Breathing is irregular during rapid eye-movement (REM) sleep, whereas it is stable during non-REM sleep. Why this is so remains a mystery. We propose that irregular breathing has a cortical origin and reflects the mental content of dreams, which often accompany REM sleep. We tested 21 patients with narcolepsy who had the exceptional ability to lucid dream in REM sleep, a condition in which one is conscious of dreaming during the dream and can signal lucidity with an ocular code. Sleep and respiration were monitored during multiple naps. Participants were instructed to modify their dream scenario so that it involved vocalizations or an apnoea, -two behaviours that require a cortical control of ventilation when executed during wakefulness. Most participants (86%) were able to signal lucidity in at least one nap. In 50% of the lucid naps, we found a clear congruence between the dream report (e.g., diving under water) and the observed respiratory behaviour (e.g., central apnoea) and, in several cases, a preparatory breath before the respiratory behaviour. This suggests that the cortico-subcortical networks involved in voluntary respiratory movements are preserved during REM sleep and that breathing irregularities during this stage have a cortical/subcortical origin that reflects dream content.

Background Heart attacks and stroke often result from occlusive thrombi following the rupture of vulnerable atherosclerotic plaques. Vascular smooth muscle cells ( VSMC s) play a pivotal role in plaque vulnerability because of their switch towards a proinflammatory/macrophage‐like phenotype when in the context of atherosclerosis. The prometastatic transcription factor Slug/Snail2 is a critical regulator of cell phenotypic transition. Here, we aimed to investigate the role of Slug in the transdifferentiation process of VSMC s occurring during atherogenesis. Methods and Results In rat and human primary aortic smooth muscle cells, Slug protein expression is strongly and rapidly increased by platelet‐derived growth factor‐BB (PDGF‐ BB ). PDGF ‐ BB increases Slug protein without affecting mRNA levels indicating that this growth factor stabilizes Slug protein. Immunocytochemistry and subcellular fractionation experiments reveal that PDGF ‐ BB triggers a rapid accumulation of Slug in VSMC nuclei. Using pharmacological tools, we show that the PDGF ‐ BB –dependent mechanism of Slug stabilization in VSMC s involves the extracellular signal‐regulated kinase 1/2 pathway. Immunohistochemistry experiments on type V and type VI atherosclerotic lesions of human carotids show smooth muscle–specific myosin heavy chain–/Slug‐positive cells surrounding the prothrombotic lipid core. In VSMC s, Slug si RNA s inhibit prostaglandin E2 secretion and prevent the inhibition of cholesterol efflux gene expression mediated by PDGF ‐ BB , known to be involved in plaque vulnerability and/or thrombogenicity. Conclusions Our results highlight, for the first time, a role of Slug in aortic smooth muscle cell transdifferentiation and enable us to consider Slug as an actor playing a role in the atherosclerotic plaque progression towards a life‐threatening phenotype. This also argues for common features between acute cardiovascular events and cancer.

Patients with sleepwalking episodes or sleep terrors (SW/ST) exhibit sudden abnormal behaviours arising from sleep, mostly from N3 sleep (American Academy of Sleep Medicine, 2014). Patients usually open their eyes, look around with a confused gaze, sit, stand, walk, talk, scream or flee their bed (Derry, Harvey, Walker, Duncan, & Berkovic, 2009). There is a continuum between the different behavioural patterns of arousal parasomnias. Specifically, the behavioural patterns of non-rapid eye movement (NREM) parasomnias appear with a hierarchical order, with arousal behaviours being the fundamental component, possibly followed by abnormal agitated conduct, which can be further accompanied by distressed emotional manifestations (Derry et al., 2009). Several clinical, polygraphical and brain functional imaging studies support the concept that these behaviours occur during local (primarily thalamo-amygdalo-cingulo-cortical) arousals from N3 sleep, disengaged from the control of the prefrontal and frontal associative cortex

In addition, the Discussion section contained an error, where, "For example, among 6 healthy lucid dreamers, who had been trained in lucid dreaming for several years, only one subject was able to perform the requested task and the ocular code after 3 full nights in a fMRI 36 " now reads: "For example, among 6 healthy lucid dreamers, who had been trained in lucid dreaming for several years, only one subject was able to perform the requested task and the ocular code after 3 full nights in an fMRI scanner 36. " These errors have now been corrected in the HTML and PDF versions of this Article.