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Introduction Among those who experience trauma, some individuals develop Adverse Posttraumatic Neuropsychiatric Sequelae (APNS). Identifying biomarkers associated with APNS is critical for predicting trajectories of recovery and informing interventions to reduce the impact of trauma. In this study, we examined objective 24-hour activity patterns and APNS in the weeks following a traumatic event. Methods Participants (n = 2,021) were recruited from emergency departments after experiencing trauma. Over 8 weeks, they wore wrist accelerometry devices to measure 24-hour activity patterns, and completed surveys assessing 10 Research Domain Criteria (RDoC) constructs associated with APNS. We aimed to 1) examine the relationship between 24-hour activity patterns and APNS symptoms, and 2) examine how 24-hour activity patterns changed over time in relation to changes in APNS over the 8-week period. A bivariate linear mixed model approach was used to model the cross-sectional and longitudinal associations with each of the 10 RDoC constructs. Results Overall, participants reporting more pain in the weeks following trauma also showed objectively less 24-hour activity variance (Pearson correlation = -0.14, p = 0.001). An improving pain trajectory over the 8 weeks was associated with increases in daily activity (Pearson correlation = -0.14, p < 0.001) variability in activity (Pearson correlation = -0.12, p < 0.001), and increases in sleep consolidation (Pearson correlation = 0.013, p < 0.001). Within subjects, an increasing number of transitions between sleep and wake over the study period was also associated with worsening self-reported anxiety (Pearson correlation = 0.06, p = 0.003) and sleep problems (Pearson correlation = 0.10, p = 0.003) Conclusion After a traumatic event, several 24-hour activity biomarkers were associated with APNS. Results suggest pain, activity, and sleep highly influence each other in the weeks following a traumatic event, and 24-hour activity patterns should be considered when making predictions about who is likely to recover from trauma. Targeted interventions for sleep and pain may promote recovery in the other domains. Support (If Any) NIMH U01MH110925, US Army Medical Research and Material Command, the One Mind Foundation, The Mayday Fund, Verily Life Sciences. LDS is supported by a Department of Veterans Affairs Career Development Award (IK2CX002032).

In this article we interrogate the claim that there is an opioid crisis: adramatic rise in drug overdose fatalities in the United States over thepast two decades that is also spreading to other countries. The usualargument is that this crisis is largely explained by errant prescriptionpractices leading to an oversupply of opioids, leading to addiction,premature mortality and drug overdose deaths, both among thoseprescribed opioids for pain relief, and those obtaining them on theillegal market. We argue, that this view is highly problematic and thatit is likely to entrench deeper problems with how substance addictionhas been perceived and known. In this article, we develop analternative picture of the addiction crisis based on four years ofresearch and collaboration with addiction neuroscientists. Drugoverdose deaths, we claim, are symptoms of what we term the‘structural distribution of social despair.’ We argue that this iscompounded by a translation crisis at the heart of addictionneuroscience. For all its dominance, the ‘dopamine hypothesis’ ofaddiction that shaped understandings for some three decades, hasstill not produced a single effective treatment. However, thistranslation crisis also represents an opportunity for ‘the memory turn’in addiction neuroscience as it seeks to translate its emergingconception of addiction as a problem of memory into effective formsof treatment. We conclude by arguing that, for the ‘memory turn’ tounderpin effective interventions into ‘the opioid crisis’, a new relationbetween neuroscientists and social scientists of addiction is needed,one that proceeds from the lived experience of human beings.

In this article, we argue that the rapid rise in drug overdose deaths in America is a tragedy that draws attention to fundamental conceptual and experimental problems in addiction science that have significant human consequences. Despite enormous economic investment, political support and claims to have revolutionised addiction medicine, neurobiological models are yet to produce a treatment for substance addiction. This is partly, we claim, because neurobiology is unable to explain essential features of addiction and relapse that neurobehavioral models of addiction are better placed to investigate. We show how addiction neuroscience turned to long-term memory to explain the chronicity of addiction and persistent relapses long after neurochemical traces have left the body. The turn to memory may in time help to close the translational gap facing addiction medicine, but it is our view in this article that the primary value of memory theory lays in its potential to create new critical friendships between biological and social sciences that are attuned to the lived experience and suffering of stigmatised people. The value of the memory turn may rest upon the capacity of these critical friendships to wean addiction science off its long-term dependence on disease concepts of human distress.

The title compound was synthesised and its structure determined by X-ray crystallography. The structure contains a hydrogen bond between the OH group of the alcohol and the phosphoryl oxygen atom. The P–N bond lengths are significantly different and the differences can be attributed to varying ρπ—dπ interactions along the bonds.