is imperative for multifunctionality integration. However, this remains a formidable task in crystal engineering due to the dynamic nature of inorganic building blocks. Herein, we develop a multi-template-guided strategy to control building blocks. The coordination modes of ligands and the spatial hindrance of anionic templates are pivotal in dictating the overall structures. Flexible multi-dentate linkers selectively promote the formation of oligomeric assembly ([TeO3(Mo2O2S2)3O2(OH)(C5O2H7)3]4- {TeMo6}) into tetrahedral cages ([(TeO3)4(Mo2O2S2)12(OH)12(C9H9O4P)6]8- {Te4Mo24} and [(AsO4)4(Mo2O2S2)12(OH)12(C9H9O6)4]12- {As4Mo24}), while steric hindrance from anionic templates further assists in assembling cages into an open quadruply twisted Möbius nanobelt ([(C6H5O3P)8(Mo2O2S2)24(OH)24(C8H10O4)12]16- {P8Mo48}). Among these structures, the hydrophilic-hydrophobic hybrid cage {Te4Mo24} emerges as an exemplary molecular model for proton conduction and serves as a prototype for humidity gradient-based power generators (HGPGs). The Te4Mo24-PVDF-based HGPG (PVDF = Poly(vinylidene fluoride)) exhibits notable stability and power generation, yielding an open-circuit voltage of 0.51 V and a current density of 77.8 nA cm-2 at room temperature and 90% relative humidity (RH). Further insights into the interactions between water molecules and microscale molecules within the generator are achieved through molecular dynamics simulations. This endeavor unveils a universal strategy for synthesizing multifunctional integration molecules.

The assembly of [Mo2O2S2]2+ based on polydentate phosphonate templates and their proton conductivity.

The assembly of [Mo2O2S2]2+ units depends on the configuration of polydentate phosphonic acid templates, leading to novel topologies with enhanced nuclearity and complexity. The variation of the assembled structures also gives rise to distinct proton-conducting properties.

Interleukin-22 alleviates alcohol-associated hepatic fibrosis, inhibits autophagy, and suppresses the PI3K/AKT/mTOR pathway in mice.

BACKGROUND: Alcohol-associated hepatic fibrosis is a widespread liver disease with no effective treatment. Recent studies have indicated that interleukin-22 (IL-22) can ameliorate alcohol-associated liver disease. However, the mechanism underlying the role of IL-22 in alcohol-associated hepatic fibrosis remains unclear. Therefore, we investigated the effect of IL-22 in a mouse model of alcohol-associated hepatic fibrosis and its underlying mechanisms. METHODS: Alcohol-associated hepatic fibrosis was induced by feeding male C57BL/6J mice with a Lieber-DeCarli liquid diet containing 4% ethyl alcohol for 8 weeks and injecting them with 5% tetrachloromethane (CCl4 ) intraperitoneally for the last 4 weeks. During the last 4 weeks, IL-22 was also administered. We investigated the role of IL-22 in autophagy and the PI3K/AKT/mTOR signaling pathway using a 3-methyladenine intraperitoneal injection in the mice treated with IL-22. The effects of IL-22 on alcohol-associated hepatic fibrosis, autophagy-related gene expression, and PI3K/AKT/mTOR activity were assessed using histopathology, biochemical analysis, transmission electron microscopy, quantitative real-time PCR, immunohistochemistry, and western blotting. RESULTS: Mice treated with ethanol and CCl4 displayed distinct liver injuries, including hepatocyte necrosis, inflammatory cell infiltration, and hepatic fibrosis, which were substantially attenuated by IL-22 treatment. In addition, we found that IL-22 regulated the expression of autophagy-related genes and inhibited the PI3K/AKT/mTOR pathway, as evidenced by the reduction in p-PI3K, p-AKT, and p-mTOR expression after IL-22 treatment. CONCLUSIONS: IL-22 exerts a marked protective effect against alcohol-associated hepatic fibrosis. Its effect may be partly related to the alteration of autophagy-related gene expression and inhibition of the PI3K/AKT/mTOR pathway in the liver.

A reusable catalyst based on CuO hexapods and a CuO-Ag composite for the highly efficient reduction of nitrophenols.

The enormous and urgent need to explore cost-effective catalysts with high efficiency has always been at the forefront of environmental protection and remediation research. This work develops a novel strategy for the fabrication of reusable CuO-based non-noble metal nanomaterials as high-efficiency catalysts. We report a facile and eco-friendly synthesis of CuO hexapods and CuO-Ag composite using uric acid as a reductant and protectant. Both exhibited high catalytic activity in the hydrogenation of 4-nitrophenol (4-NP) to 4-aminophenol (4-AP) by sodium borohydride (NaBH4), with the CuO-Ag composite showing superior catalytic performance. Notably, the highest turnover frequency of CuO-Ag reached 7.97 × 10-2 s-1, which was much higher than numerous noble-metal nanomaterials. In addition, CuO hexapods and CuO-Ag composite were also shown to act as highly efficient and recyclable catalysts in the degeneration of 4-NP. Both CuO hexapods and the CuO-Ag composite exhibited outstanding catalytic durability, with no significant loss of activity over more than 10 cycles in the hydrogenation of 4-NP.

Theoretical exploration about nitro-substituted derivatives of pyrimidine as high-energy-density materials.

A series of pyrimidine derivatives were constructed by replacing hydrogen atoms with nitro groups. To explore their thermal stability and kinetic stability, heat of formation (HOF) and dissociation energies (BDE) are calculated based on the density functional theory with the B3PW91/6-311+G(d,p)//MP2/6-311+G(d,p) method. Based on our calculations, all derivatives are confirmed stable enough to be synthesized in laboratory. To explore the detonation characters, the detonation velocity and detonation pressure are calculated by using the empirical Kamlet-Jacobs equation and good detonation parameters were confirmed for most of title molecules. Based on our calculations, four molecules (2,4,5,6-tetranitropyrimidine, 4,5,6-trinitropyrimidine, 2,4,6-trinitropyrimidine, 2,4,5-trinitropyrimidine ) are screened out as potential high-energy-density materials for further research.

[Inhibitory effect of lentivirus-mediated hTERTp-TK combined with hTERTp-tumstatin on human hepatocarcinoma HepG2 cells].

OBJECTIVE: To observe targeted expression of recombinant lentivirus-mediated (Lv)-hTERTp-TK and Lv-hTERTp-tumstatin in HepG2 cells, and explore the inhibitory effect of their combination on HepG2 cells both in vitro and in vivo. METHODS: Lv-hTERTp-TK and Lv-hTERTptumstatin were used to infect HepG2 and L02 cells at different MOIs. Transfection efficiency was observed by fluorescence microscopy. Expression of TK and tumstatin mRNA was detected by reverse-transcriptase PCR. Proliferation and apoptosis were detected by MTT and flow cytometry, respectively. The HepG2 cells were examined by real time-PCR and western blotting to determine expression level of bcl-2 and VEGF mRNA and protein.A murine hepatocellular carcinoma model was established by injecting 1 * 10(7) HepG2 cells into 30 BALB/c nude mice. The modeled mice were randomly divided into a control group, mock group, Lv-hTERTp-tumstatin group, Lv-hTERTp-TK group, and combination group for four weeks of injections at regular intervals of PBS, Lv-hTERTp-null, Lv-hTERTp-tumstatin, Lv-hTERTp-TK, and Lv-hTERTp-tumstatin plus Lv-hTERTp-TK, respectively.Changes in tumor volume and weight, and cell morphology of tumor and major organs, were assessed by hematoxylin-eosin staining.Microvascular density of tumor tissue and cell apoptosis were assessed by immunohistochemical and TUNEL staining, respectively. RESULTS: The Lv-infected HepG2 cells, and not the Lv-infected L02 cells, expressed TK and tumstatin. Lv-hTERTp-TK and Lv-hTERTp-tumstatin, alone or in combination, inhibited proliferation and increased apoptosis of the HepG2 cells, but the combination was more effective than either alone (P less than 0.05). None of the treatments affected proliferation or apoptosis of the L02 cells (P more than 0.05). The combination also led to a greater reduction of bcl-2 and VEGF than either alone (all, P less than 0.05). Tumor growth was significantly inhibited by the combination (P less than 0.05). In vivo, the combination treatment induced the greatest amount of apoptosis of the HepG2 cells. Cell morphology of major organs such as liver, spleen and kidney were similar to the control group. The combination also produced the most significant effect on tumor microvascular density (P less than 0.05) and the highest apoptosis index (P less than 0.05). CONCLUSION: The HTERT promoter can induce targeted expression of TK and tumstatin in HepG2 cells. Lv-hTERTp-TK combined with Lv-hTERTp-tumstatin can significantly inhibit proliferation and induce apoptosis of human HepG2 cells in vitro and in vivo, which may be related to down-regulation ofbcl-2 and VEGF.