232 research outputs found
MBR Technology: future research directions
Cutting down the operational costs of MBR technology will be the key driver for research. This article outlines some research areas and specific topics that potentially will contribute to lower costs. Special attention to these topics should be given the coming years. Long term research should focus on sustainable MBR concepts. A few innovative developments will be presente
Cyanobacterial growth and cyanophycin production with urea and ammonium as nitrogen source
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Scenario Analysis of Nutrient Removal from Municipal Wastewater by Microalgal Biofilms
Microalgae can be used for the treatment of municipal wastewater. The application of microalgal biofilms in wastewater treatment systems seems attractive, being able to remove nitrogen, phosphorus and COD from wastewater at a short hydraulic retention time. This study therefore investigates the area requirement, achieved effluent concentrations and biomass production of a hypothetical large-scale microalgal biofilm system treating municipal wastewater. Three scenarios were defined: using microalgal biofilms: (1) as a post-treatment; (2) as a second stage of wastewater treatment, after a first stage in which COD is removed by activated sludge; and (3) in a symbiotic microalgal/heterotrophic system. The analysis showed that in the Netherlands, the area requirements for these three scenarios range from 0.32 to 2.1 m2 per person equivalent. Moreover, it was found that it was not possible to simultaneously remove all nitrogen and phosphorus from the wastewater, because of the nitrogen:phosphorus ratio in the wastewater. Phosphorus was limiting in the post-treatment scenario, while nitrogen was limiting in the two other scenarios. Furthermore, a substantial amount of microalgal biomass was produced, ranging from 13 to 59 g per person equivalent per day. These findings show that microalgal biofilm systems hold large potential as seasonal wastewater treatment systems and that it is worthwhile to investigate these systems furthe
Mechanism of trifluorothymidine potentiation of oxaliplatin-induced cytotoxicity to colorectal cancer cells
Oxaliplatin (OHP) is an anticancer agent that acts by formation of Platinum-DNA (Pt-DNA) adducts resulting in DNA-strand breaks and is used for the treatment of colorectal cancer. The pyrimidine analog trifluorothymidine (TFT) forms together with a thymidine phosphorylase inhibitor (TPI) the anticancer drug formulation TAS-102, in which TPI enhances the bioavailability of TFT in vivo. In this in vitro study the combined cytotoxic effects of OHP with TFT were investigated in human colorectal cancer cells as a model for TAS-102 combinations. In a panel of five colon cancer cell lines (WiDr, H630, Colo320, SNU-C4 and SW1116) we evaluated the OHP-TFT drug combinations using the multiple drug–effect analysis with CalcuSyn software, in which the combination index (CI) indicates synergism (CI<0.9), additivity (CI=0.9–1.1) or antagonism (CI>1.1). Drug target analysis was used for WiDr, H630 and SW1116 to investigate whether there was an increase in Pt-DNA adduct formation, DNA damage induction, cell cycle delay and apoptosis. Trifluorothymidine combined with OHP resulted in synergism for all cell lines (all CI<0.9). This was irrespective of schedule in which either one of the drugs was kept at a constant concentration (using variable drug ratio) or when the two drugs were added in a 1 : 1 IC50-based molar ratio. Synergism could be increased for WiDr using sequential drug treatment schedules. Trifluorothymidine increased Pt-DNA adduct formation significantly in H630 and SW1116 (14.4 and 99.1%, respectively; P<0.05). Platinum-DNA adducts were retained best in SW1116 in the presence of TFT. More DNA-strand breaks were induced in SW1116 and the combination increased DNA damage induction (>20%) compared with OHP alone. Exposure to the drugs induced a clear cell-cycle S-phase arrest, but was dose schedule and cell line dependent. Trifluorothymidine (TFT) and OHP both induced apoptosis, which increased significantly for WiDr and SW1116 after TFT–OHP exposure (18.8 and 20.6% respectively; P<0.05). The basal protein levels of ERCC1 DNA repair enzyme were not related to the DNA damage that was induced in the cell lines. In conclusion, the combination of TFT with the DNA synthesis inhibitor OHP induces synergism in colorectal cancer cells, but is dependent on the dose and treatment schedule used
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