Hypermethylation of the non-imprinted maternal MEG3 and paternal MEST alleles is highly variable among normal individuals.

Imprinted genes show parent-specific activity (functional haploidy), which makes them particularly vulnerable to epigenetic dysregulation. Here we studied the methylation profiles of oppositely imprinted genes at single DNA molecule resolution by two independent parental allele-specific deep bisulfite sequencing (DBS) techniques. Using Roche (GSJunior) next generation sequencing technology, we analyzed the maternally imprinted MEST promoter and the paternally imprinted MEG3 intergenic (IG) differentially methylated region (DMR) in fetal cord blood, adult blood, and visceral adipose tissue.

DNA methylation signatures in cord blood of ICSI children.

Study Question: Does ICSI induce specific DNA methylation changes in the resulting offspring?

Summary Answer: Although several thousand analyzed CpG sites (throughout the genome) displayed significant between-group methylation differences, both ICSI and spontaneously conceived children varied within the normal range of methylation variation.

What Is Known Already: Children conceived by ART have increased risks for medical problems at birth and to the extent of present knowledge also in later life (i.e.

Epigenetic signatures of gestational diabetes mellitus on cord blood methylation.

Background: Intrauterine exposure to gestational diabetes mellitus (GDM) confers a lifelong increased risk for metabolic and other complex disorders to the offspring. GDM-induced epigenetic modifications modulating gene regulation and persisting into later life are generally assumed to mediate these elevated disease susceptibilities. To identify candidate genes for fetal programming, we compared genome-wide methylation patterns of fetal cord bloods (FCBs) from GDM and control pregnancies.

Subjective expansion of extended time-spans in experienced meditators.

Experienced meditators typically report that they experience time slowing down in meditation practice as well as in everyday life. Conceptually this phenomenon may be understood through functional states of mindfulness, i.e.

The impact of insulin treatment on the expression of vascular endothelial cadherin and Beta-catenin in human fetoplacental vessels.

Vascular endothelial cadherin and β-catenin play a key role in establishment and maintenance of the endothelial monolayer integrity, regulation of vascular barrier function, and initiation of angiogenesis. The cadherin-catenin complex has been shown to be reduced in type 1 diabetic placenta, but the exact relationship between histopathologic findings and clinical data is not known. Immunohistochemistry of placental tissue from type 1, type 2, and gestational diabetes showed that diabetes per se might be compatible with normal levels of vascular endothelial (VE)-cadherin and β-catenin in fetoplacental vessels as long as the patient has not been treated with insulin.