New insight into the effects of Ca(II) on cake layer structure in submerged membrane bioreactors.

The effects of Ca(II) on the structure of the cake layer in submerged membrane bioreactors (SMBRs) were investigated in this study. Three parallel laboratory-scale SMBRs were operated with synthetic municipal wastewater with three Ca(II) levels (82, 208 and 410 mg l(-1)). As the Ca(II) concentration increased, the sludge floc size increased and the molecular weight of the soluble microbial products (SMP) in the bulk liquid decreased. These observations were attributed to the neutralization and bridging function of Ca(II). Furthermore, Ca(II) addition did not change the thickness of the cake layer, but inhibited the deposition of other elements, such as Al, Si, Mg, and Fe. As a result of Ca(II) addition, the cake layer became less compact and more porous. The interspaces among the flocs in the cake layer helped to reduce the membrane fouling potential.

Effects of low-concentration Cr(VI) on the performance and the membrane fouling of a submerged membrane bioreactor in the treatment of municipal wastewater.

The effects of low-concentration Cr(VI) (0.4 mg l(-1)) on the performance of a submerged membrane bioreactor (SMBR) in the treatment of municipal wastewater, as well as membrane fouling were investigated. Compared with the SMBR for control municipal wastewater, the SMBR for Cr(VI)-containing municipal wastewater had a higher concentration of soluble microbial products (SMP) with lower molecular weights, and smaller sludge particle sizes. Furthermore, low-concentration Cr(VI) induced membrane fouling, especially irreversible membrane pore blocking, which markedly shortened the service life of the membrane.

Cyclic RGD functionalized liposomes encapsulating urokinase for thrombolysis.

Thrombosis, a critical event in blood vessels, not only is associated with myocardial infarction and stroke, but also accounts for considerable morbidity and mortality. Thrombolytic drugs are usually applied to the treatment of acute myocardial infarction, acute cerebral infarction and pulmonary embolism. However, thrombolytic drugs show limited efficacy in clinical practice because of the short half-life in plasma and systemic side effects. In this study, the cyclic RGD (cRGD) functionalized liposomes were prepared to encapsulate urokinase, a cheap and widely used thrombolytic drug in clinic and better thrombolysis efficacy was achieved. The flow cytometry analysis showed that the cRGD liposomes could bind to the activated platelets while not to the resting platelets. In vitro release study revealed that the release percentage reached plateau in about 5 h with 60% urokinase being released from liposomes. Results from the in vitro thrombolysis experiments demonstrated a good thrombolysis potential of the cRGD urokinase liposomes. The in vivo thrombolysis study demonstrated that the cRGD liposomes could significantly reduce the dose of urokinase by 75% while achieving the equivalent thrombolysis effect as the free urokinase in mouse mesenteric thrombosis model. In conclusion, the cRGD liposomes encapsulating urokinase hold great promise in clinic for better thrombolytic efficacy. STATEMENT OF SIGNIFICANCE: In this paper, the cRGD liposomes were prepared to encapsulate urokinase for targeted thrombolysis therapy. The cRGD liposomes could specifically bind to the activated platelets and could stably and continuously release its loaded urokinase. The mouse mesenteric thrombosis model was established to evaluate the thrombolysis effect of the cRGD urokinase liposomes. The results demonstrated that the cRGD liposomes could improve the thrombolytic efficacy by almost 4-fold over free urokinase. In conclusion, the cRGD liposomes encapsulating urokinase had great potential for the clinical treatment of thrombosis.

Tracking human footprints in Antarctica through passive sampling of polycyclic aromatic hydrocarbons in inland lakes.

Freely dissolved polycyclic aromatic hydrocarbons (PAHs) were monitored in seven inland lakes of Antarctica by a polyethylene (PE)-based passive sampling technique, with the objective of tracking human footprints. The measured concentrations of PAHs were in the range of 14-360 ng L(-1) with the highest values concentrated around the Russian Progress II Station, indicating the significance of human activities to the loading of PAHs in Antarctica. The concentrations of PAHs in the inland lakes were in the upper part of the PAHs levels in aquatic environments from remote and background regions across the globe. The composition profiles of PAHs indicated that PAHs in the inland lakes were derived mainly from local oil spills, which was corroborated by a large number of fuel spillage reports from ship and plane crash incidents in Antarctica during recent years. Clearly, local human activities, rather than long-range transport, are the dominant sources of PAH contamination to the inland lakes. Finally, the present study demonstrates the efficacy of PE-based passive samplers for investigating PAHs in the aquatic environment of Antarctica under complex field conditions.

Effects of suspended titanium dioxide nanoparticles on cake layer formation in submerged membrane bioreactor.

Effects of the suspended titanium dioxide nanoparticles (TiO2 NPs, 50 mg/L) on the cake layer formation in a submerged MBR were systematically investigated. With nanometer sizes, TiO2 NPs were found to aggravate membrane pore blocking but postpone cake layer fouling. TiO2 NPs showed obvious effects on the structure and the distribution of the organic and the inorganic compounds in cake layer. Concentrations of fatty acids and cholesterol in the cake layer increased due to the acute response of bacteria to the toxicity of TiO2 NPs. Line-analysis and dot map of energy-dispersive X-ray were also carried out. Since TiO2 NPs inhibited the interactions between the inorganic and the organic compounds, the inorganic compounds (especially SiO2) were prevented from depositing onto the membrane surface. Thus, the postponed cake layer fouling was due to the changing features of the complexes on the membrane surface caused by TiO2 NPs.