NLRP3-mediated autophagy dysfunction links gut microbiota dysbiosis to tau pathology in chronic sleep deprivation

Emerging evidence indicates that sleep deprivation(SD)can lead to Alzheimer’s disease(AD)-related pathological changes and cognitive decline.However,the underlying mechanisms remain obscure.In the present study,we identified the existence of a microbiota-gut-brain axis in cognitive deficits resulting from chronic SD and revealed a potential pathway by which gut microbiota affects cognitive functioning in chronic SD.Our findings demonstrated that chronic SD in mice not only led to cognitive decline but also induced gut microbiota dysbiosis,elevated NLRP3 inflammasome expression,GSK-3βactivation,autophagy dysfunction,and tau hyperphosphorylation in the hippocampus.Colonization with the“SD microbiota”replicated the pathological and behavioral abnormalities observed in chronic sleep-deprived mice.Remarkably,both the deletion of NLRP3 in NLRP3-/-mice and specific knockdown of NLRP3 in the hippocampus restored autophagic flux,suppressed tau hyperphosphorylation,and ameliorated cognitive deficits induced by chronic SD,while GSK-3βactivity was not regulated by the NLRP3 inflammasome in chronic SD.Notably,deletion of NLRP3 reversed NLRP3 inflammasome activation,autophagy deficits,and tau hyperphosphorylation induced by GSK-3βactivation in primary hippocampal neurons,suggesting that GSK-3β,as a regulator of NLRP3-mediated autophagy dysfunction,plays a significant role in promoting tau hyperphosphorylation.Thus,gut microbiota dysbiosis was identified as a contributor to chronic SD-induced tau pathology via NLRP3-mediated autophagy dysfunction,ultimately leading to cognitive deficits.Overall,these findings highlight GSK-3βas a regulator of NLRP3-mediated autophagy dysfunction,playing a critical role in promoting tau hyperphosphorylation.

Alterations of sleep deprivation on brain function:A coordinatebased resting-state functional magnetic resonance imaging metaanalysis

BACKGROUND Sleep deprivation is a prevalent issue that impacts cognitive function.Although numerous neuroimaging studies have explored the neural correlates of sleep loss,inconsistencies persist in the reported results,necessitating an investigation into the consistent brain functional changes resulting from sleep loss.AIM To establish the consistency of brain functional alterations associated with sleep deprivation through systematic searches of neuroimaging databases.Two metaanalytic methods,signed differential mapping(SDM)and activation likelihood estimation(ALE),were employed to analyze functional magnetic resonance imaging(fMRI)data.METHODS A systematic search performed according to PRISMA guidelines was conducted across multiple databases through July 29,2023.Studies that met specific inclusion criteria,focused on healthy subjects with acute sleep deprivation and reported whole-brain functional data in English were considered.A total of 21 studies were selected for SDM and ALE meta-analyses.RESULTS Twenty-one studies,including 23 experiments and 498 subjects,were included.Compared to pre-sleep deprivation,post-sleep deprivation brain function was associated with increased gray matter in the right corpus callosum and decreased activity in the left medial frontal gyrus and left inferior parietal lobule.SDM revealed increased brain functional activity in the left striatum and right central posterior gyrus and decreased activity in the right cerebellar gyrus,left middle frontal gyrus,corpus callosum,and right cuneus.CONCLUSION This meta-analysis consistently identified brain regions affected by sleep deprivation,notably the left medial frontal gyrus and corpus callosum,shedding light on the neuropathology of sleep deprivation and offering insights into its neurological impact.

Overexpression of Sirt6 ameliorates sleep deprivation induced-cognitive impairment by modulating glutamatergic neuron function

Sleep benefits the restoration of energy metabolism and thereby suppo rts neuronal plasticity and cognitive behaviors.Sirt6 is a NAD+-dependent protein deacetylase that has been recognized as an essential regulator of energy metabolism because it modulates various transcriptional regulators and metabolic enzymes.The aim of this study was to investigate the influence of Sirt6 on cerebral function after chronic sleep deprivation(CSD).We assigned C57BL/6J mice to control or two CSD groups and subjected them to AAV2/9-CMV-EGFP or AAV2/9-CMV-Sirt6-EGFP infection in the prelimbic cortex(PrL).We then assessed cerebral functional connectivity(FC) using resting-state functional MRI,neuron/astrocyte metabolism using a metabolic kinetics analysis;dendritic spine densities using sparse-labeling;and miniature excitato ry postsynaptic currents(mEPSCs) and action potential(AP) firing rates using whole-cell patchclamp recordings.In addition,we evaluated cognition via a comprehensive set of behavioral tests.Compared with controls,Sirt6 was significantly decreased(P<0.05) in the PrL after CSD,accompanied by cognitive deficits and decreased FC between the PrL and accumbens nucleus,piriform cortex,motor co rtex,somatosensory co rtex,olfactory tubercle,insular cortex,and cerebellum.Sirt6 ove rexpression reve rsed CSD-induced cognitive impairment and reduced FC.Our analysis of metabolic kinetics using [1-13C] glucose and [2-13C] acetate showed that CSD reduced neuronal Glu4and GABA2synthesis,which could be fully restored via forced Sirt6 expression.Furthermore,Sirt6 ove rexpression reversed CSD-induced decreases in AP firing rates as well as the frequency and amplitude of mEPSCs in PrL pyramidal neurons.These data indicate that Sirt6 can improve cognitive impairment after CSD by regulating the PrL-associated FC network,neuronal glucose metabolism,and glutamatergic neurotransmission.Thus,Sirt6 activation may have potential as a novel strategy for treating sleep disorder-related diseases.

ADJUSTING EFFECTS OF APPLICATION OF GARLIC PASTE AT SHNQU (神阙 CV8) ON THE CIRCADIAN RHYTHM OF BODY TEMPERATURE INDUCED BY SLEEP DEPRIVATION

Objective To observe the effect of application of garlic paste at Shenque （神阙 CV8） on the circadian rhythm in sleep deprivation young students. Metheds Twenty healthy volunteer young male students from Southern Medical University were randomly divided into three groups： normal group （A）, sleep deprivation group （B） and treatment group （C）. Volunteers in group B and C received 48 h sleep deprivation （SD）, and in the mean time volunteers in group C were treated by garlic paste at Shenque （神阙 CV8）, while those in group A had no any treatment. The body temperature of all the volunteers was detected at 6：00 am, 12：00 am, 6：00 pm and 0：00 am, respectively, after the treatment. Results The mean body temperature values in group A and C both were highest at 6： 00 pm and lowest at 6： 00 am which had a significant difference in each group （P〈0.01）; in group B, the mean body temperature was highest at 0：00 am and lowestat 6：00 am, no significant difference was found between them （P〉0.05）. Results of cosine analysis showed that in subjects of group B the circadian rhythm of body temperature still kept going well after SD, but the peak amplitude and amplitude of vibration were higher than those of group A, and the acrophase of group B was obviously lower than that of group C and A. The 3 indexes of group C were similar to those of group A, denoting that garlic paste application of Shenque （神阙 CV8） could prevent disorders of circadian rhythm of the body temperature. Conclusion The garlic paste application at Shenque （神阙 CV8） can adjust circadian rhythm and accelerate the recovery processes of circadian rhythm in SD young students.

Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa

AIM: To investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense. METHODS: Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7d sleep deprivation. RT-PCR, immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70. Ethanol (500mL.L(-1), i.g.) was used to induce gastric mucosa damage. RESULTS: RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL.L(-1) ethanol challenge, the ulcer area found in the rats with 7d sleep deprivation (19.15 +/- 4.2)mm(2) was significantly lower (P【0.01) than the corresponding control (53.7 +/- 8.1) mm(2). CONCLUSION: Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection.

Gene expression profiles in gastric mucosa of sleep deprivation rats

INTRODUCTIONStress has been shown to induce gastric mucosallesions and lower the effectiveness of the mucosa asa barrier.In rats,gastric ulcers can beproduced by cold-restraint stress and it isfrequently employed as a model for the study of themechanisms of stress on ulcer formation.Cold-restraint stress however is not normally

nfluence of paradoxical sleep deprivation and sleep recovery on testosterone level in rats of different ages

This study was performed to assess serum testosterone alterations induced by paradoxical sleep deprivation （PSD） and to verify their attenuation during sleep recovery （SR） based on different durations and ages. Wistar male rats aged 12 weeks for the younger group and 20 weeks for the elder group were randomly distributed into one of the following groups： a control group （cage and platform）, 3-day SD, 5-day SD, 7-day SD, 1-day SR, 3-day SR and 5-day SR groups. For PSD, the modified multiple platform method was used to specifically limit rapid eye movement （REM） sleep. Differences in the testosterone and luteinizing hormone levels between the younger group and the elder group according to duration of PSD and SR recovery were analysed. Testosterone continued to fall during the sleep deprivation period in a time-dependent manner in both the younger （P=-0.001, correlation coefficient r=-0.651） and elder groups （P=0.001, correlation coefficient r=-0.840）. The elder group showed a significantly lower level of testosterone compared with the younger group after PSD. Upon SR after 3 days of PSD, the testosterone level continued to rise for 5 days after sleep recovery in the younger group （P=0.013）, whereas testosterone concentrations failed to recover until day 5 in the elder group. PSD caused a more detrimental effect on serum testosterone in the elder group compared to the younger group with respect to decreases in luteinizing hormone （LH） levels. The replenishment of serum testosterone level was prohibited in the elder group suggesting that the effects of SD/SR may be age-dependent. The mechanism by which SD affects serum testosterone and how age may modify the process are still unclear.

Progressive paradoxical sleep deprivation impairs partial memory following learning tasks in rats

BACKGROUND： Complex learning tasks result in a greater number of paradoxical sleep phases, which can improve memory. The effect of paradoxical sleep deprivation, induced by ＂flower pot＂ technique, on spatial reference memory and working memory require further research. OBJECTIVE： To observe the effect of progressive paradoxical sleep deprivation in rats, subsequent to learning, on memory using the Morris Water Maze. DESIGN, TIME AND SETTING： Controlled observation experiment. The experiment was performed at the Laboratory of Neurobiology, Department of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Lanzhou University from December 2006 to October 2007. MATERIALS： Twenty-eight, male, Wistar rats, 3-4 months old, were provided by the Experimental Animal Center of Lanzhou University. The Morris Water Maze and behavioral analyses system was purchased from Genheart Company, Beijing, China. METHODS： All animals, according to a random digits table, were randomly divided into paradoxical sleep deprivation, tank control, and home cage control groups. Paradoxical sleep deprivation was induced by the ＂flower pot＂ technique for 72 hours, housing the rats on small platforms over water. Rats in the ＂tank control＂ and ＂home cage control＂ groups were housed either in a tank with large platforms over the water or in normal cages without paradoxical sleep deprivation. MAIN OUTCOME MEASURES： Morris Water Maze was employed for task learning and spatial memory testing. Rats in all groups were placed at six random starting points each day for four consecutive days. Each placement was repeated for two trials; the first trial represented reference memory and the second working memory. Rats in the first trial were allowed to locate the submerged platform within 120 seconds. Data, including swimming distance, escape latency, swimming velocity, percentage of time in correct quarter, and memory scores were recorded and analyzed automatically by behavioral analyses systems for Morris Water Maze. RESULTS： Twenty-eight rats were included in the final analysis, without any loss. In the first trial, between day 2 and 4, escape latency and swimming distance increased significantly in the paradoxical sleep deprivation group compared to the home cage control and tank control groups （P 〈 0.01）; percentage of time in correct quarter and memory scores, however, decreased in the paradoxical sleep deprivation group compared to the home cage control and tank control groups （P 〈 0.01）. The escape latency, swimming distance, percentage of time in correct quarter, and memory scores in the second trial was not significantly different among the three groups （P 〉 0.05）. CONCLUSION： Paradoxical sleep deprivation inhibits spatial reference memory, but not working memory.

Maternal sleep deprivation induces gut microbial dysbiosis and neuroinflammation in offspring rats

Maternal sleep deprivation(MSD)is a global public health problem that affects the physical and mental development of pregnant women and their newborns.The latest research suggests that sleep deprivation(SD)disrupts the gut microbiota,leading to neuroinflammation and psychological disturbances.However,it is unclear whether MSD affects the establishment of gut microbiota and neuroinflammation in the newborns.In the present study,MSD was performed on pregnant SpragueDawley rats in the third trimester of pregnancy(gestational days 15-21),after which intestinal contents and brain tissues were collected from offspring at different postnatal days(P1,P7,P14,and P56).Based on microbial profiling,microbial diversity and richness increased in pregnant rats subjected to MSD,as reflected by the significant increase in the phylum Firmicutes.In addition,microbial dysbiosis marked by abundant Firmicutes bacteria was observed in the MSD offspring.Furthermore,quantitative real-time polymerase chain reaction(q RT-PCR)and enzyme-linked immunosorbent assay(ELISA)showed that the expression levels of proinflammatory cytokines interleukin 1β(IL-1β)and tumor necrosis factorα(TNF-α)were significantly higher in the MSD offspring at adulthood(P56)than in the control group.Through Spearman correlation analysis,IL-1βand TNF-αwere also shown to be positively correlated with Ruminococcus_1 and Ruminococcaceae_UCG-005 at P56,which may determine the microbiota-host interactions in MSDrelated neuroinflammation.Collectively,these results indicate that MSD changes maternal gut microbiota and affects the establishment of neonatal gut microbiota,leading to neuroinflammation in MSD offspring.Therefore,understanding the role of gut microbiota during physiological development may provide potential interventions for cognitive dysfunction in MSD-impacted offspring.

Effects of sleep deprivation on cognitive functions

Sleep deprivation （SD） is a common condition that afflicts many people in modem life. Deficits in daytime perfor- mance due to SD are experienced universally. Recent evidence indicates that SD causes impairments in cognitive functions. However, the mechanisms that SD impairs cognitive functions are not clear. This review will focus on the behavioral and neural effects of SD with the aim to elucidate the possible mechanisms of SD-induced deterioration in cognitive functions and to identify directions for future research.

Melatonin modulates adiponectin expression on murine colitis with sleep deprivation

AIM To determine adiponectin expression in colonic tissue of murine colitis and systemic cytokine expression after melatonin treatments and sleep deprivation.METHODS The following five groups of C57BL/6 mice were used in this study:(1) group Ⅰ,control;(2) group Ⅱ,2% DSS induced colitis for 7 d;(3) group Ⅲ,2% DSS induced colitis and melatonin treatment;(4) group Ⅳ,2% DSS induced colitis with sleep deprivation(SD) using specially designed and modified multiple platform water baths; and(5) group V,2% DSS induced colitis with SD and melatonin treatment. Melatonin(10 mg/kg) or saline was intraperitoneally injected daily to mice for 4 d. The body weight was monitored daily. The degree of colitis was evaluated histologically after sacrificing the mice. Immunohistochemical staining and Western blot analysis was performed using anti-adiponectin antibody. After sampling by intracardiac punctures,levels of serum cytokines were measured by ELISA. RESULTS Sleep deprivation in water bath exacerbated DSS induced colitis and worsened weight loss. Melatonin injection not only alleviated the severity of mucosal injury,but also helped survival during stressful condition. The expression level of adiponectin in mucosa was decreased in colitis,with the lowest level observed in colitis combined with sleep deprivation. Melatonin injection significantly(P < 0.05) recovered the expression of adiponectin. The expression levels of IL-6 and IL-17 were increased in the serum of mice with DSS colitis but decreased after melatonin injection. CONCLUSION This study suggested that melatonin modulated adiponectin expression in colonic tissue and melatonin and adiponectin synergistically potentiated antiinflammatory effects on colitis with sleep deprivation.

Role of Cannabinoid CB1 Receptor in Object Recognition Memory Impairment in Chronically Rapid Eye Movement Sleep-deprived Rats

Objective We aimed to investigate whether antagonism of the cannabinoid CB1 receptor(CB1R)could affect novel object recognition(NOR)memory in chronically rapid eye movement sleep-deprived(RSD)rats.Methods The animals were examined for recognition memory following a 7-day chronic partial RSD paradigm using the multiple platform technique.The CB1R antagonist rimonabant(1 or 3 mg/kg,i.p.)was administered either at one hour prior to the sample phase for acquisition,or immediately after the sample phase for consolidation,or at one hour before the test phase for retrieval of NOR memory.For the reconsolidation task,rimonabant was administered immediately after the second sample phase.Results The RSD episode impaired acquisition,consolidation,and retrieval,but it did not affect the reconsolidation of NOR memory.Rimonabant administration did not affect acquisition,consolidation,and reconsolidation;however,it attenuated impairment of the retrieval of NOR memory induced by chronic RSD.Conclusions These findings,along with our previous report,would seem to suggest that RSD may affect different phases of recognition memory based on its duration.Importantly,it seems that the CB1R may,at least in part,be involved in the adverse effects of chronic RSD on the retrieval,but not in the acquisition,consolidation,and reconsolidation,of NOR memory.

G-protein coupled receptors and synaptic plasticity in sleep deprivation

Insufficient sleep has been correlated to many physiological and psychoneurological disorders.Over the years,our understanding of the state of sleep has transcended from an inactive period of rest to a more active state involving important cellular and molecular processes.In addition,during sleep,electrophysiological changes also occur in pathways in specific regions of the mammalian central nervous system(CNS).Activity mediated synaptic plasticity in the CNS can lead to long-term and sometimes permanent strengthening and/or weakening synaptic strength affecting neuronal network behaviour.Memory consolidation and learning that take place during sleep cycles,can be affected by changes in synaptic plasticity during sleep disturbances.G-protein coupled receptors(GPCRs),with their versatile structural and functional attributes,can regulate synaptic plasticity in CNS and hence,may be potentially affected in sleep deprived conditions.In this review,we aim to discuss important functional changes that can take place in the CNS during sleep and sleep deprivation and how changes in GPCRs can lead to potential problems with therapeutics with pharmacological interventions.

Effects of 72 Hours Sleep Deprivation on Liver Circadian Clock Gene Expression and Oxidative Stress in Rats

Objective: To investigate the effects of 72 hours continuous sleep deprivation (SD) on circadian clock gene expression and oxidative stress in the rat liver. Methods: Twenty healthy male Sprague-Dawley rats were divided into 2 groups (n = 10 each) using a random number table: normal control group (group C), sleep deprivation group (group SD). Group SD was treated with a modified multiple platform water environment method. After 72 hours sleep deprived, the levels of AST (Aspartate transaminase ) and ALT (Alanine aminotransferase) in serum were determined. The contents of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the liver tissue of the rats were examined in both two groups. The expression levels of CLOCK, BMAL1 and CRY1 protein in liver tissue were examined by Western blotting. Results: Compared with group C, the content of MDA, and the levels of AST and ALT in serum were significantly increased (P Conclusion: 72 hours continuous sleep deprivation can downregulate the expression of circadian clock gene and promote oxidative stress in rats.

Melatonin modifies SOX2^+ cell proliferation in dentate gyrus and modulates SIRT1 and MECP2 in long-term sleep deprivation

Melatonin is a pleiotropic molecule that,after a short-term sleep deprivation,promotes the proliferation of neural stem cells in the adult hippocampus.However,this effect has not been observed in long-term sleep deprivation.The precise mechanism exerted by melatonin on the modulation of neural stem cells is not entirely elucidated,but evidence indicates that epigenetic regulators may be involved in this process.In this study,we investigated the effect of melatonin treatment during a 96-hour sleep deprivation and analyzed the expression of epigenetic modulators predicted by computational text mining and keyword clusterization.Our results showed that the administration of melatonin under sleep-deprived conditions increased the MECP2 expression and reduced the SIRT1 expression in the dentate gyrus.We observed that let-7 b,mir-132,and mir-124 were highly expressed in the dentate gyrus after melatonin administration,but they were not modified by sleep deprivation.In addition,we found more Sox2^+/5-bromo-2’-deoxyuridine(BrdU)^+cells in the subgranular zone of the sleep-deprived group treated with melatonin than in the untreated group.These findings may support the notion that melatonin modifies the expression of epigenetic mediators that,in turn,regulate the proliferation of neural progenitor cells in the adult dentate gyrus under long-term sleep-deprived conditions.All procedures performed in this study were approved by the Animal Ethics Committee of the University of Guadalajara,Mexico(approval No.CI-16610)on January 2,2016.

Twenty-Hour Sleep Deprivation Does Not Affect Perceived Vection Strength

We examined the effect of sleep deprivation on self-motion perception (vection). We measured the strength of vection, its latency, and its duration in two conditions: Sleep-Deprivation and Normal-Sleep (by using the between-subject design). For the Sleep-Deprivation condition, participants did not sleep for about 20 hours. We also recorded subjective sleepiness with a subjective rating scale that was filled out by the participants. Results showed that vection strength did not differ between the two conditions. Sleep deprivation did not have any clear effect on vection. As expected, subjective sleepiness significantly increased following sleep deprivation. Further, subjective sleepiness significantly correlated with vection latency and duration only in the Normal-Sleep condition. Vection was immune to sleep deprivation. We conclude that when people are not deprived of sleep, sleepiness can enhance the perceived strength of vection.

Sleep Deprivation Affects Working Memory in Low but Not in High Complexity for the N-Back Test

Sleep clearly influences learning and memory since sleep deprivation and stress impairs both cognitive processes. Working memory is an essential cognitive process and refers to a short-term holding of incoming information required to update the long-term mnemonic storage and to manipulate new elements in order to solve problems and make decisions. Nevertheless, the influence of sleep deprivation on working memory has scarcely been studied. In this study we evaluated working memory using the N-back test after increasing periods of wakefulness. Healthy young males were kept awake for 36 hours and the two N-back tasks with low (1-Back) and high (3-Back) levels of complexity were applied every 6 hours. Additionally, salivary cortisol was determined along the study. Unlike the control non-deprived participants, the sleep deprived volunteers showed a significant decrease in their efficiency to solve the 1-Back task after 24 hours of sleep deprivation. However, no differences were observed after 30 and 36 hours of sleep deprivation. Concerning the 3-Back task no differences were observed after sleep deprivation. Regarding reaction time, the deprived group manifested slower responses for the 1-Back task and for the 3-Back task after 30 hours and 36 hours of sleep deprivation, respectively. Cortisol levels presented the normal daily oscillation and no differences were observed between groups. This data suggests that sleep deprivation affects basal states of attention instead of working memory while performing simple tasks. The impact of sleep deprivation on the cognitive performance depends on the moment of day when the task is applied and the complexity of the tests used to assess these mnemonic skills.

The Effects of Sleep Deprivation on the Biophysical Properties of Facial Skin

Lack of sleep is a problem in today’s society, and many people are concerned about changes in their outward appearance due to lack of sleep. People generally come up with some noticeable skin attributes as symptoms of sleep deficiency including rough, dull, and dry skin as well as droopy eyelids and dark eye circles. Several previous reports also suggested that poor sleep could affect the skin condition. The purpose of this study was to evaluate the effect of one night of sleep deprivation on various skin biophysical properties. Twenty four healthy females participated in a study of one night of sleep deprivation. Subjects were kept awake for one night in a laboratory with controlled temperature and relative humidity. The skin condition of each subject was evaluated after normal sleep pattern and after one night of sleep deprivation. The measured skin biophysical parameters included transepidermal water loss, facial pore size, and skin tone, hydration, elasticity, desquamation, translucency, and blood flow. The cheek, eye, and lip areas were evaluated. After one night of sleep deprivation, multiple skin biophysical parameters showed changes when compared to the baseline measurements. A significant decrease in skin hydration and impaired barrier function were observed (p < 0.05). Decreased hydration led to decreased skin elasticity and translucency and increased skin scaling (p < 0.05). Facial pores were more conspicuous, and skin lightness decreased significantly (p < 0.05). Furthermore, skin blood flow decreased prominently (p < 0.05). The results demonstrated that the skin features that are recognized as symptoms of sleep deficiency actually showed remarkable differences after a period of sleep deprivation, and some of these features were confirmed in the eye, lip, as well as the cheek areas. This study revealed a significant association between sleep deprivation and skin biophysical properties by scientific measuring.

Correlation between interaction anxiousness and sleep deprivation among undergraduate students

Sleep deprivation is a common problem among university students,it causes lowered cognitive skills,higher tend of suicide,risk-taking behavior and interaction anxiety.By using the Pittsburgh sleep quality index(PSQI)and Interaction Anxiousness Scale(IAS),the survey on the sleep quality and interaction anxiousness was carried out among 124 undergraduate students,in order to found the correlation between sleep deprivation and interaction anxiousness.The results showed a strong positive correlation between them.This study also investigates the difference of PSQI and IAS among students with varied disciplines and grades,and findings illustrated a poor sleep quality as well as poor interpersonal communication situation among university students.

The Role of Sleep Deprivation in Arrhythmias

Sleep is essential to the normal psychological and physiological activities of the human body.Increasing evidence indicates that sleep deprivation is associated with the occurrence,development,and poor treatment effects of various arrhythmias.Sleep deprivation affects not only the peripheral nervous system but also the central nervous system,which regulates the occurrence of arrhythmias.In addition,sleep deprivation is associated with apoptotic pathways,mitochondrial energy metabolism disorders,and immune system dysfunction.Although studies increasingly suggest that pathological sleep patterns are associated with various atrial and ventricular arrhythmias,further research is needed to identify specific mechanisms and recommend therapeutic interventions.This review summarizes the findings of sleep deprivation in animal experiments and clinical studies,current challenges,and future research directions in the field of arrhythmias.