Analysis of the effect of green roof substrate amended with biochar on water quality and quantity of rainfall runoff.

Green roofs are becoming a popular ecological alternative in urban areas worldwide. In this study, we constructed two modular green roofs (commercial substrate green roof and biochar substrate green roof) and analyzed the effects that the green roof substrate amended with biochar on the runoff retention capacity, water quality, pollutants releasing characteristic, and pollution load by simulating rainfall experiment (rainfall levels 10~80 mm). Results showed that the mean retention ratio was no significant differences between the commercial substrate (72.54%) and the biochar substrate (72.08%). Both the two kinds of substrates showed that the concentrations of total nitrogen (TN), total phosphorus (TP), chemical oxygen demand (COD), and iron (Fe) decreased gradually with the extension of rainfall time. Electrical conductivity (EC) and pH, as well as mean concentrations of TN, COD, TP, total suspended solids (TSS), and Fe, showed no differences between the green roof runoff of two kind of substrate. However, the neutralizing capacity of biochar substrate for the pH of green roof runoff was stronger than the commercial substrate, and the mean concentration of the TN and COD in the commercial substrate (16.14 mg/L and 171.79 mg/L, respectively) was about two times higher than the biochar substrate (9.85 mg/L and 97.31 mg/L, respectively). Similarly, the pollution load of TN and COD in the commercial substrate was significantly higher than that in the biochar substrate. Therefore, the biochar substrate could effectively reduce the pollution load of TN and COD in the runoff of green roof. Consequently, we suggest that the biochar could be applied to green roof substrates in order to reduce the impact of city non-point pollution on receiving water bodies.

Isorhamnetin protects endothelial cells model CRL1730 from oxidative injury by hydrogen peroxide.

To explore the protective effect and mechanism of isorhamnetin against oxidative injury caused by H2O2 to endothelial cell strain CRL1730 of human umbilical vein. H2O2 and endothelial cell strain CRL1730 were used, as a model of injured endothelial cell. Three levels of crude drugs areorhamnetin, 22.8µg/ml, 11.4µg/mL and 5.7µg/mL was added to the injured cell strain CRL1730 respectively. The cell injury was measured in terms of necrotic rate, quantities of von Wilebr and factor (vWf) and thrombomodulin (TM), lactate dehydrogenase (LDH) and intracellular free calcium ions through flow cytometry, ELISA, fluorescent spectrometer and laser scanning confocal microscopy respectively. Isorhamnetins @ 11.4µg/mL and 5.7µg/mL has significantly decreased EC necrotic rate, while the increased vWf concentration due to oxidant (200mol/L of H2O2) was significantly decreased by 5.7µg/mL versus 11.4 and 22.8µg/mL isorhamnetin. Also, the increased in TM and LDH in injured cells was reversed to normal level with 5.7 to 11.4µg/mL isorhamnetin. These results suggest that isorhamnetin protect the integrity of cell membranes. Similarly, H2O2 treatment of cells elicited the release of intracellular calcium, however, 5.7µg/mL and 11.4µ g/mL isorhamnetin dramatically inhibited transient release of intracellular calcium. This suggests that isorhamnetin, at lower concentration, could inhibit the IP3-sensitive calcium pool from releasing calcium, protecting VECs from injury by H2O2. Traditional Chinese herbs, hippophaerhamnoides have been recognized as safe and as a source of flavonoids, with strong cardiovascular protection. The results of this study revealed that isorhamnetin produce a strong effect on some targetspresent in ECs and thus, provide a basis for the future work targeted towards endothelial cells protection.

Doxorubicin-loaded fluorescent carbon dots with PEI passivation as a drug delivery system for cancer therapy.

In this work, we reported a novel and effective cancer treatment strategy by fabricating carbon dot (CD)-polyethylenimine (PEI)-doxorubicin (DOX) antitumor drug complexes from a combination of PEI-passivated CDs (CD-PEI) and DOX. CD-PEI was synthesized by the one-step microwave hydrothermal carbonization of a mixture of glycerol and PEI-25k, enabling simultaneous synthesis and surface passivation of CDs. DOX was loaded onto CD-PEI by electrostatic interactions. The results show that this system not only improves selective drug release but also prolongs the drug release time and improves the killing effect on tumors. Compared with free DOX, the CD-PEI-DOX complex has a stronger killing effect on liver cancer cells (MHCC-97L and Hep3B cells) but a very low killing effect on normal liver cells (L02). Studies have also confirmed that compared with DOX alone, CD-PEI-DOX nanoparticles can effectively inhibit tumors because of the larger amount of drugs localized in tumor cells and the higher apoptosis rate of MHCC-97L cells. In vivo experiments confirmed that CD-PEI-DOX has a stronger inhibitory effect on tumor growth, indicating that CD-PEI-DOX nanomedicine has inhibitory effects on tumors.

The combination of a synthetic promoter and a CMV promoter improves foreign gene expression efficiency in myocytes.

Skeletal muscle is becoming an attractive target tissue for gene therapy. Nevertheless, the low level of gene therapeutic expression in this tissue is the major limitation to it becoming an ideal target for gene transfer. The promoter is important element for gene transcription; however, the gene expression efficiencies and specificities of viral promoters and skeletal muscle-specific promotors are in themselves limiting factors. In this study, we established a dual-promoters system in skeletal muscle using a cytomegalovirus (CMV) promoter and a skeletal muscle-specific synthetic promoter. Mouse myoblast cell line C2C12 cells were transfected with the system. We demonstrated that the dual-promoters system could significantly improve exogenous gene expression rate in vitro when compared with a single CMV promoter system and a skeletal muscle-specific synthetic promoter system in C2C12 cell line, by 69.48% and 41.93%, respectively. Next, we evaluated the system efficiency in vivo, the results showed that the dual-promoters system increased gene expression in mice 1.23-fold and 1.60-fold, respectively compared with expression controlled by the two single promoter vectors. Finally, we tested the dual-promoters system in growth hormone-releasing hormone (GHRH) gene therapy, and revealed that when these two promoters co-drove the GHRH gene expression in vivo animal growth was enhanced significantly. All these results indicate that use of the dual-promoter vector was more efficient for gene expression in skeletal muscle tissue than use of the single promoter vectors. These finding could, hopefully, lead to the development of a high efficiency expression system in myocytes and form an ideal approach for gene therapy.