Insights from studying human sleep disorders

Problems with sleep are one of the commonest reasons for seeking medical attention. Knowledge gained from basic research into sleep in animals has led to marked advances in the understanding of human sleep, with important diagnostic and therapeutic implications. At the same time, research guided by human sleep disorders is leading to important basic sleep concepts. For example, sleep may not be a global, but rather a local, brain phenomenon. Furthermore, contrary to common assumptions, wakefulness, rapid eye movement (REM) and non-REM sleep are not mutually exclusive states. This striking realization explains a fascinating range of clinical phenomena.     

Effects of sleep deprivation on gamma oscillation of waking human EEG

This study compares and evaluates the effect of sleep deprivation （SD） on human brain cognition by analyzing the recorded EEG data under normal and 24 h sleep deprived states. EEG auditory event-related potentials were collected from 14 healthy volunteers, and the statistical values of wavelet-transformed EEG in gamma band were decomposed by parallel factor analysis （PARAFAC） to identify where the differences appeared in the time, frequency and spatial domains. The results showed that the changes of brain states caused by SD appeared around 40 Hz at about 400 ms after stimulation on prefrontal and frontal lobes. Negative effects of SD on neuronal activity and oscillation were observed. The analysis of the EEG data by the wavelet transform and PARAFAC can be an integrated way to estimate the change of brain states in the three domains.     

Phagocyte-derived catecholamines enhance acute inflammatory injury

It is becoming increasingly clear that the autonomic nervous system and the immune system demonstrate cross-talk during inflammation by means of sympathetic and parasympathetic pathways. We investigated whether phagocytes are capable of de novo production of catecholamines, suggesting an autocrine/paracrine self-regulatory mechanism by catecholamines during inflammation, as has been described for lymphocytes. Here we show that exposure of phagocytes to lipopolysaccharide led to a release of catecholamines and an induction of catecholamine-generating and degrading enzymes, indicating the presence of the complete intracellular machinery for the generation, release and inactivation of catecholamines. To assess the importance of these findings in vivo, we chose two models of acute lung injury. Blockade of alpha2-adrenoreceptors or catecholamine-generating enzymes greatly suppressed lung inflammation, whereas the opposite was the case either for an alpha2-adrenoreceptor agonist or for inhibition of catecholamine-degrading enzymes. We were able to exclude T cells or sympathetic nerve endings as sources of the injury-modulating catecholamines. Our studies identify phagocytes as a new source of catecholamines, which enhance the inflammatory response.     

电脑与人脑

定义了电脑功能函数Ｃ（ｘｊ）与人脑功能函数Ｂ（ｘｊ），论证了△＝Ｂ－Ｃ〉０不等式关系，提出了发展电脑及人脑科学技术一条途径。     

Local sleep and learning

Human sleep is a global state whose functions remain unclear. During much of sleep, cortical neurons undergo slow oscillations in membrane potential, which appear in electroencephalograms as slow wave activity (SWA) of <4 Hz. The amount of SWA is homeostatically regulated, increasing after wakefulness and returning to baseline during sleep. It has been suggested that SWA homeostasis may reflect synaptic changes underlying a cellular need for sleep. If this were so, inducing local synaptic changes should induce local SWA changes, and these should benefit neural function. Here we show that sleep homeostasis indeed has a local component, which can be triggered by a learning task involving specific brain regions. Furthermore, we show that the local increase in SWA after learning correlates with improved performance of the task after sleep. Thus, sleep homeostasis can be induced on a local level and can benefit performance.