A CO2-imprinted adsorbent was synthesized by crosslinking the CO2 pre-adsorbed amino-terminated hyperbranched polymer, which was prepared through the Michael addition reaction between amines and methyl acrylate (MA) at 0 °C, followed by self-condensation of the addition reaction products at 100 °C and 140 °C.

Background This study aimed to explore the effect of long non-coding RNA (LncRNA) H19 on the proliferation and invasion of lung carcinoma cells A549, and to determine its molecular targets. Methods A549 cells were with either LncRNA H19 or LncRNA H19 shRNA, and the expression levels of LncRNA H19 were evaluated by quantitative real-time PCR (RT-PCR). We measured cell proliferation using the CCK-8 assay, cell counting assays, and colony formation assay in response to shLncRNA H19-2. Cell migration and invasion were assessed by wound healing assay and Transwell assay, respectively. The mRNA and protein expression levels of E-cadherin, N-cadherin, and vimentin were determined by RT-PCR and western blot, respectively. Results The three LncRNA H19 shRNAs used in our study significantly reduced the expression levels of LncRNA H19 in A549 cells ( P <0.05). Moreover, LncRNA H19 shRNA 2 (shLncRNA-2) was the most potent inhibitor of LncRNA H19 expression, and was selected for further experimentation. Transfection with shLncRNA H19-2 significantly decreased the proliferation, migration, and invasion of A549 cells, while overexpression of LncRNA H19 had the opposite effect in these cells ( P <0.05). In response to shLncRNA H19-2, the expression levels of E-cadherin were notably elevated ( P <0.05), while the expression levels of N-cadherin and vimentin were decreased ( P <0.05). In contrast, overexpression of LncRNA H19 induced the expression of E-cadherin, and blocked the expression of N-cadherin, and vimentin ( P <0.05). Conclusion Our results suggest that LncRNA H19 mediates the proliferation and invasion of lung cancer cells via upregulation of N-cadherin and vimentin, and downregulation of E-cadherin.

A carbon dioxide imprinted solid amine adsorbent (IPEIA-R) with polyethylenimine (PEI) as a skeleton was conveniently prepared by using glutaraldehyde to cross-link carbon dioxide-preadsorbed PEI. As confirmed by FTIR, FT-Raman, and C NMR spectroscopy, CO preadsorbed on PEI could occupy the reactive sites of amino groups and act as a template for imprinting in the cross-linking process. The imino groups formed from the cross-linking reaction between glutaraldehyde and PEI could be reduced by NaBH to form CO -adsorbable amino groups. The adsorption results indicated that CO imprinting and reduction of imino groups by NaBH endowed the adsorbent with a higher CO adsorption capacity. Compared with PEI-supported mesoporous adsorbents, the solid amine adsorbent with PEI as a skeleton can avoid serious pore blockage and CO diffusion resistance, even with a high amine content. The solid amine adsorbent with PEI as a skeleton showed a remarkable CO adsorption capacity (8.56 mmol g ) in the presence of water at 25 °C, owing to the high amine content and good swelling properties. It also showed promising regeneration performance and could maintain almost the same CO adsorption capacity after 15 adsorption-desorption cycles.

Celastrol is an active compound extracted from the root bark of Triptergium wilfordii Hook F., also known as 'Thunder of God Vine'. It is a well-known Chinese medicinal herb that was found to inhibit tumor cell growth and promote apoptosis in several tumor cell lines. However, research into its effects on osteosarcoma cell apoptosis is still extremely limited. The present study was undertaken to determine the effect of celastrol on viability and apoptosis of osteosarcoma cells and furthermore, to illuminate the molecular mechanism of celastrol-induced osteosarcoma cell apoptosis. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay was used to evaluate the viability of the cells following treatment with celastrol. The effect of celastrol on the apoptotic rate of the cells was evaluated by flow cytometry using Annexin V-PE/7-AAD staining assay. Fluorescence microscopy was used to detect the morphological changes in the human osteosarcoma U-2OS cell lines. The expression of Bcl-2 family proteins, caspase-3, caspase-8, caspase-9, cytochrome c and PARP was measured by western blotting. We found that celastrol significantly inhibited the growth of osteosarcoma cells in a dose-dependent manner, particularly U-2OS cells. Furthermore, we observed that celastrol upregulated the expression of the pro-apoptotic proteins Bax and cytochrome c and altered the ratio of Bax/Bcl-2, and triggered the mitochondrial apoptotic pathway, resulting in caspase-3 and -9 activation and PARP cleavage. To conclude, the results indicate that celastrol inhibits the proliferation of human osteosarcoma cancer cells by inducing apoptosis via the mitochondrial-dependent pathway.