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- Sumaila, U. Rashid, et al.
(författare)
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WTO must ban harmful fisheries subsidies
- 2021
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 374:6567, s. 544-544
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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- Chapin, III F.S., et al.
(författare)
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Resilience-based stewardship : Strategies for navigating sustainable pathways in a changing world.
- 2009
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Ingår i: Principles of ecosystem stewardship. - New York : Springer Verlag. - 9780387730332 ; , s. 319-337
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Bokkapitel (populärvet., debatt m.m.)abstract
- Accelerated global changes in climate, environment, and social–ecological systems demand a transformation in human perceptions of our place in nature and patterns of resource use. The biology and culture of Homo sapiens evolved for about 95% of our species’ history in hunting-and-gathering societies before the emergence of settled agriculture. We have lived in complex societies for about 3%, and in industrial societies using fossil fuels for about 0.1% of our history. The pace of cultural evolution, including governance arrangements and resource-use patterns, appears insufficient to adjust to the rate and magnitude of technological innovations, human population increases, and environmental impacts that have occurred. Many of these changes are accelerating, causing unsustainable exploitation of ecosystems, including many boreal and tropical forests, drylands, and marine fisheries. The net effect has been serious degradation of the planet’s life-support system on which societal development ultimately depends (see Chapters 2 and 14.
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- Nording, Malin L, et al.
(författare)
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Bioactive lipid profiling reveals drug target engagement of a soluble epoxide hydrolase inhibitor in a murine model of tobacco smoke exposure
- 2015
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Ingår i: Journal of metabolomics. - : Herbert publications. - 2059-0008. ; 1:1
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Tidskriftsartikel (refereegranskat)abstract
- The inflammatory process underlying chronic obstructive pulmonary disease (COPD) may be caused by tobacco smoke (TS) exposure. Previous studies show that epoxyeicosatrienoic acids (EETs) possess promising anti-inflammatory properties, therefore stabilization of EETs and other fatty acid epoxides through inhibition of soluble epoxide hydrolase (sEH) was investigated in mouse models of acute and subchronic inflammation caused by TS exposure. During the entire TS exposure, the potent sEH inhibitor 1-(1-methylsulfonyl-piperidin-4-yl)-3-(4-trifluoromethoxy-phenyl)-urea (TUPS) was given via drinking water. To assess drug target engagement of TUPS, a tandem mass spectrometry method was used for bioactive lipid profiling of a broad range of fatty acid metabolites, including EETs, and their corresponding diols (DHETs) derived from arachidonic acid, as well as epoxides and diols derived from other fatty acids. Several, but not all, plasma epoxide/diol ratios increased in mice treated with sEH inhibitor, compared to non-treated mice, suggesting a wider role for sEH involving more fatty acid precursors besides arachidonic acid. This study supports qualitative use of epoxide/diol ratios explored by bioactive lipid profiling to indicate drug target engagement in mouse models of TS exposure relevant to COPD, which may have ramifications for future therapeutic interventions of sEH.
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- Rich, Rebecca L., et al.
(författare)
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A global benchmark study using affinity-based biosensors
- 2009
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Ingår i: Analytical Biochemistry. - : Elsevier BV. - 0003-2697 .- 1096-0309. ; 386:2, s. 194-216
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Tidskriftsartikel (refereegranskat)abstract
- To explore the variability in biosensor studies, 150 participants from 20 countries were given the same protein samples and asked to determine kinetic rate constants for the interaction. We chose a protein system that was amenable to analysis using different biosensor platforms as well as by users of different expertise levels. The two proteins (a 50-kDa Fab and a 60-kDa glutathione S-transferase [GST] antigen) form a relatively high-affinity complex, so participants needed to optimize several experimental parameters, including ligand immobilization and regeneration conditions as well as analyte concentrations and injection/dissociation times. Although most participants collected binding responses that could be fit to yield kinetic parameters, the quality of a few data sets could have been improved by optimizing the assay design. Once these outliers were removed, the average reported affinity across the remaining panel of participants was 620 pM with a standard deviation of 980 pM. These results demonstrate that when this biosensor assay was designed and executed appropriately, the reported rate constants were consistent, and independent of which protein was immobilized and which biosensor was used.
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- Sandberg, Kenneth, 1945, et al.
(författare)
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Fetal nicotine exposure increases airway responsiveness and alters airway wall composition in young lambs.
- 2011
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Ingår i: Respiratory physiology & neurobiology. - : Elsevier BV. - 1878-1519 .- 1569-9048. ; 176:1-2, s. 57-67
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Tidskriftsartikel (refereegranskat)abstract
- To test the hypotheses that fetal nicotine exposure alters airway wall composition and enhances the airway response to inhaled methacholine (MCh), lambs were exposed during the last fetal trimester to (1) a low dose (LN) (n=13, 0.5mg/kg/d (maternal weight) of free base nicotine, (2) a moderate dose (MN) (n=10, 1.5mg/kg/d) or (3) saline (n=14). Studies were performed at postnatal days 12, 26 and 52. Prenatal nicotine exposure induced a dose- and age-related hyper-responsiveness to MCh in the proximal airways. Moment analysis of nitrogen decay curves showed no nicotine or MCh effects on ventilation homogeneity or gas-mixing efficiency in the distal airways during MCh inhalations suggesting a bimodal response. Fetal nicotine exposure increased epithelial mucosubstance volume in central (LN, MN) and distal bronchi (LN), increased smooth muscle volume in distal bronchi and bronchioles (LN) and decreased bronchiolar diameter (MN). In conclusion, third trimester nicotine exposure causes hyperreactive proximal airways and alters proximal airway wall composition associated with airflow limitation.
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