Exercise prescription improves exercise tolerance in young children with CHD:a randomised clinical trial

Objective The main objective of this study was to ascertain if a structured intervention programme can improve the biophysical health of young children with congenital heart disease (CHD). The primary end point was an increase in measureable physical activity levels following the intervention.Methods Patients aged 5–10 years with CHD were identified and invited to participate. Participants completed a baseline biophysical assessment, including a formal exercise stress test and daily activity monitoring using an accelerometer. Following randomisation, the intervention group attended a 1 day education session and received an individual written exercise plan to be continued over the 4-month intervention period. The control group continued with their usual level of care. After 4 months, all participants were reassessed in the same manner as at baseline.Results One hundred and sixty-three participants (mean age 8.4 years) were recruited, 100 of whom were male (61.3%). At baseline, the majority of the children were active with good exercise tolerance. The cyanotic palliated subgroup participants, however, were found to have lower levels of daily activity and significantly limited peak exercise performance compared with the other subgroups. One hundred and fifty-two participants (93.2%) attended for reassessment. Following the intervention, there was a significant improvement in peak exercise capacity in the intervention group. There was also a trend towards increased daily activity levels.Conclusion Overall physical activity levels are well preserved in the majority of young children with CHD. A structured intervention programme significantly increased peak exercise capacity and improved attitudes towards positive lifestyle changes

Energy compensation in the real world. Good compensation for small portions of chocolate and biscuits over short time periods in complicit consumers using commercially available foods.

While investigations using covert food manipulations tend to suggest that individuals are poor at adjusting for previous energy intake, in the real world adults rarely consume foods with which they are ill-informed. This study investigated the impact in fully complicit consumers of consuming commercially available dark chocolate, milk chocolate, sweet biscuits and fruit bars on subsequent appetite. Using a repeated measures design, participants received four small portions (4 × 10-11 g) of either dark chocolate, milk chocolate, sweet biscuits, fruit bars or no food throughout five separate study days (counterbalanced in order), and test meal intake, hunger, liking and acceptability were measured. Participants consumed significantly less at lunch following dark chocolate, milk chocolate and sweet biscuits compared to no food (smallest t(19) = 2.47, p = 0.02), demonstrating very good energy compensation (269-334%). No effects were found for fruit bars (t(19) = 1.76, p = 0.09), in evening meal intakes (F(4,72) = 0.62, p = 0.65) or in total intake (lunch + evening meal + food portions) (F(4,72) = 0.40, p = 0.69). No differences between conditions were found in measures of hunger (largest F(4,76) = 1.26, p = 0.29), but fruit bars were significantly less familiar than all other foods (smallest t(19) = 3.14, p = 0.01). These findings demonstrate good compensation over the short term for small portions of familiar foods in complicit consumers. Findings are most plausibly explained as a result of participant awareness and cognitions, although the nature of these cognitions cannot be discerned from this study. These findings however, also suggest that covert manipulations may have limited transfer to real world scenarios

Lack of MEF2A Δ7aa mutation in Irish families with early onset ischaemic heart disease, a family based study

BACKGROUND: Ischaemic heart disease (IHD) is a complex disease due to the combination of environmental and genetic factors. Mutations in the MEF2A gene have recently been reported in patients with IHD. In particular, a 21 base pair deletion (Δ7aa) in the MEF2A gene was identified in a family with an autosomal dominant pattern of inheritance of IHD. We investigated this region of the MEF2A gene using an Irish family-based study, where affected individuals had early-onset IHD. METHODS: A total of 1494 individuals from 580 families were included (800 discordant sib-pairs and 64 parent-child trios). The Δ7aa region of the MEF2A gene was investigated based on amplicon size. RESULTS: The Δ7aa mutation was not detected in any individual. Variation in the number of CAG (glutamate) and CCG (proline) residues was detected in a nearby region. However, this was not found to be associated with IHD. CONCLUSION: The Δ7aa mutation was not detected in any individual within the study population and is unlikely to play a significant role in the development of IHD in Ireland. Using family-based tests of association the number of tri-nucleotide repeats in a nearby region of the MEF2A gene was not associated with IHD in our study group

Zirconium complexes of bipyrrolidine derived salan ligands for the isoselective polymerisation of rac-lactide

We report a series of Zr(iv) 2,2′-bipyrrolidine–salan derived complexes and their exploitation for the ROP of rac-lactide to afford highly isotactically enriched PLA.</p

Abdominal aortic aneurysm is associated with a variant in low-density lipoprotein receptor-related protein 1

Abdominal aortic aneurysm (AAA) is a common cause of morbidity and mortality and has a significant heritability. We carried out a genome-wide association discovery study of 1866 patients with AAA and 5435 controls and replication of promising signals (lead SNP with a p value &lt; 1 × 10-5) in 2871 additional cases and 32,687 controls and performed further follow-up in 1491 AAA and 11,060 controls. In the discovery study, nine loci demonstrated association with AAA (p &lt; 1 × 10-5). In the replication sample, the lead SNP at one of these loci, rs1466535, located within intron 1 of low-density-lipoprotein receptor-related protein 1 (LRP1) demonstrated significant association (p = 0.0042). We confirmed the association of rs1466535 and AAA in our follow-up study (p = 0.035). In a combined analysis (6228 AAA and 49182 controls), rs1466535 had a consistent effect size and direction in all sample sets (combined p = 4.52 × 10-10, odds ratio 1.15 [1.10-1.21]). No associations were seen for either rs1466535 or the 12q13.3 locus in independent association studies of coronary artery disease, blood pressure, diabetes, or hyperlipidaemia, suggesting that this locus is specific to AAA. Gene-expression studies demonstrated a trend toward increased LRP1 expression for the rs1466535 CC genotype in arterial tissues; there was a significant (p = 0.029) 1.19-fold (1.04-1.36) increase in LRP1 expression in CC homozygotes compared to TT homozygotes in aortic adventitia. Functional studies demonstrated that rs1466535 might alter a SREBP-1 binding site and influence enhancer activity at the locus. In conclusion, this study has identified a biologically plausible genetic variant associated specifically with AAA, and we suggest that this variant has a possible functional role in LRP1 expression