Comparison of the volatile components of two cultivars of potato cooked by boiling, conventional baking and microwave baking

Tubers of two cultivars (Estima and Maris Piper) of potato were cooked by three different procedures, ie boiling, conventional baking and microwave baking. Peeled and sliced tubers were boiled, while intact potatoes were baked in their skins. Flavour components from the boiled slices and the flesh of the baked tubers were isolated by headspace adsorption onto Tenax and analysed by gas chromatography-mass spectrometry (GC-MS). For all cooking procedures, Estima gave stronger isolates than Maris Piper. The two main sources of flavour compounds (regardless of cooking procedure) were lipid degradation and the Maillard reaction and/or sugar degradation. The ratio (yield derived from lipid)/(yield derived from Maillard reaction and/or sugar) decreased from 8.5-9.1 (boiling) to 2.7-3.4 (microwave baking) and to 0.4-1.1 (conventional baking). Quantitative and qualitative differences among the cooking procedures are explained in terms of the variations in heat and mass transfer processes that occurred. Each cooking procedure resulted in a unique profile of flavour compounds. (C) 2002 Society of Chemical Industry.

Genome-wide association meta-analysis of human longevity identifies a novel locus conferring survival beyond 90 years of age

The genetic contribution to the variation in human lifespan is approximately 25%.  Despite the large number of identified disease-susceptibility loci, it is not known which loci influence population mortality.  We performed a genome-wide association meta-analysis of 7729 long-lived individuals of European descent (≥ 85 years) and 16121 younger controls (< 65 years) followed by replication in an additional set of 13060 long-lived individuals and 61156 controls. In addition, we performed a subset analysis in cases ≥ 90 years. We observed genome-wide significant association with longevity, as reflected by survival to ages beyond 90 years, at a novel locus, rs2149954, on chromosome 5q33.3 (OR = 1.10, P =1.74 x 10-8). We also confirmed association of rs4420638 on chromosome 19q13.32 (OR = 0.72, P = 3.40 x 10-36), representing the TOMM40/APOE/APOC1 locus. In a prospective meta-analysis (n = 34103) the minor allele of rs2149954 (T) on chromosome 5q33.3 associates with increased survival (HR = 0.95, P = 0.003). This allele has previously been reported to associate with low blood pressure in middle age. Interestingly, the minor allele (T) associates with decreased cardiovascular mortality risk, independent of blood pressure. We report on the first GWAS-identified longevity locus on chromosome 5q33.3 influencing survival in the general European population. The minor allele of this locus associates with low blood pressure in middle age, although the contribution of this allele to survival may be less dependent on blood pressure. Hence, the pleiotropic mechanisms by which this intragenic variation contributes to lifespan regulation have to be elucidated.

The role of adiposity in cardiometabolic traits:a Mendelian randomization analysis

The association between adiposity and cardiometabolic traits is well known from epidemiological studies. Whilst the causal relationship is clear for some of these traits, for others it is not. We aimed to determine whether adiposity is causally related to various cardiometabolic traits using the Mendelian randomization approach.

Electrical conduction and rheological behaviour of composites of poly(epsilon-caprolactone) and MWCNTs

Two mechanisms of conduction were identified from temperature dependent (120 K-340 K) DC electrical resistivity measurements of composites of poly(c-caprolactone) (PCL) and multi-walled carbon nanotubes (MWCNTs). Activation of variable range hopping (VRH) occurred at lower temperatures than that for temperature fluctuation induced tunneling (TFIT). Experimental data was in good agreement with the VRH model in contrast to the TFIT model, where broadening of tunnel junctions and increasing electrical resistivity at T > T-g is a consequence of a large difference in the coefficients of thermal expansion of PCL and MWCNTs. A numerical model was developed to explain this behavior accounting for a thermal expansion effect by supposing the large increase in electrical resistivity corresponds to the larger relative deformation due to thermal expansion associated with disintegration of the conductive MWCNT network. MWCNTs had a significant nucleating effect on PCL resulting in increased PCL crystallinity and an electrically insulating layer between MWCNTs. The onset of rheological percolation at similar to 0.18 vol% MWCNTs was clearly evident as storage modulus, G' and complex viscosity, vertical bar eta*vertical bar increased by several orders of magnitude. From Cole-Cole and Van Gurp-Palmen plots, and extraction of crossover points (G(c)) from overlaying plots of G' and G '' as a function of frequency, the onset of rheological percolation at 0.18 vol% MWCNTs was confirmed, a similar MWCNT loading to that determined for electrical percolation. 

Age- and Sex-Specific Causal Effects of Adiposity on Cardiovascular Risk Factors

Observational studies have reported different effects of adiposity on cardiovascular risk factors across age and sex. Since cardiovascular risk factors are enriched in obese individuals, it has not been easy to dissect the effects of adiposity from those of other risk factors. We used a Mendelian randomization approach, applying a set of 32 genetic markers to estimate the causal effect of adiposity on blood pressure, glycemic indices, circulating lipid levels, and markers of inflammation and liver disease in up to 67,553 individuals. All analyses were stratified by age (cutoff 55 years of age) and sex. The genetic score was associated with BMI in both nonstratified analysis (P = 2.8 × 10(-107)) and stratified analyses (all P < 3.3 × 10(-30)). We found evidence of a causal effect of adiposity on blood pressure, fasting levels of insulin, C-reactive protein, interleukin-6, HDL cholesterol, and triglycerides in a nonstratified analysis and in the <55-year stratum. Further, we found evidence of a smaller causal effect on total cholesterol (P for difference = 0.015) in the ≥55-year stratum than in the <55-year stratum, a finding that could be explained by biology, survival bias, or differential medication. In conclusion, this study extends previous knowledge of the effects of adiposity by providing sex- and age-specific causal estimates on cardiovascular risk factors.

Adiposity as a cause of cardiovascular disease: a Mendelian randomization study

Background: Adiposity, as indicated by body mass index (BMI), has been associated with risk of cardiovascular diseases in epidemiological studies. We aimed to investigate if these associations are causal, using Mendelian randomization (MR) methods.

Methods: The associations of BMI with cardiovascular outcomes [coronary heart disease (CHD), heart failure and ischaemic stroke], and associations of a genetic score (32 BMI single nucleotide polymorphisms) with BMI and cardiovascular outcomes were examined in up to 22 193 individuals with 3062 incident cardiovascular events from nine prospective follow-up studies within the ENGAGE consortium. We used random-effects meta-analysis in an MR framework to provide causal estimates of the effect of adiposity on cardiovascular outcomes.

Results: There was a strong association between BMI and incident CHD (HR = 1.20 per SD-increase of BMI, 95% CI, 1.12–1.28, P = 1.9·10−7), heart failure (HR = 1.47, 95% CI, 1.35–1.60, P = 9·10−19) and ischaemic stroke (HR = 1.15, 95% CI, 1.06–1.24, P = 0.0008) in observational analyses. The genetic score was robustly associated with BMI (β = 0.030 SD-increase of BMI per additional allele, 95% CI, 0.028–0.033, P = 3·10−107). Analyses indicated a causal effect of adiposity on development of heart failure (HR = 1.93 per SD-increase of BMI, 95% CI, 1.12–3.30, P = 0.017) and ischaemic stroke (HR = 1.83, 95% CI, 1.05–3.20, P = 0.034). Additional cross-sectional analyses using both ENGAGE and CARDIoGRAMplusC4D data showed a causal effect of adiposity on CHD.

Conclusions: Using MR methods, we provide support for the hypothesis that adiposity causes CHD, heart failure and, previously not demonstrated, ischaemic stroke.