The Internationalisation of Tobacco Control, 1950-2010.

This article explores the internationalisation of tobacco control as a case study in the history of international health regulation. Contrary to the existing literature on the topic, it argues that the history of international anti-smoking efforts is longer and richer than the making of the World Health Organisation's Framework Convention on Tobacco Control in the early twenty-first century. It thereby echoes the point made by other scholars about the importance of history when making sense of contemporary global health. Specifically, the article shows how the internationalisation of tobacco control started in the 1950s through informal contacts between scientists working on cancer research and how these initial interactions were followed by a growing number of more formal initiatives, from the World Conferences on Tobacco or Health to the Bloomberg Initiative to Reduce Tobacco Use. Rather than arranging these efforts in a linear narrative of progress culminating with the Framework Convention on Tobacco Control, we take anthropological claims about global health's uneven terrain seriously and portray a history of international tobacco control marked by ruptures and discontinuities. Specifically, we identify three successive periods, with each of them characterised by specific understandings of international action, tobacco control expertise, advocacy networks and funding strategies

Cognition-Enhancing Doses of Methylphenidate Preferentially Increase Prefrontal Cortex Neuronal Responsiveness

Background Despite widespread use of low-dose psychostimulants for the treatment of attention deficit hyperactivity disorder (ADHD), the neural basis for the therapeutic actions of these drugs are not well-understood. We recently demonstrated that low-dose methylphenidate (MPH) increases catecholamine efflux preferentially within the prefrontal cortex (PFC), suggesting the PFC is a principal site of action in the behavioral-calming and cognition-enhancing effects of low-dose psychostimulants. To better understand the neural mechanisms involved in the behavioral actions of low-dose stimulants, the current study examined the effects of low-dose MPH on the discharge properties of individual and ensembles of PFC neurons. Methods Extracellular activity of multiple individual PFC neurons was recorded in freely moving rats using multi-channel recording techniques. Behavioral studies identified optimal, working memory-enhancing doses of intraperitoneal MPH. The effects of these low-doses of MPH on PFC neuronal discharge properties were compared to: 1) the effects of high-dose MPH on PFC neuronal discharge; 2) the effects of low-dose MPH on neuronal discharge within the somatosensory cortex. Results Only working memory-enhancing doses of MPH increased the responsivity of individual PFC neurons and altered neuronal ensemble responses within the PFC. These effects were not observed outside the PFC (i.e. within somatosensory cortex). In contrast, high-dose MPH profoundly suppressed evoked discharge of PFC neurons. Conclusions These observations suggest that preferential enhancement of signal processing within the PFC, including alterations in the discharge properties of individual PFC neurons and PFC neuronal ensembles, underlie the behavioral/cognitive actions of low-dose psychostimulants

Psychostimulants as Cognitive Enhancers: The Prefrontal Cortex, Catecholamines and Attention Deficit Hyperactivity Disorder

Psychostimulants exert behavioral-calming and cognition-enhancing actions in the treatment of attention deficit hyperactivity disorder (ADHD). Contrary to early views, extensive research demonstrates that these actions are not unique to ADHD. Specifically, when administered at low and clinically-relevant doses, psychostimulants improve a variety of behavioral and cognitive processes dependent on the prefrontal cortex (PFC) in subjects with and without ADHD. Despite the longstanding clinical use of these drugs, the neural mechanisms underlying their cognition-enhancing/therapeutic actions have only recently begun to be examined. At behaviorally-activating doses, psychostimulants produce large and widespread increases in extracellular levels of brain catecholamines. In contrast, cognition-enhancing doses of psychostimulants exert regionally-restricted actions, elevating extracellular catecholamine levels and enhancing neuronal signal processing preferentially within the PFC. Additional evidence suggests a prominent role of PFC α2- and D1 receptors in the behavioral and electrophysiological actions of low-dose psychostimulants. These and other observations indicate a pivotal role of PFC catecholamines in the cognition-enhancing and therapeutic actions of psychostimulants as well as other drugs used in the treatment of ADHD. This information may be particularly relevant for the development of novel pharmacological treatments for ADHD and other conditions associated with PFC dysregulation

Children in care or in need:educational progress at home and in care

By age 16 the attainment of most children in or on the edge of out of home care has fallen well behind the average for their age. This paper uses the English National Pupil Database to examine how much of this falling behind occurs before the age 7, and how any subsequent decline relates to time in care as against time outside it. We compare the previous progress of three groups of 16-year-olds: 5,175 looked after by the state (CLA), 17,392 in need but not in care (CIN), and 22,567 children matched with the CLA or CIN on initial attainment, special educational needs and eligibility for free school meals. We found that the attainment of the CIN and those CLA not yet in care was around one standard deviation below the cohort average at age 7. It then fell relative to their peers while their rate of unauthorised absences and exclusions grew. Removal from home to care appeared to halt or greatly reduce this decline but did not, on average, reverse it. We conclude that educational interventions for CLA should also include CIN, start before 7, target both school and family, and exploit the educational opportunity which care provides

Stress-Induced Impairment of a Working Memory Task: Role of Spiking Rate and Spiking History Predicted Discharge

Stress, pervasive in society, contributes to over half of all work place accidents a year and over time can contribute to a variety of psychiatric disorders including depression, schizophrenia, and post-traumatic stress disorder. Stress impairs higher cognitive processes, dependent on the prefrontal cortex (PFC) and that involve maintenance and integration of information over extended periods, including working memory and attention. Substantial evidence has demonstrated a relationship between patterns of PFC neuron spiking activity (action-potential discharge) and components of delayed-response tasks used to probe PFC-dependent cognitive function in rats and monkeys. During delay periods of these tasks, persistent spiking activity is posited to be essential for the maintenance of information for working memory and attention. However, the degree to which stress-induced impairment in PFC-dependent cognition involves changes in task-related spiking rates or the ability for PFC neurons to retain information over time remains unknown. In the current study, spiking activity was recorded from the medial PFC of rats performing a delayed-response task of working memory during acute noise stress (93 db). Spike history-predicted discharge (SHPD) for PFC neurons was quantified as a measure of the degree to which ongoing neuronal discharge can be predicted by past spiking activity and reflects the degree to which past information is retained by these neurons over time. We found that PFC neuron discharge is predicted by their past spiking patterns for nearly one second. Acute stress impaired SHPD, selectively during delay intervals of the task, and simultaneously impaired task performance. Despite the reduction in delay-related SHPD, stress increased delay-related spiking rates. These findings suggest that neural codes utilizing SHPD within PFC networks likely reflects an additional important neurophysiological mechanism for maintenance of past information over time. Stress-related impairment of this mechanism is posited to contribute to the cognition-impairing actions of stress