) that is subject to high gene flow from a lake and is thus maladapted to stream conditions. In this system, maladaptation increases with distance along the stream, and this increase is associated with decreasing population densities until stickleback are no longer present (2.5 km from the lake). We conducted field experiments to inform whether this association might reflect a negative role for gene flow in constraining population size and therefore causing a local range limit. We specifically tested predictions deriving from theory: peripheral populations should show partial local selleck adaptation, be under strong selection and not simply be maintained by dispersal. First,
a transplant experiment suggested a weak home-site advantage in the peripheral 3-Methyladenine clinical trial population. Second, a mark-recapture study showed directional selection for a stream-adapted phenotype in 1 of 2 years. Third, another mark-recapture experiment showed that dispersal is limited to the point that positive demographic effects of dispersal are probably minimal. We conclude that, although gene flow does constrain
morphological maladaptation in the outlet stream population, the evidence for its contribution to population size and range limits is mixed. We discuss the implications of our work for the study of factors influencing the evolution of species’ ranges.”
“BACKGROUND: Coronary allograft vasculopathy (CAV) is the major limiting factor for long term survival after heart transplantation. The aim of this study was to identify gene candidates implicated in human CAV using a rat aortic allograft model in tandem with microarrays and quantitative real time PCR (Q-PCR).
METHODS: Rat abdominal aortas were isografted (5) or allografted (5) from Brown-Norway to Lewis rats
and grafts were harvested after day 8, 25 and 60. Agilent microarrays were then used to highlight differentially expressed genes between Defactinib isografted and allografted rat aortas. Further investigation of a selected candidate gene was performed on human coronary arteries.
RESULTS: 1829, 2582 and 1925 genes (fold changes >2 or <2 and p values <0.05) were differentially expressed at day 8, 25 and 60 respectively between isografs and allografts. Seventeen candidate genes were selected according to significant differential expression at day 60. These rat candidate genes were then validated by quantitative real time polymerase chain reaction (Q-PCR). One of these candidate genes, T-Cadherin (T-Cad) was further investigated, using immunohistochemistry (IHC), in human coronary arteries showing CAV compared to classical atherosclerosis present in ischemic cardiomyopathy (ICM) and normal coronary arteries present in dilated cardiomyopathy (DCM). Results showed an over expression of T-Cad in CAV and classical atherosclerosis compared to normal coronary arteries.
CONCLUSIONS: T-Cad was found to be over expressed in CAV.