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Publikasjoner

NIBIOs ansatte publiserer flere hundre vitenskapelige artikler og forskningsrapporter hvert år. Her finner du referanser og lenker til publikasjoner og andre forsknings- og formidlingsaktiviteter. Samlingen oppdateres løpende med både nytt og historisk materiale. For mer informasjon om NIBIOs publikasjoner, besøk NIBIOs bibliotek.

2015

Sammendrag

The scanning electron microscopy (SEM), x-ray fluorescence spectrometry (XRF) and inductively coupled plasma mass spectrometry (ICP-MS) methods were used for investigation of manganese dioxide (MnO2)–containing composite sorbents and their sorption properties were evaluated as well. A characterization of the sorbents was performed by SEM and XRF. Diatomite and silicagel were used as the porous carrier for the MnO2 (which provides the functionality of the sorbents). The silica component was prepared by co-precipitation of water glass with manganese dioxide. Potassium permanganate is used as a source of manganese dioxide. Deposition of MnO2 was carried on the pore surfaces of porous materials (silica, diatomite) by means of hydrogen peroxide and formaldehyde. The sorbent prepared under the previously described procedure was tested for compounds containing potassium (K+).

Sammendrag

The woodland strawberry (Fragaria vesca) has become the model plant for the economically important, but genetically complex, octoploid F. × ananassa. Crown rot caused by the oomycete Phytophthora cactorum is a major problem for the strawberry industry and the identification and incorporation of efficient resistance genes into superior cultivars are important for breeding. In the present study, two experimental populations were used in inoculation experiments under controlled greenhouse condition. Studies of a sparse diallel cross between resistant and susceptible F. vesca genotypes concluded that resistance to crown rot is inherited as a dominant trait under nuclear control. Subsequently, an F2 population derived from the grandparents Bukammen (resistant) and Haugastøl 3 (susceptible) collected in Norway, were phenotyped in infection experiments and genotyped using genotyping-by-sequencing. A 416.2-cM linkage map was constructed, and a single major gene locus was identified on linkage group 6 that we attributed to resistance to Phytopthora infection. We propose to name the resistance locus RPc-1 (Resistance to Phytophthora cactorum 1). Gene prediction of the 3.3 Mb QTL recovered 801 genes of which 69 had a potential role in plant disease resistance.

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Sammendrag

In the context of reducing CO2 emissions to the atmosphere, chemical absorption with amines is emerging as the most advanced technology for post-combustion CO2 capture from exhaust gases of fossil fuel power plants. Despite amine solvent recycling during the capture process, degradation products are formed and released into the environment, among them aliphatic nitramines, for which the environmental impact is unknown. In this study, we determined the acute and chronic toxicity of two nitramines identified as important transformation products of amine-based carbon capture, dimethylnitramine and ethanolnitramine, using a multi-trophic suite of bioassays. The results were then used to produce the first environmental risk assessment for the marine ecosystem. In addition, the in vivo genotoxicity of nitramines was studied by adapting the comet assay to cells from experimentally exposed fish. Overall, based on the whole organism bioassays, the toxicity of both nitramines was considered to be low. The most sensitive response to both compounds was found in oysters, and dimethylnitramine was consistently more toxic than ethanolnitramine in all bioassays. The Predicted No Effect Concentrations for dimethylnitramine and ethanolnitramine were 0.08 and 0.18 mg/L, respectively. The genotoxicity assessment revealed contrasting results to the whole organism bioassays, with ethanolnitramine found to be more genotoxic than dimethylnitramine by three orders of magnitude. At the lowest ethanolnitramine concentration (1 mg/L), 84% DNA damage was observed, whereas 100 mg/L dimethylnitramine was required to cause 37% DNA damage. The mechanisms of genotoxicity were also shown to differ between the two compounds, with oxidation of the DNA bases responsible for over 90% of the genotoxicity of dimethylnitramine, whereas DNA strand breaks and alkali-labile sites were responsible for over 90% of the genotoxicity of ethanolnitramine. Fish exposed to > 3 mg/L ethanolnitramine had virtually no DNA left in their red blood cells.