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Burton, T.

Publications and source records attributed to Burton, T..

2 recordsLinked to original sources

Evolution of Daphnia population dynamics following invasion by a non-native predator

O_LIPredators are frequently observed to cause evolutionary responses in prey phenotypes, which may, in turn, translate into evolutionary shifts in prey population dynamics. Although a link between predation and population growth has been demonstrated in experimental evolution studies, insights from natural populations are lacking. C_LIO_LIHere we tested for evolutionary changes in the population dynamics of the herbivorous water flea Daphnia pulicaria in response to the invasion of the predatory spiny water flea (Bythotrephes longimanus) in the Great Lakes region, USA. Using a resurrection ecological approach and a 3-month population growth experiment (in the absence of predation) we compared population dynamics in daphnia from pre- and post-invasion time periods. C_LIO_LIPost-invasion daphnia were able to maintain an overall higher population abundance throughout the growth experiment, both in terms of the number of individuals (28% higher) and total population biomass (33% higher). Estimation of population dynamics parameters from a theta-logistic model suggested that this was achieved through an increase in intrinsic population growth rate as well as increased carrying capacity. C_LIO_LIThe observed difference in intrinsic rate of increase could not be predicted based on previous measurements of life-history traits in these clones. This indicates that care should be taken when extrapolating from a few life history traits measured in isolated individuals under controlled conditions to population dynamics. C_LIO_LIWhereas previous experimental evolution studies of predator-prey interactions have demonstrated that genotypes that have evolved under predation have inferior population growth when the predator is absent, this was not the case for the Daphnia. We suggest that complexities in ecological interactions of natural ecosystems, such as the potential for spatial and temporal avoidance of predation, makes it challenging to provide general predictions about evolutionary responses in population dynamics to predators. C_LI

evolutionary biology↗

The role of sodium thiocyanate supplementation during dextran sodium sulphate-stimulated experimental colitis

Ulcerative colitis is a condition characterised by the infiltration of leukocytes into the gastrointestinal wall. Leukocyte-MPO catalyses hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN) formation from chloride (Cl-) and thiocyanous (SCN-) anions, respectively. While HOCl indiscriminately oxidises biomolecules, HOSCN primarily targets low-molecular weight protein thiols. Oxidative damage mediated by HOSCN may be reversible, potentially decreasing MPO-associated host tissue destruction. This study investigated the effect of SCN- supplementation in a model of acute colitis. Female mice were supplemented dextran sodium sulphate (DSS, 3% w/v) in the presence of 10 mM Cl- or SCN- in drinking water ad libitum, or with salts (NaCl and NaSCN only) or water only (controls). Behavioural studies showed mice tolerated NaSCN and NaCl-treated water with water-seeking frequency. Ion-exchange chromatography showed increased fecal and plasma SCN- levels in thiocyanate supplemented mice; plasma SCN- reached similar fold-increase for smokers. Overall there was no difference in weight loss and clinical score, mucin levels, crypt integrity and extent of cellular infiltration between DSS/SCN- and DSS/Cl- groups. Neutrophil recruitment remained unchanged in DSS-treated mice, as assessed by fecal calprotectin levels. Total thiol and tyrosine phosphatase activity remained unchanged between DSS/Cl- and DSS/SCN- groups, however, colonic tissue showed a trend in decreased 3-chlorotyrosine (1.5-fold reduction, p<0.051) and marked increase in colonic GCLC, the rate-limiting enzyme in glutathione synthesis. These data suggest that SCN- administration can modulate MPO activity towards a HOSCN-specific pathway, however, this does not alter the development of colitis within a DSS murine model.HighlightsSodium thiocyanate (SCN-) supplementation increased plasma and fecal SCN- level.Thiocyanate supplementation diverted HOCl-mediated oxidative damage in mice colon.Thiocyanate supplementation stimulated thiol synthesis in the DSS colitis model.Thiocyanate provides no protection in an acute experimental model of UC.Competing Interest StatementThe authors have declared no competing interest.AbbreviationsCDCrohn’s Disease3-Cl-Tyr3-chlorotyrosineDSSDextran Sodium SulphateGAPDHGlyceraldehyde 3-phosphate dehydrogenaseGCLCGlutamate-Cysteine Ligase Catalytic SubunitGIGastrointestinalGSHGlutathioneGSSGGlutathione DisulfideHOBrHypobromous AcidHOClHypochlorous AcidHCN-Hydrogen; CyanideHOSCNHypothiocyanous AcidIBDInflammatory Bowel DiseaseMPOMyeloperoxidaseNrf2Nuclear factor erythroid 2-related Factor 2PMNsPolymorphonuclear NeutrophilsPTPProtein Tyrosine PhosphatasesROSReactive Oxygen SpeciesSCN-ThiocyanateUCUlcerative ColitisView Full Text

pathology↗