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Predator-prey relationships belong to the most important and well-studied ecological interactions in nature. Understanding the underlying mechanisms is important to predict community dynamics and to estimate coexistence probability. Historically, evolution has been considered to be too slow to affect such ecological interactions. However, evolution can occur within ecological time scales, potentially affecting predator-prey communities. In an antagonistic pair-wise relationship the prey might evolve to minimize the effect caused by the predator (e.g. mortality), while the predator might evolve to maximize the effect (e.g. food intake). Evolution of one of the species or even co-evolution of both species in predator-prey relationships is often difficult to estimate from population dynamics without measuring of trait changes in predator and/or prey population. Particularly in microbial systems, where microorganisms evolve quickly, determining whether co-evolution occurs in predator-prey systems is challenging. We simulate observational data using quantitative trait evolution models and show that the interaction between bacteria and ciliates can be best explained as a co-evolutionary process, where both the prey and predator evolve. Evolution by prey alone explains the data less well, whereas the models with predator evolution alone or no evolution are both failing. We conclude that that ecology and evolution both interact in shaping community dynamics in microcosms. Ignoring the contribution of evolution might lead to incorrect conclusions., (Copyright © 2019. Published by Elsevier Ltd.)

Macrophage class A scavenger receptor types I and II (SR-AI and II) mediate the uptake of oxidized LDL in atherosclerotic lesions. The recently described type III receptor (SR-AIII), which lacks amino acids encoded by exon 10 of the SR-A gene, is unable to mediate the uptake of ligands and acts as a dominant negative regulator in the trimeric SR-A molecule. To find out whether SR-AIII might play a role in the regulation of SR-A activity in the arterial wall, we studied its expression in normal and atherosclerotic aortic intima-medias of Watanabe heritable hyperlipidemic (WHHL) and cholesterol-fed New Zealand white (NZW) rabbits. SR-A mRNA was amplified by reverse transcription-polymerase chain reaction (RT-PCR) with a SR-AIII-specific primer pair and with a primer pair suitable for both SR-AI and III. Very low SR-AI expression and no SR-AIII expression was found in the lesion-free aortic intima-medias of WHHL rabbits and control NZW rabbits. WHHL rabbit fatty streaks contained abundant SR-AI expression and low-level SR-AIII expression. In contrast, the numerous fatty streaks and fatty plaques appearing in the aortas of cholesterol-fed (14 weeks) NZW rabbits, and the fatty plaques of WHHL rabbits contained clearly detectable SR-AIII expression in addition to the abundant SR-AI expression. In addition, SR-AIII mRNA was detected in NZW and WHHL rabbit livers. The results suggest that in advanced atherosclerotic lesions, cells may protect themselves from the excessive uptake of oxidized lipoproteins by generating SR-A molecules which cannot bind modified LDL.

Atherosclerosis is characterized by the presence of lipid-loaded cells which are derived from macrophages and smooth muscle cells. Several lipoprotein receptors may be involved in cellular lipid uptake. These receptors include: scavenger receptor(s); LDL receptor-related protein/alpha2-macroglobulin receptor (LRP); LDL receptor; and VLDL receptor. With the exception of the LDL receptor, all of these receptors are expressed in atherosclerotic lesions. While scavenger receptors are mostly expressed in macrophages, the LRP and VLDL receptor may play an important role in mediating lipid uptake in smooth muscle cells. It is evident that no single receptor pathway is solely responsible for the increased lipid uptake in lesion cells but several redundant mechanisms may contribute to the uptake and degradation of lipoproteins in atherosclerotic lesions.

We describe a method developed for the quantitative analysis of hydroxy fatty acids derived from fatty acid monohydroperoxides formed during lipoprotein oxidation. The procedure starts with catalytic hydrogenation of the lipid extract, whereby hydroperoxyl groups are converted to hydroxyl groups and double bonds are eliminated, and the risk for lipid oxidation during the rest of the procedure is eliminated. The fatty acids are converted to methyl esters, which are fractionated by gas chromatography on a nonpolar column. The major differences to existing methods are that a mass spectrometer is not required and that the specificity thus lost is replaced by gas chromatography before and after acetylation of the hydroxyl groups. This changes the retention times of the hydroxyacids with respect to the unsubstituted fatty acids moving them to positions usually occupied by trace components only. The method allows quantification of monohydroxy fatty acids derived from 18-, 20- and 22-carbon polyunsaturated fatty acids. Positional isomers are separated from each other to some extent. The method has been mainly used for analysis of hydroperoxides in human low density lipoprotein preparations and for following lipoprotein oxidation in vitro.