Nitrous oxide and methane in the Atlantic Ocean between 50 degrees North and 52 degrees South: Latitudinal distribution and sea-to-air flux

We discuss nitrous oxide (N2O) and methane (CH4) distributions in 49 vertical profiles covering the upper 300 m of the water column along two 13,500 km transects between 50°N and 52°S during the Atlantic Meridional Transect (AMT) programme (AMT cruises 12 and 13). Vertical N2O profiles were amenable to analysis on the basis of common features coincident with Longhurst provinces. In contrast, CH4 showed no such pattern. The most striking feature of the latitudinal depth distributions was a well-defined “plume” of exceptionally high N2O concentrations coincident with very low levels of CH4, located between 23.5°N and 23.5°S; this feature reflects the upwelling of deep waters containing N2O derived from nitrification, as identified by an analysis of N2O, apparent oxygen utilization (AOU) and NO3-, and presumably depleted in CH4 by bacterial oxidation. Sea-to-air emissions fluxes for a region equivalent to 42% of the Atlantic Ocean surface area were in the range 0.40–0.68 Tg N2O yr-1 and 0.81–1.43 Tg CH4 yr-1. Based on contemporary estimates of the global ocean source strengths of atmospheric N2O and CH4, the Atlantic Ocean could account for 6–15% and 4–13%, respectively, of these source totals. Given that the Atlantic Ocean accounts for around 20% of the global ocean surface, on unit area basis it appears that the Atlantic may be a slightly weaker source of atmospheric N2O than other ocean regions but it could make a somewhat larger contribution to marine-derived atmospheric CH4 than previously thought

Familial Risk for Mood Disorder and the Personality Risk Factor, Neuroticism, Interact in Their Association with Frontolimbic Serotonin 2A Receptor Binding

Life stress is a robust risk factor for later development of mood disorders, particularly for individuals at familial risk. Likewise, scoring high on the personality trait neuroticism is associated with an increased risk for mood disorders. Neuroticism partly reflects stress vulnerability and is positively correlated to frontolimbic serotonin 2A (5-HT2A) receptor binding. Here, we investigate whether neuroticism interacts with familial risk in relation to frontolimbic 5-HT2A receptor binding. Twenty-one healthy twins with a co-twin history of mood disorder and 16 healthy twins without a co-twin history of mood disorder were included. They answered self-report personality questionnaires and underwent [18F]altanserin positron emission tomography. We found a significant interaction between neuroticism and familial risk in predicting the frontolimbic 5-HT2A receptor binding (p=0.026) in an analysis adjusting for age and body mass index. Within the high-risk group only, neuroticism and frontolimbic 5-HT2A receptor binding was positively associated (p=0.0037). In conclusion, our data indicate that familial risk and neuroticism interact in their relation to frontolimbic 5-HT2A receptor binding. These findings point at a plausible neurobiological link between genetic and personality risk factors and vulnerability to developing mood disorders. It contributes to our understanding of why some people at high risk develop mood disorders while others do not. We speculate that an increased stress reactivity in individuals at high familial risk for mood disorders might enhance the effect of neuroticism in shaping the impact of potential environmental stress and thereby influence serotonergic neurotransmission

Challenges and opportunities in genome-wide environmental interaction (GWEI) studies.

The interest in performing gene-environment interaction studies has seen a significant increase with the increase of advanced molecular genetics techniques. Practically, it became possible to investigate the role of environmental factors in disease risk and hence to investigate their role as genetic effect modifiers. The understanding that genetics is important in the uptake and metabolism of toxic substances is an example of how genetic profiles can modify important environmental risk factors to disease. Several rationales exist to set up gene-environment interaction studies and the technical challenges related to these studies-when the number of environmental or genetic risk factors is relatively small-has been described before. In the post-genomic era, it is now possible to study thousands of genes and their interaction with the environment. This brings along a whole range of new challenges and opportunities. Despite a continuing effort in developing efficient methods and optimal bioinformatics infrastructures to deal with the available wealth of data, the challenge remains how to best present and analyze genome-wide environmental interaction (GWEI) studies involving multiple genetic and environmental factors. Since GWEIs are performed at the intersection of statistical genetics, bioinformatics and epidemiology, usually similar problems need to be dealt with as for genome-wide association gene-gene interaction studies. However, additional complexities need to be considered which are typical for large-scale epidemiological studies, but are also related to "joining" two heterogeneous types of data in explaining complex disease trait variation or for prediction purposes