Conceptualising and historicising the US foreign policy establishment in a racialised class structure

In recent years critical scholars of U.S. foreign policy have challenged the mainstream paradigm that fails to account for the racial dimensions of international relations. This article introduces a conceptual and historical analysis of the US foreign policy establishment that posits race and racism at its centre. While alluding to conventional theories of American power such as pluralism and statism, the article also highlights classical Marxism’s failure to acknowledge that US exceptionalism and racism conjoined in a manner that conferred a racial dimension to class politics. The article argues that the U.S. foreign policy establishment has been presided over by an elite or ruling elite; and irrespective of challenges from below, increasing diversity, or the insistence that America is a meritocratic classless society, the U.S establishment is at heart, elitist, racialised and generally Anglo-centric. The article identifies links between the racial dimensions of U.S. foreign policy and the identity profile of the power elite. The paper extends and critiques C. Wright Mills’ definition of the power elite by mapping its racial dimension. Finally the article argues that although the election of Obama represented a more inclusive and cosmopolitan version of the establishment, Obama’s presence has helped to consolidate the status quo as the structural constraints on the executive branch and symbolism associated with the election of the first African-American president has generally silenced the Left and quietly fostered the suggestion that an unconventional identity profile will not necessarily result in the change we can believe in

Excess of serotonin affects neocortical pyramidal neuron migration

The serotonin transporter (SERT) is a key molecule involved in the homeostasis of extracellular levels of serotonin and is regulated developmentally. Genetic deletion of SERT in rodents increases extracellular levels of serotonin and affects cellular processes involved in neocortical circuit assembly such as barrel cortex wiring and cortical interneuron migration. Importantly, pharmacological blockade of SERT during brain development leads to phenotypes relevant to psychiatry in rodents and to an increased risk for autism spectrum disorders in humans. Furthermore, developmental adversity interacts with genetically-driven variations of serotonin function in humans and nonhuman primates to increase the risk for a variety of stress-related phenotypes. In this study, we investigate whether an excess of serotonin affects the migration of neocortical pyramidal neurons during development. Using in utero electroporation combined with time-lapse imaging to specifically monitor pyramidal neurons during late mouse embryogenesis, we show that an excess of serotonin reversibly affects the radial migration of pyramidal neurons. We further identify that the serotonin receptor 5-HT6 is expressed in pyramidal neuron progenitors and that 5-HT6 receptor activation replicates the effects of serotonin stimulation. Finally, we show that the positioning of superficial layer pyramidal neurons is altered in vivo in SERT knockout mice. Taken together, these results indicate that a developmental excess of serotonin decreases the migration speed of cortical pyramidal neurons, affecting a fundamental step in the assembly of neural circuits. These findings support the hypothesis that developmental dysregulation of serotonin homeostasis has detrimental effects on neocortical circuit formation and contributes to increased vulnerability to psychiatric disorders

Effect of a primary health-care-based controlled trial for cardiorespiratory fitness in refugee women

BACKGROUND: Refugee women have a high risk of coronary heart disease with low physical activity as one possible mediator. Furthermore, cultural and environmental barriers to increasing physical activity have been demonstrated. The aim of the study was to evaluate the combined effect of an approximate 6-month primary health care- and community-based exercise intervention versus an individual written prescription for exercise on objectively assessed cardiorespiratory fitness in low-active refugee women. METHODS: A controlled clinical trial, named "Support for Increased Physical Activity", was executed among 243 refugee women recruited between November 2006 and April 2008 from two deprived geographic areas in southern Stockholm, Sweden. One geographic area provided the intervention group and the other area the control group. The control group was on a higher activity level at both baseline and follow-up, which was taken into consideration in the analysis by applying statistical models that accounted for this. Relative aerobic capacity and fitness level were assessed as the two main outcome measures. RESULTS: The intervention group increased their relative aerobic capacity and the percentage with an acceptable fitness level (relative aerobic capacity > 23 O2 mlxkgxmin-1) to a greater extent than the control group between baseline and the 6-month follow-up, after adjusting for possible confounders (P = 0.020). CONCLUSIONS: A combined primary health-care and community-based exercise programme (involving non-profit organizations) can be an effective strategy to increase cardiorespiratory fitness among low-active refugee women. TRIAL REGISTRATION: ClinicalTrials.gov ID: NCT00747942

Hedonic and incentive signals for body weight control

Here we review the emerging neurobiological understanding of the role of the brain’s reward system in the regulation of body weight in health and in disease. Common obesity is characterized by the over-consumption of palatable/rewarding foods, reflecting an imbalance in the relative importance of hedonic versus homeostatic signals. The popular ‘incentive salience theory’ of food reward recognises not only a hedonic/pleasure component (‘liking’) but also an incentive motivation component (‘wanting’ or ‘reward-seeking’). Central to the neurobiology of the reward mechanism is the mesoaccumbal dopamine system that confers incentive motivation not only for natural rewards such as food but also by artificial rewards (eg. addictive drugs). Indeed, this mesoaccumbal dopamine system receives and integrates information about the incentive (rewarding) value of foods with information about metabolic status. Problematic over-eating likely reflects a changing balance in the control exerted by hypothalamic versus reward circuits and/or it could reflect an allostatic shift in the hedonic set point for food reward. Certainly, for obesity to prevail, metabolic satiety signals such as leptin and insulin fail to regain control of appetitive brain networks, including those involved in food reward. On the other hand, metabolic control could reflect increased signalling by the stomach-derived orexigenic hormone, ghrelin. We have shown that ghrelin activates the mesoaccumbal dopamine system and that central ghrelin signalling is required for reward from both chemical drugs (eg alcohol) and also from palatable food. Future therapies for problematic over-eating and obesity may include drugs that interfere with incentive motivation, such as ghrelin antagonists