The formation of porous metal oxide networks using mixed titania/zirconia precursor solutions was achieved by a polymer gel templating technique. The inorganic porous materials result from a coating of the initial template with obvious structural similarities between the polymer gel and the final inorganic network. The mixed TiO2/ZrO2 network structures exhibit higher surface areas than a corresponding pure titania network, and in a certain range of metal oxide compositions X-ray amorphous mixed glasses are obtained upon calcination at 500 °C. The photocatalytic efficiencies of the TiO2 and TiO2/ZrO2 networks have been assessed by monitoring the photodecomposition of two organic molecules:  salicylic acid and 2-chlorophenol. The TiO2 network was found to exhibit an efficiency of ≈60% and ≈65% of the standard Degussa P25 TiO2 (of nanoparticulate morphology) for the salicylic acid and 2-chlorophenol reactions, respectively. For both photocatalytic reactions the presence of zirconia in the titania network (at a molar ratio of 1:9) resulted in enhanced photocatalytic activity relative to the pure TiO2 network (80% and 100% the efficiency of Degussa P25), which is believed to be due to a number of factors including an increased surface area and a decrease of the anatase to rutile crystal phase transformation. A further increase in the zirconia-to-titania ratio leads to decreased activity as amorphous materials are obtained and zirconia itself does not act as a photocatalyst under the experimental conditions used.

A variety of polymer gels with different chemical composition, architecture, porosity, and surface area have been used as templating materials for the fabrication of porous TiO2 networks. Titanium isopropoxide was incorporated in the bicontinuous polymer structure where hydrolysis and condensation reactions were carried out, producing a hybrid of polymer and amorphous titania. Calcination of this hybrid resulted in the formation of a continuous, purely inorganic network of either the anatase or rutile crystal phase, with the individual titanium dioxide particles contacting a number of neighbors, thereby forming a continuous three-dimensional structure. The resulting networks have vastly different structures, with porosities as high as 99% and surface areas ranging from 5 to 100 m2 g-1. These structures may be of importance to various fields of research, including photovoltaics and photocatalysis, because the open “coral-like” network structure of the titanium dioxide allows high access of the titanium dioxide surface to the reaction medium. The potential of the gel coating technology for the construction of more complex chemical systems was illustrated by the assembling of a noble metal/oxide semiconductor hybrid where homogeneously dispersed platinum nanoparticles are integrated within the TiO2 network. Preliminary studies have shown the titanium dioxide materials to exhibit 75% of the photocatalytic activity of Degussa P25.

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This study was implemented to figure out whether lncRNA HOTAIR/miR‐17‐5p/PTEN axis played a role that was opposite to Shenqifuzheng (SQFZ) injection in regulating the chemosensitivity of gastric cancer cells. The gastric cancer tissues were gathered and four gastric cancer cell lines were prepared, including BGC‐823, MGC‐803, SGC‐7901, and MKN28. Moreover, cisplatin, adriamycin, mitomycin, and 5‐fluoroura were managed as the chemo‐therapeutics, and SQFZ was prepared as a Chinese medicine. Striking distinctions of HOTAIR, miR‐17‐5p, and PTEN expressions were observed between gastric cancer tissues and para‐carcinoma normal tissues (P < 0.05). MKN28 was associated with the highest resistance to cisplatin, adriamycin, mitomycin, and 5‐fluoroura among all the cell types, and SQFZ significantly improved the MKN28 cells’ sensitivity to the drugs (P < 0.05). The over‐expressed HOTAIR and miR‐17‐5p, as well as under‐expressed PTEN tended to significantly facilitate the viability, EMT process and proliferation of MKN28 cells that were subject to treatment of chemo‐therapies (P < 0.05). SQFZ could amplify the effects of si‐HOTAIR, miR‐17‐5p inhibitor, and pcDNA‐PTEN on boosting the chemosensitivity of gastric cancer cells (P < 0.05). In addition, HOTAIR was also found to directly target miR‐17‐5p, and PTEN appeared to be subject to the modification of HOTAIR and miR‐17‐5p in its acting on the viability, proliferation, EMT process, and apoptosis of gastric cancer cells. The HOTAIR/miR‐17‐5p/PTEN axis could be regarded as the potential treatment targets for gastric cancer, and adjuvant therapy of SQFZ injection could assist in further improving the treatment efficacy of chemo‐therapies for gastric cancer.

The current investigation explored the synthetic contribution of lncRNA H19, miR‐130a‐3p, and miR‐17‐5p to radio‐resistance and chemo‐sensitivity of cardiac cancer cells. Totally 284 human cardiac cancer tissues were gathered, and they have been pathologically diagnosed. The cardiac cancer cells were isolated with utilization of the mechanic method. Moreover, cisplatin, adriamycin, mitomycin, and 5‐fluorouracil were designated as the chemotherapies, and single‐dose X‐rays were managed as the radiotherapy for cardiac cancer cells. We also performed luciferase reporter gene assay to verify the targeted relationship between H19 and miR‐130a‐3p, as well as between H19 and miR‐17‐5p. Finally, mice models were established to examine the functions of H19, miR‐130a‐3p, and miR‐17‐5p on the development of cardiac cancer. The study results indicated that H19, miR‐130a‐3p, and miR‐17‐5p expressions within cardiac cancer tissues were significantly beyond those within adjacent nontumor tissues (P < 0.05), and H19 expression was positively correlated with both miR‐130a‐3p (rs = 0.43) and miR‐17‐5p (rs = 0.49) expressions. The half maximal inhibitory concentrations (IC50) of cisplatin, adriamycin, mitomycin, and 5‐fluorouracil for cardiac cancer cells were, respectively, determined as 2.01 μg/mL, 8.35 μg/mL, 24.44 μg/mL, and 166.42 μg/mL. The overexpressed H19, miR‐130a‐3p, and miR‐17‐5p appeared to improve the survival rate and viability of cardiac cancer cells that were exposed to chemotherapies and X‐rays (all P < 0.05). It was also drawn from luciferase reporter gene assay that H19 could directly target miR‐130a‐3p and miR‐17‐5p, thereby modifying the sensitivity of cardiac cancer cells to drugs and X‐rays (P < 0.05). Finally, the mice models also produced larger tumor size and higher tumor weight, when H19, miR‐130a‐3p, or miR‐17‐5p expressions were up‐regulated within them (P < 0.05). In conclusion, H19 could act on miR‐130a‐3p or miR‐17‐5p to alter the radio‐ and chemo‐sensitivities of cardiac cancer cells, helping to improve the radio‐/chemotherapies for cardiac cancer.

Primary gallbladder cancer (GBC) is the most common malignancy of the digestive system. Due to its resistance to standard chemotherapy, no effective treatments are available at present. Artemisinin, a plant-derived anti‑malarial drug, has recently been shown to have anti-proliferative effects on a range of human cancer cell types. However, the efficacy of artemisinin against gallbladder cancer has not been reported. The present study investigated the effects of artemisinin on the proliferation, cell cycle and apoptosis of gallbladder cancer cell lines. A cell viability assay and an in vivo xenograft study demonstrated that artemisinin significantly inhibited the growth of gallbladder cancer. Western blot analysis indicated that artemisinin induced the expression of p16, while down‑regulating phosphorylated extracellular signal‑regulated kinase (ERK)1/2, CDK4 and cyclin D1 expression, leading to inhibition of the ERK1/2 pathway. Furthermore, flow cytometry and western blot analysis showed that artemisinin caused G1-phase arrest of the cell cycle, promoted the generation of reactive oxygen species (ROS), led to a collapse of the mitochondrial membrane potential and to triggered cytochrome c release from the mitochondria into the cytoplasm, which finally activated caspase‑3‑mediated apoptosis. In conclusion, the present study demonstrated that artemisinin inhibits the proliferation of gallbladder cancer cells in vitro as well as in vivo and induces apoptosis via induction of ROS and cell cycle arrest. These results suggested that artemisinin may be suitable for the treatment of gallbladder cancer.