Here we review the progress made in addressing the influence of a compromised in utero environment on the behavior of imprinted genes. We also examine whether these

environmental influences may have an impact on the later development of human disease. (C) 2009 Elsevier Ltd. All rights reserved.”
“Background: The methylation status of the human glucocorticoid receptor gene NR3C1 in newborns has been reported to be sensitive to prenatal maternal mood. This study investigates both the association between maternal cortisol and emotional state during pregnancy and the methylation state of the promoter region of NR3C1 gene.\n\nMethods: We examined 83 pregnant women. Psychological data and diurnal cortisol check details data were assessed to evaluate maternal stress once each trimester. DNA methylation at different loci of the NR3C1 gene, including exon 1(B), 1(D)

and 1(F). was analyzed in genomic DNA from cord blood mononuclear cells.\n\nResults: Univariable analyses indicated pregnancy related anxiety to be the strongest psychological parameter throughout pregnancy. Most significant findings concerned 1(F). Particularly the methylation state of CpG9 was significantly associated with maternal emotional wellbeing. In a multivariable model the proportion of variance in methylation state of F9 explained (PVE) by pregnancy related anxiety was 7.8% (p = 0.023) during T1.\n\nFurthermore different CpG-units located at the nerve growth factor CHIR-99021 in vivo inducible protein A (NGFI-A) binding sites of 1(F) were associated with maternal anxiety [(F20.21: PC PRAQ and fear of integrity in T1: respectively PVE:8.9% and PVE:9.0%; Fear of delivery T2: PVE:8.0%, Fear of integrity T2: PVE:6.0% and STAI T2: PVE:5.9%) - (F12.13: PC PRAQ T1: PVE:6.9%, fear of integrity T2: JQ-EZ-05 order PVE:6.0%

and fear of delivery T2: PVE:8.0%)] and cortisol (F38.39: PVE:8.9%) in T2.\n\nConclusion: These data indicate that prenatal maternal emotional state, particularly pregnancy related anxiety, are associated with the methylation state of the NR3C1 gene in the child. (C) 2013 Elsevier Ltd. All rights reserved.”
“The evolution of host resistance to parasites, shaped by associated fitness costs, is crucial for epidemiology and maintenance of genetic diversity. Selection imposed by multiple parasites could be a particularly strong constraint, as hosts either accumulate costs of multiple specific resistances or evolve a more costly general resistance mechanism. We used experimental evolution to test how parasite heterogeneity influences the evolution of host resistance. We show that bacterial host populations evolved specific resistance to local bacteriophage parasites, regardless of whether they were in single or multiple-phage environments, and that hosts evolving with multiple phages were no more resistant to novel phages than those evolving with single phages.