Invasive rodents detrimentally affect native bird species on many islands worldwide, and rodent eradication is a useful tool to safeguard endemic and threatened species. However, especially on tropical islands, rodent eradications can fail for various reasons, and it is unclear whether the temporary reduction of a rodent population during an unsuccessful eradication operation has beneficial effects on native birds. Here we examine the response of four endemic land bird species on subtropical Henderson Island in the Pitcairn Island Group, South Pacific Ocean, following an unsuccessful rodent eradication in 2011. We conducted point counts at 25 sampling locations in 14 survey periods between 2011 and 2015, and modelled the abundance trends of all species using binomial mixture models accounting for observer and environmental variation in detection probability. Henderson Reed Warbler Acrocephalus taiti more than doubled in abundance (2015 population estimate: 7,194-28,776), and Henderson Fruit Dove Ptilinopus insularis increased slightly between 2011 and 2015 (2015 population estimate: 4,476–10,072), while we detected no change in abundance of the Henderson Lorikeet Vini stepheni (2015 population estimate: 554–3014). Henderson Crake Zapornia atra increased to pre-eradication levels following anticipated mortality during the operation (2015 population estimate: 4,960–20,783). A temporary reduction of rat predation pressure and rat competition for fruit may have benefitted the reed warbler and the fruit dove, respectively. However, a long drought may have naturally suppressed bird populations prior to the rat eradication operation in 2011, potentially confounding the effects of temporary rat reduction and natural recovery. We therefore cannot unequivocally ascribe the population recovery to the temporary reduction of the rat population. We encourage robust monitoring of island biodiversity both before and after any management operation to better understand responses of endemic species to failed or successful operations.

Diurnal preference is an individual's preference for daily activities and sleep timing and is strongly correlated with the underlying circadian clock and the sleep-wake cycle validating its use as an indirect circadian measure in humans. Recent research has implicated DNA methylation as a mechanism involved in the regulation of the circadian clock system in humans and other mammals. In order to evaluate the extent of epigenetic differences associated with diurnal preference, we examined genome-wide patterns of DNA methylation in DNA from monozygotic (MZ) twin-pairs discordant for diurnal preference. MZ twins were selected from a longitudinal twin study designed to investigate the interplay of genetic and environmental factors in the development of emotional and behavioral difficulties. Fifteen pairs of MZ twins were identified in which one member scored considerably higher on the Horne–Ostberg Morningness–Eveningness Questionnaire (MEQ) than the other. Genome-wide DNA methylation patterns were assessed in twins’ buccal cell DNA using the Illumina Infinium HumanMethylation450 BeadChips. Quality control and data pre-processing was undertaken using the wateRmelon package. Differentially methylated probes (DMPs) were identified using an analysis strategy taking into account both the significance and the magnitude of DNA methylation differences. Our data indicate that DNA methylation differences are detectable in MZ twins discordant for diurnal preference. Moreover, downstream gene ontology (GO) enrichment analysis on the top-ranked diurnal preference associated DMPs revealed significant enrichment of pathways that have been previously associated with circadian rhythm regulation, including cell adhesion processes and calcium ion binding.

A trend toward greater body size in dizygotic (DZ) than in monozygotic (MZ) twins has been suggested by some but not all studies, and this difference may also vary by age. We analyzed zygosity differences in mean values and variances of height and body mass index (BMI) among male and female twins from infancy to old age. Data were derived from an international database of 54 twin cohorts participating in the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins), and included 842,951 height and BMI measurements from twins aged 1 to 102 years. The results showed that DZ twins were consistently taller than MZ twins, with differences of up to 2.0 cm in childhood and adolescence and up to 0.9 cm in adulthood. Similarly, a greater mean BMI of up to 0.3 kg/m2 in childhood and adolescence and up to 0.2 kg/m2 in adulthood was observed in DZ twins, although the pattern was less consistent. DZ twins presented up to 1.7% greater height and 1.9% greater BMI than MZ twins; these percentage differences were largest in middle and late childhood and decreased with age in both sexes. The variance of height was similar in MZ and DZ twins at most ages. In contrast, the variance of BMI was significantly higher in DZ than in MZ twins, particularly in childhood. In conclusion, DZ twins were generally taller and had greater BMI than MZ twins, but the differences decreased with age in both sexes.

For over 100 years, the genetics of human anthropometric traits has attracted scientific interest. In particular, height and body mass index (BMI, calculated as kg/m2) have been under intensive genetic research. However, it is still largely unknown whether and how heritability estimates vary between human populations. Opportunities to address this question have increased recently because of the establishment of many new twin cohorts and the increasing accumulation of data in established twin cohorts. We started a new research project to analyze systematically (1) the variation of heritability estimates of height, BMI and their trajectories over the life course between birth cohorts, ethnicities and countries, and (2) to study the effects of birth-related factors, education and smoking on these anthropometric traits and whether these effects vary between twin cohorts. We identified 67 twin projects, including both monozygotic (MZ) and dizygotic (DZ) twins, using various sources. We asked for individual level data on height and weight including repeated measurements, birth related traits, background variables, education and smoking. By the end of 2014, 48 projects participated. Together, we have 893,458 height and weight measures (52% females) from 434,723 twin individuals, including 201,192 complete twin pairs (40% monozygotic, 40% same-sex dizygotic and 20% opposite-sex dizygotic) representing 22 countries. This project demonstrates that large-scale international twin studies are feasible and can promote the use of existing data for novel research purposes.

Childhood depressive symptoms may arise from genetic and environmental risks, which act to bias the ways in which children process emotional information. Previous studies show that several “cognitive biases” are heritable and share genetic and environmental risks with depressive symptoms. Past research suggests that many cognitive biases only reflect genetic risks for depressive symptoms from adolescence. The present study sought to identify (a) when interpersonal cognitions mature as risk factors for depressive symptoms by examining whether these factors are stable and predict symptoms across time in childhood, and (b) the extent to which interpersonal cognitions reflect inherited/environmental risks on children's depressive symptoms. Results showed that there was some stability for interpersonal cognitive biases from age 8 to 10 years (rs = .32–.43). Only the absence of positive self/other perceptions, and negative peer and mother expectations at age 8 predicted depressive symptoms at age 10 (after controlling for depressive symptoms at age 8). The absence of positive self/other perceptions shared genetic influences with depressive symptoms within and across time. Across middle to late childhood, interpersonal cognitions begin to operate as vulnerability-trait factors for depressive symptoms, gradually reflecting distal genetic risks on symptoms.

The Genesis 12–19 (G1219) Study is an ongoing longitudinal study of a sample of UK twin pairs, non-twin sibling pairs, and their parents. G1219 was initially designed to examine the role of gene–environment interplay in adolescent depression. However, since then data have continued to be collected from both parents and their offspring into young adulthood. This has allowed for longitudinal analyses of depression and has enabled researchers to investigate multiple phenotypes and to ask questions about intermediate mechanisms. The study has primarily focused on emotional development, particularly depression and anxiety, which have been assessed at multiple levels of analysis (symptoms, cognitions, and relevant environmental experiences). G1219 has also included assessment of a broader range of psychological phenotypes ranging from antisocial behaviors and substance use to sleep difficulties, in addition to multiple aspects of the environment. DNA has also been collected. The first wave of data collection began in the year 1999 and the fifth wave of data collection will be complete before the end of 2012. In this article, we describe the sample, data collection, and measures used. We also summarize some of the key findings to date.

Consistent evidence shows both genetic and stress-related risks on child and adolescent anxiety, yet few studies have considered the degree to which genetic effects are moderated by stress (gene–environment interaction). We used longitudinal data from both a child and adolescent sample of twins to examine three novel issues on the presence of gene–environment interaction on anxiety symptoms. First, we assessed moderation of genetic risks on anxiety symptoms by negative life events in each age group. Second, by distinguishing between “stable” and “age-specific” genetic factors, we explored the continuity of gene–environment interaction across time and/or its emergence at specific ages. Third, we compared the presence of gene–environment interaction across different symptom types (general, panic, social, and separation). Genetic effects on separation anxiety symptoms in childhood (mean age = 8 years, 6 months) and panic anxiety symptoms in adolescence (mean age = 15 years) increased across independent negative life events. Shared environmental effects on separation anxiety symptoms and nonshared environmental effects on general anxiety symptoms in adolescence were also moderated by negative life events. We interpret these preliminary findings tentatively in the context of gene–environment interaction on anxiety in general, and on early separation and later panic anxiety in particular.

The present study investigated the role of cognitive processes in the maintenance of clinically significant sleep disturbance across two cultures. A questionnaire was administered to 60 Japanese and 60 English university students to assess the presence of sleep disturbance, predominance of pre-sleep cognitive activity, use of thought management strategies to control pre-sleep cognitive activity, and the content of pre-sleep cognitive activity. The results indicated that across both cultures poor sleepers attributed their sleep disturbance to the presence of uncontrollable pre-sleep cognitive activity. Minor differences between the Japanese and English samples included the strategies employed to control pre-sleep cognitive activity. The English participants were more likely to engage in reappraisal whereas the Japanese sample were more likely to engage in punishment and worry. These results are suggestive of the cross-cultural applicability of cognitive models of insomnia.