While there is a developing understanding of the influence of sleep on cardiovascular autonomic activity in humans, there remain unresolved issues. In particular, the effect of time within the sleep period, independent of sleep stage, has not been investigated. Further, the influence of sleep on central sympathetic nervous system (SNS) activity is uncertain because results using the major method applicable to humans, the low frequency (LF) component of heart rate variability (HRV), have been contradictory, and because the method itself is open to criticism. Sleep and cardiac activity were measured in 14 young healthy subjects on three nights. Data was analysed in 2‐min epochs. All epochs meeting specified criteria were identified, beginning 2 h before, until 7 h after, sleep onset. Epoch values were allocated to 30‐min bins and during sleep were also classified into stage 2, slow wave sleep (SWS) and rapid eye movement (REM) sleep. The measures of cardiac activity were heart rate (HR), blood pressure (BP), high frequency (HF) and LF components of HRV and pre‐ejection period (PEP). During non‐rapid eye movement (NREM) sleep autonomic balance shifted from sympathetic to parasympathetic dominance, although this appeared to be more because of a shift in parasympathetic nervous system (PNS) activity. Autonomic balance during REM was in general similar to wakefulness. For BP and the HF and LF components the change occurred abruptly at sleep onset and was then constant over time within each stage of sleep, indicating that any change in autonomic balance over the sleep period is a consequence of the changing distribution of sleep stages. Two variables, HR and PEP, did show time effects reflecting a circadian influence over HR and perhaps time asleep affecting PEP. While both the LF component and PEP showed changes consistent with reduced sympathetic tone during sleep, their pattern of change over time differed.

ChemoEd holds promise to improve patient treatment-related concerns and some physical/psychological outcomes; however, further research is required on more diverse patient populations to ensure generalisability.

The mammalian neocortex is generated by waves of migrating cells originating from the ventricular zone. Radial migration along radial glia has been proposed as the dominant mechanism for this process. The radial unit hypothesis is poorly supported by retroviral lineage studies, however, and although some clones show limited radial organization, the emphasis appears to be on widespread tangential dispersion. Here we investigate the pattern of cortical cell dispersion using transgenic mice in which roughly half of the brain cells are coloured by a transgene. We find that the neocortex is randomly divided into diffused bands, the majority of cells within each band have the same colour, and their radial orientation suggests radial dispersion. Superimposed upon this was a significant contribution by tangentially dispersed cells that did not respect clonal borders. These observations indicate that cortical specification is not dependent upon a single mechanism of cell allocation, but that both radial mosaicism and tangential cell migration are involved.

The TCW model holds some promise; however, additional work in at-risk populations is required before we recommend implementation.