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Silver-based nanoparticles (Ag-b-NPs) emitted by wastewater treatment plants (WWTPs) are considered to be widely present in the natural environment. However, there is much that is unknown about the effect of WWTP effluent on the occurrence of Ag-b-NPs in surface waters. On the basis of field analysis of representative WWTPs in Germany, we demonstrate that more than 96.4% of Ag-b-NPs from wastewater influent are removed through WWTPs, even though influent contains Ag-b-NP concentrations of tens to hundreds ng L(-1), resulting in effluent Ag-b-NP concentrations of 0.7-11.1 ng L(-1) over the seasons. The estimated flux of Ag-b-NPs associated with WWTPs effluent discharge is ∼33 kg y(-1) in Germany. WWTPs effluent increases Ag-b-NP levels of the River Isar to 2.0-8.6 ng L(-1), while remarkable decreases are observed at sites ∼1.5 km downstream of each discharge point, and Ag-b-NP levels then keep stable (0.9-2.3 ng L(-1)) until the next discharge point, showing subtle differences in Ag-b-NP levels between the river and reference lakes without industrial sources and WWTPs effluent discharge. Our results demonstrate that WWTPs effluent can exert a clear influence on the occurrence of Ag-b-NPs in surface waters.

IkappaBzeta belongs to the nuclear members of the IkappaB protein family. Its function in regulating the activity of the transcription factor NFkappaB is poorly understood. Here, we demonstrate that human IkappaBzeta is posttranscriptionally regulated by microRNA (miR)-124a. In HepG2 cells miR-124a was not endogenously expressed, but upon enforced expression dramatically inhibited the interleukin-1beta-induced protein expression of IkappaBzeta. The predicted binding site for miR-124a in the 3'UTR of the IkappaBzeta mRNA revealed an imperfect match resulting in miR-124a-mediated suppression of IkappaBzeta expression through translational repression. Reporter gene analyses revealed that miR-124a targets IkappaBzeta mRNA through base pairing to the partially complementary sequence in the 3'UTR that was predicted as a binding site by in silico analysis. Furthermore, we demonstrate that the 7mer seed match is sufficient for recognition of the IkappaBzeta mRNA. Together, our data identify IkappaBzeta as a target of miR-124a that might be involved in the fine-tuning of NF-kappaB-mediated gene expression.

A better understanding of wastewater treatment with soil filters is important to optimise plant operation and reduce the risk of clogging. The article presents results of a treatment concept which uses a combination of SBR and vertical-flow sand filter technology. The SBR was mainly used for denitrification and sedimentation of substances in particulate form. Efficient nitrification was achieved by the planted sand filter. Degradation rates of 10gNH(4)-N/(m(2)xd) were measured for periods with peak loadings. The two-dimensional dynamic model reproduces the biofilm growth and decay of heterotrophic and autotrophic biomass. It is capable of describing the clogging of the sand filter by combining a biochemical and a geometric model. After calibration, the model was used for the calculation of maximum nitrogen degradation performances. Maximum degradation rates of 12gNH(4)-N/(m(2)xd) can be achieved if the COD/TKN ratio is reduced before to a level lower than that of municipal wastewater. The COD was further degraded in the filter than we expected comparing it with activated sludge plants. Within the soil filter a biofilm thickness of up to 110microm is simulated depending on the embankment of gravel and grains of sand. Sensitivity analysis of model parameters showed the high impact of the maximum autotrophic growth rate, the autotrophic yield, the diffusion coefficient for oxygen and the number of contact points of the single grains of sand.

A novel member of the IkappaB family, human IkappaB-zeta, was identified by a differential screening approach of apoptosis-sensitive and -resistant tumor cells. The protein consists of 6 ankyrin repeats at its COOH terminus and shares about 30% identity with other IkappaB members. IkappaB-zeta associates with both the p65 and p50 subunit of NF-kappaB and inhibits the transcriptional activity as well as the DNA binding of the transcription factor. Interestingly, IkappaB-zeta is localized in the nucleus where it aggregates in matrix-associated deacetylase bodies, indicating that IkappaB-zeta regulates nuclear NF-kappaB activity rather than its nuclear translocation from the cytoplasm. IkappaB-zeta expression itself was regulated by NF-kappaB, suggesting that its activity is controlled in a negative feedback loop. Unlike classical IkappaB proteins, IkappaB-zeta was not degraded upon cell stimulation. Treatment with tumor necrosis factor-alpha, interleukin-1beta, and lipopolysaccharide induced a strong induction of IkappaB-zeta transcripts. Expression of IkappaB-zeta was detected in different tissues including lung, liver, and in leukocytes but not in the brain. Suppression of endogenous IkappaB-zeta by RNA interference rendered cells more resistant to apoptosis, whereas overexpression of IkappaB-zeta was sufficient to induce cell death. Our results, therefore, suggest that IkappaB-zeta functions as an additional regulator of NF-kappaB activity and, hence, provides another control level for the activation of NF-kappaB-dependent target genes.