The emerging prevalence of obesity within families in europe and its associations with family socio-demographic characteristics and lifestyle factors; a cross-sectional analysis of baseline data from the feel4diabetes study

The Feel4Diabetes study is a type 2 diabetes prevention program that recruited 12,193 children [age: 8.20 (±1.01) years] and their parents from six European countries. The current work used pre-intervention data collected from 9576 children–parents pairs, to develop a novel family obesity variable and to examine its associations with family sociodemographic and lifestyle characteristics. Family obesity, defined as the presence of obesity in at least two family members, had a prevalence of 6.6%. Countries under austerity measures (Greece and Spain) displayed higher prevalence (7.6%), compared to low-income (Bulgaria and Hungary: 7%) and high-income countries (Belgium and Finland: 4.5%). Family obesity odds were significantly lower when mothers (OR: 0.42 [95% CI: 0.32, 0.55]) or fathers (0.72 [95% CI: 0.57, 0.92]) had higher education, mothers were fully (0.67 [95% CI: 0.56, 0.81]) or partially employed (0.60 [95% CI: 0.45, 0.81]), families consumed breakfast more often (0.94 [95% CI: 0.91 0.96]), more portions of vegetables (0.90 [95% CI: 0.86, 0.95]), fruits (0.96 [95% CI: 0.92, 0.99]) and wholegrain cereals (0.72 [95% CI: 0.62, 0.83]), and for more physically active families (0.96 [95% CI: 0.93, 0.98]). Family obesity odds increased when mothers were older (1.50 [95% CI: 1.18, 1.91]), with the consumption of savoury snacks (1.11 [95% CI: 1.05, 1.17]), and increased screen time (1.05 [95% CI: 1.01, 1.09]). Clinicians should familiarise themselves with the risk factors for family obesity and choose interventions that target the whole family. Future research should explore the causal basis of the reported associations to facilitate devising tailored family-based interventions for obesity prevention

Cortical Contributions to Saccadic Suppression

The stability of visual perception is partly maintained by saccadic suppression: the selective reduction of visual sensitivity that accompanies rapid eye movements. The neural mechanisms responsible for this reduced perisaccadic visibility remain unknown, but the Lateral Geniculate Nucleus (LGN) has been proposed as a likely site. Our data show, however, that the saccadic suppression of a target flashed in the right visual hemifield increased with an increase in background luminance in the left visual hemifield. Because each LGN only receives retinal input from a single hemifield, this hemifield interaction cannot be explained solely on the basis of neural mechanisms operating in the LGN. Instead, this suggests that saccadic suppression must involve processing in higher level cortical areas that have access to a considerable part of the ipsilateral hemifield

Genomic analysis of LexA binding reveals the permissive nature of the Escherichia coli genome and identifies unconventional target sites

Genomes of eukaryotic organisms are packaged into nucleosomes that restrict the binding of transcription factors to accessible regions. Bacteria do not contain histones, but they have nucleoid-associated proteins that have been proposed to function analogously. Here, we combine chromatin immunoprecipitation and high-density oligonucleotide microarrays to define the in vivo DNA targets of the LexA transcriptional repressor in Escherichia coli. We demonstrate a near-universal relationship between the presence of a LexA sequence motif, LexA binding in vitro, and LexA binding in vivo, suggesting that a suitable recognition site for LexA is sufficient for binding in vivo. Consistent with this observation, LexA binds comparably to ectopic target sites introduced at various positions in the genome. We also identify ∼20 novel LexA targets that lack a canonical LexA sequence motif, are not bound by LexA in vitro, and presumably require an additional factor for binding in vivo. Our results indicate that, unlike eukaryotic genomes, the E. coli genome is permissive to transcription factor binding. The permissive nature of the E. coli genome has important consequences for the nature of transcriptional regulatory proteins, biological specificity, and evolution

Canine Disorder Mirrors Human Disease: Exonic Deletion in <i>HES7</i> Causes Autosomal Recessive Spondylocostal Dysostosis in Miniature Schnauzer Dogs

<div><p>Spondylocostal dysostosis is a congenital disorder of the axial skeleton documented in human families from diverse racial backgrounds. The condition is characterised by truncal shortening, extensive hemivertebrae and rib anomalies including malalignment, fusion and reduction in number. Mutations in the Notch signalling pathway genes <i>DLL3</i>, <i>MESP2</i>, <i>LFNG</i>, <i>HES7</i> and <i>TBX6</i> have been associated with this defect. In this study, spondylocostal dysostosis in an outbred family of miniature schnauzer dogs is described. Computed tomography demonstrated that the condition mirrors the skeletal defects observed in human cases, but unlike most human cases, the affected dogs were stillborn or died shortly after birth. Through gene mapping and whole genome sequencing, we identified a single-base deletion in the coding region of <i>HES7</i>. The frameshift mutation causes loss of functional domains essential for the oscillatory transcriptional autorepression of HES7 during somitogenesis. A restriction fragment length polymorphism test was applied within the immediate family and supported a highly penetrant autosomal recessive mode of inheritance. The mutation was not observed in wider testing of 117 randomly sampled adult miniature schnauzer and six adult standard schnauzer dogs; providing a significance of association of <i>P</i>_raw = 4.759e^-36 (genome-wide significant). Despite this apparently low frequency in the Australian population, the allele may be globally distributed based on its presence in two unrelated sires from geographically distant locations. While isolated hemivertebrae have been observed in a small number of other dog breeds, this is the first clinical and genetic diagnosis of spontaneously occurring spondylocostal dysostosis in a non-human mammal and offers an excellent model in which to study this devastating human disorder. The genetic test can be utilized by dog breeders to select away from the disease and avoid unnecessary neonatal losses.</p></div

Comma defect PCR-RFLP test results for 11 miniature schnauzers.

<p>Samples in lanes 1–9 are homozygous for the wild-type genotype; lane 10 shows a carrier for the deletion; lane 11 is homozygous for the mutant allele. L = ladder (100 bp).</p

List of candidate functional mutations observed in genome sequence of pups affected with Comma defect.

<p>JBrowse references are provided for each mutant mouse skeletal phenotype. The number of quality sequence reads supporting the reference and alternate allele respectively are shown in brackets for each genotype.</p><p>List of candidate functional mutations observed in genome sequence of pups affected with Comma defect.</p

Three-generation pedigree for the miniature schnauzer family producing litters affected with Comma defect.

<p>Individuals with USCF identifiers (<i>n</i> = 10) are those that have been phenotyped and for which DNA samples are available. Genotypes as determined by PCR-RFLP are indicated (Wt = wild type; Mu = mutant). Unsampled animals are depicted by grey outlines.</p

Photograph of miniature schnauzer pup USCF137 affected with Comma defect.

<p>Photograph of miniature schnauzer pup USCF137 affected with Comma defect.</p

CT scans of miniature schnauzer pups affected with Comma defect and an age-matched unrelated control.

<p>(a) Unaffected Nova Scotia duck tolling retriever pup sampled for unrelated reasons. (b) Affected miniature schnauzer pup USCF134. (c) Affected miniature schnauzer pup USCF136. (d) Affected miniature schnauzer pup USCF137.</p

Genome-wide association analysis for Comma defect.

<p>The analysis included three cases and seven controls genotyped on the Canine HD BeadChip. Coordinates shown are from the canFam2 assembly. (a) Haploview plot of -log₁₀ transformed <i>P</i> values for 73,921 SNPs tested for association using PLINK. (b) Haploview plot of -log₁₀ transformed <i>P</i> values for SNPs on CFA5.</p