Research has shown that therapeutic sleep deprivation (SD) has rapid antidepressant effects in the majority of depressed patients. Investigation of factors preceding and accompanying these effects may facilitate the identification of the underlying biological mechanisms. This exploratory study aimed to examine clinical and genetic factors predicting response to SD and determine the impact of SD on illness course. Mood during SD was also assessed via visual analogue scale. Depressed inpatients (n = 78) and healthy controls (n = 15) underwent ~36 h of SD. Response to SD was defined as a score of ≤ 2 on the Clinical Global Impression Scale for Global Improvement. Depressive symptom trajectories were evaluated for up to a month using self/expert ratings. Impact of genetic burden was calculated using polygenic risk scores for major depressive disorder. In total, 72% of patients responded to SD. Responders and non-responders did not differ in baseline self/expert depression symptom ratings, but mood differed. Response was associated with lower age (p = 0.007) and later age at life-time disease onset (p = 0.003). Higher genetic burden of depression was observed in non-responders than healthy controls. Up to a month post SD, depressive symptoms decreased in both patients groups, but more in responders, in whom effects were sustained. The present findings suggest that re-examining SD with a greater focus on biological mechanisms will lead to better understanding of mechanisms of depression.

In academic debates about environmental protection and social equity, neoliberalism has supplanted globalization as the newest catchphrase. A growing body of literature on neoliberalism, particularly in the fields of political ecology, political economy, and geography, has shown the concept to be at least as unwieldy as its predecessor. Neoliberal Environments: False Promises and Unnatural Consequences emerges specifically from this expansive proliferation of scholarship with the aim to collect and represent a particular focus on the``connections and common problems'' between neoliberal approaches and environmental governance, change, and policies (page 9).The editors frame neoliberalism as the most current form of capitalism and stress its intent tò`e xpand opportunities for capital investment and accumulation by re-working state^market^civil society relations to allow for the stretching and deepening of commodity production, circulation and exchange'' (page 10). Recognizing the challenge of giving this idea of neoliberalism an identifiable form, the editors use many case studies and commentaries in four topical sections to illustrate the conviction that, while neoliberal ideas and policies vary widely, they frequently result in environmental degradation and socioeconomic disparity.The opening section,``Enclosure and privatization'', examines attempts to define natural systems in terms of access and property. Case studies in this section show how the privatization of property does not actually lessen government interference, but rather requires new forms of state regulation, or reregulation. The second section,``Commodification and marketization'', is a series of case studies that look at how natural systems become fungible commodities and are exchanged in markets. For example, Morgan Robertson examines the development of wetland banking systems, in which natural wetland and human-made wetland are equivalent`goods' to be bought, sold, and even`banked' to fulfill certain regulatory obligations. His analysis demonstrates the difficulty inherent in creating standards of measurement and governance when commodifying these complex natural processes.The third section,``Devolution and neoliberal governmentalities'', provides four instances of neoliberal ideology in governance and policy making, each of which underscores the variable forms that neoliberal policies can take. Also illustrated are the ways in which neoliberal policies have a tendency to reinforce and entrench their own logic, further encouraging devolution and privatization, possibly at the expense of environmental and social gain. The final section,`R esistance'', shows how neoliberalism is inherently uneven in its institutionalization, implementation, and governance: instead of being concerned with equity, neoliberalism values equity as a secondary outcome that occurs`naturally' as a result of efficient markets or correct pricing. As a result, the inequities created by neoliberal policies have a tendency to breed resistance. In``New Mexico: sustained yiel...

Therapeutic sleep deprivation (SD) rapidly induces robust, transient antidepressant effects in a large proportion of major mood disorder patients suffering from a depressive episode, but underlying biological factors remain poorly understood. Research suggests that these patients may have altered circadian molecular genetic ‘clocks’ and that SD functions through ‘resetting’ dysregulated genes; additional factors may be involved, warranting further investigation. Leveraging advances in microarray technology enabling the transcriptome-wide assessment of gene expression, this study aimed to examine gene expression changes accompanying SD and recovery sleep in patients suffering from an episode of depression. Patients (N = 78) and controls (N = 15) underwent SD, with blood taken at the same time of day before SD, after one night of SD and after recovery sleep. A transcriptome-wide gene-by-gene approach was used, with a targeted look also taken at circadian genes. Furthermore, gene set enrichment, and longitudinal gene set analyses including the time point after recovery sleep, were conducted. Circadian genes were significantly affected by SD, with patterns suggesting that molecular clocks of responders and non-responders, as well as patients and controls respond differently to chronobiologic stimuli. Notably, gene set analyses revealed a strong widespread effect of SD on pathways involved in immune function and inflammatory response, such as those involved in cytokine and especially in interleukin signalling. Longitudinal gene set analyses showed that in responders these pathways were upregulated after SD; in non-responders, little response was observed. Our findings emphasize the close relationship between circadian, immune and sleep systems and their link to etiology of depression at the transcriptomic level.