Tongan adolescents' eating patterns : opportunities for intervention

The purpose of this mixed methods study was to examine the sources of food and dietary patterns of Tongan adolescents (n = 2084) and their perceptions of sociocultural influences. The study incorporated anthropometric measurements, a behavioral survey, and qualitative interviews. More adolescent Tongan females (82.5%) than males (74.3%) reported sourcing morning tea and/or lunch (females 81.9%, males 72.6%) from school canteens or nearby food outlets. More females than males reported consuming obesity-promoting foods such as packaged snack foods (females 38.2%, males 21.3%), chocolates (females 24.7%, males 15.0%), and soft drinks (females 55.3%, males 50.4%). Food purchased for consumption at schools was predominantly energy dense and nutrient poor. Ensuring that students have access to foods of high nutritional quality sourced from school or home, and restricting access to local food outlets that supply unhealthy products would improve the nutrition status of adolescents in Tonga. Furthermore, it is important that obesity prevention interventions are informed by culture-specific influences to optimize uptake of healthy diets.

A gene expression signature for insulin resistance

Insulin resistance is a heterogeneous disorder caused by a range of genetic and environmental factors, and we hypothesize that its aetiology varies considerably between individuals. This heterogeneity provides significant challenges to the development of effective therapeutic regimes for long-term management of type 2 diabetes. We describe a novel strategy, using large-scale gene expression profiling, to develop a Gene Expression Signature (GES) that reflects the overall state of insulin resistance in cells and patients. The GES was developed from 3T3-L1 adipocytes that were made ‘insulin resistant’ by treatment with tumour necrosis factor-alpha (TNFα) and then reversed with aspirin and troglitazone (‘re-sensitized’). The GES consisted of five genes whose expression levels best discriminated between the insulin resistant and insulin re-sensitized states. We then used this GES to screen a compound library for agents that affected the GES genes in 3T3- L1 adipocytes in a way that most closely resembled the changes seen when insulin resistance was successfully reversed using aspirin and troglitazone. This screen identified both known and new insulin sensitizing compounds including non-steroidal anti inflammatory agents, β-adrenergic antagonists, beta-lactams and sodium channel blockers. We tested the biological relevance of this GES in participants in the San Antonio Family Heart Study (n = 1,240) and showed that patients with the lowest GES scores were more insulin resistant (according to HOMA_IR and fasting plasma insulin levels, P < 0.001). These findings show that GES technology can be used for both the discovery of insulin sensitizing compounds and the characterization of patients into subtypes of insulin resistance according to GES scores, opening the possibility of developing a personalized medicine approach to type 2 diabetes.

Does migration of hybrids contribute to post-zygotic isolation in flycatchers?

In the face of hybridization, species integrity can only be maintained through post-zygotic isolating barriers (PIBs). PIBs need not only be intrinsic (i.e. hybrid inviability and sterility caused by developmental incompatibilities), but also can be extrinsic due to the hybrid's intermediate phenotype falling between the parental niches. For example, in migratory species, hybrid fitness might be reduced as a result of intermediate migration pathways and reaching suboptimal wintering grounds. Here, we test this idea by comparing the juvenile to adult survival probabilities as well as the wintering grounds of pied flycatchers (Ficedula hypoleuca), collared flycatchers (Ficedula albicollis) and their hybrids using stable isotope ratios of carbon (δ13C) and nitrogen (δ15N) in feathers developed at the wintering site. Our result supports earlier observations of largely segregated wintering grounds of the two parental species. The isotope signature of hybrids clustered with that of pied flycatchers. We argue that this pattern can explain the high annual survival of hybrid flycatchers. Hence, dominant expression of the traits of one of the parental species in hybrids may substantially reduce the ecological costs of hybridization.

Questioning the construct of 'susceptibility' in the causal link between tobacco industry promotion and adolescent smoking

The first article to report on a causal connection between tobacco industry promotion and adolescent smoking (Pierce et al. 1998) had, and continues to have, a significant influence on the marketing of cigarettes in many parts of the world. A key construct in determining causality was the ability to identify the respondents’ “susceptibility to smoke”. Through an analysis of the questions, and reanalysis of the original data used by Pierce et al. (1998), it is shown that the construct is flawed, and needs revision before a causal link can be claimed with the original data.

The developmental stress hypothesis: A special case of the evolution of condition-dependent sexual traits

The idea that sexually selected traits might be condition dependent is far from novel (Zahavi 1975); however, the developmental stress hypothesis was proposed as a special case because of a highly plausible mechanism: the development of the neural circuits controlling song output coincides with a period of time during which developing birds are likely to be susceptible to stress. The elegant aspect of the hypothesis is that the mechanism is defined and effects can be readily tested (Nowicki et al. 1998; Buchanan et al. 2003). Compared with more general hypotheses about the evolution of condition-dependent sexual traits (Buchanan 2000), the second particularly interesting aspect of the developmental stress hypothesis is that, in some species, individuals may suffer historical markers of stress. This is because in species with a fixed period for neural growth and song learning, there is no possibility for compensation in later life for stress experienced during early development. Females using such a marker of stress may benefit by obtaining a partner whose other cognitive functions have not been impaired by stress.

RAP1 controls rhoptry targeting of RAP2 in the malaria parasite Plasmodium falciparum

Rhoptry associated protein 1 (RAP1) and 2 (RAP2), together with a poorly described third protein RAP3, form the low molecular weight complex within the rhoptries of Plasmodium falciparum. These proteins are thought to play a role in erythrocyte invasion by the extracellular merozoite and are important vaccine candidates. We used gene-targeting technology in P.falciparum blood-stage parasites to disrupt the RAP1 gene, producing parasites that express severely truncated forms of RAP1. Immunoprecipitation experiments suggest that truncated RAP1 species did not complex with RAP2 and RAP3. Consistent with this were the distinct subcellular localizations of RAP1 and 2 in disrupted RAP1 parasites, where RAP2 does not traffic to the rhoptries but is instead located in a compartment that appears related to the lumen of the endoplasmic reticulum. These results suggest that RAP1 is required to localize RAP2 to the rhoptries, supporting the hypothesis that rhoptry biogenesis is dependent in part on the secretory pathway in the parasite. The observation that apparently host-protective merozoite antigens are not essential for efficient erythrocyte invasion has important implications for vaccine design.

Prospects for epigenetic epidemiology

Epigenetic modification can mediate environmental influences on gene expression and can modulate the disease risk associated with genetic variation. Epigenetic analysis therefore holds substantial promise for identifying mechanisms through which genetic and environmental factors jointly contribute to disease risk. The spatial and temporal variance in epigenetic profile is of particular relevance for developmental epidemiology and the study of aging, including the variable age at onset for many common diseases. This review serves as a general introduction to the topic by describing epigenetic mechanisms, with a focus on DNA methylation; genetic and environmental factors that influence DNA methylation; epigenetic influences on development, aging, and disease; and current methodology for measuring epigenetic profile. Methodological considerations for epidemiologic studies that seek to include epigenetic analysis are also discussed.