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Repeated nicotine administration has been associated with increased paradoxical sleep in rats and antinociceptive properties, whereas paradoxical sleep deprivation (PSD) elicits pronociceptive and inflammatory responses. Thus, we aimed to evaluate the effect of repeated nicotine administration and its withdrawal combined with PSD on pain sensitivity and inflammatory markers. Sixty adult male Wistar rats were subjected to repeated injections of saline (SAL) or nicotine (NIC) for 12 days or 7 days of nicotine followed by acute mecamylamine administration on day 8 to precipitate nicotine abstinence (ABST). On day 9, the animals were submitted to PSD for 72 h or remained in control condition (CTRL); on day 12, thermal pain threshold was assessed by the hot plate test. PSD significantly decreased the latency to paw withdrawal in all groups compared to their respective controls. ABST-PSD animals presented higher levels of interleukin (IL)-6 compared to all groups, except ABST-CTRL. After adjustment for weight loss, IL-6, IL-4 and tumor necrosis factor alpha, ABST-PSD was associated with the lowest pain threshold. Nicotine and IL-4 levels were predictors of higher pain threshold. Hyperalgesia induced by PSD prevailed over the antinociceptive action of nicotine, while the association between PSD and ABST synergistically increased IL-6 concentrations and decreased pain threshold.

Purpose A role for circadian rhythm abnormalities in the pathogenesis of bipolar disorder (BD) has been suggested. The present study assessed circadian preference, a subjective preference for activities in the morning or evening related to chronotype. Methods The sample was comprised of 81 outpatients with BD in remission and 79 control subjects. Circadian preference was derived from an interview evaluating biological rhythms and sleep pattern from the Pittsburgh Sleep Quality Index. Results Patients were significantly more likely to have an evening preference than control subjects. Circadian preference was also associated with sleep latency. Conclusions The association of evening preference and longer sleep latency may be related to the frequent clinical observation of a sleep/wake cycle reversal in bipolar disorder.

the accumulation of visceral fat in kidney disease. The rise in obesity may result, at least in part, from changes in lifestyle, currently characterized by sedentary, poor eating, and sleep habits. The reduction in sleep duration is known to predispose individuals to obesity by increasing the white adipose tissue deposits such as visceral fat.4,5 Of note, obesity and visceral fat accumulation are etiopathological factors for both chronic kidney disease (CKD) and sleep disorders.6,7 View the original paper by Xu et al

Pogo transposable element-derived protein with ZNF domain (POGZ) gene encodes a chromatin regulator and rare variants on this gene have been associated with a broad spectrum of neurodevelopmental disorders, such as White-Sutton syndrome. Patient clinical manifestations frequently include developmental delay, autism spectrum disorder and obesity. Sleep disturbances are also commonly observed in these patients, yet the biological pathways which link sleep traits to the POGZ-associated syndrome remain unclear. We screened for sleep implications among individuals with causative POGZ variants previously described. Sleep disturbances were observed in 52% of patients, and being obese was not observed as a risk factor for sleep problems. Next, we identified genes associated with sleep-associated traits among the POGZ regulatory targets, aiming to uncover the molecular pathways that, when disrupted by POGZ loss of function, contribute to the aetiology of sleep phenotypes in these patients. The intersect between POGZ targets and sleep-related genes was used in a pathway enrichment analysis. Relevant pathways among these overlapping genes are involved in the regulation of circadian rhythm, tau protein binding, ATPase activator activity. This study may represent the beginning for novel functional investigations on shared molecular mechanisms between sleep disturbances and rare developmental syndromes related to POGZ and its regulatory targets.

Introduction There are reports of non-medical use of clonazepam, a benzodiazepine, after cocaine consumption in order to ameliorate cocaine side-effects. The potential impact of this combination on health is still scarcely studied, however. We aimed at evaluating the effects of cocaine and clonazepam association on behavior and sleep in male Wistar rats. Methods Animals were allocated in 4 treatment groups: CTRL group (1 ml/kg saline); COC group (7mg/kg cocaine); CLN group (1.25 mg/kg clonazepam) and COCCLN group (7mg/kg cocaine and, after a 1-hour interval, 1.25 mg/kg clonazepam). Animals received intraperitoneal injections according to their group for 16 days. Acute sleep recording was performed for 24 hours following the first injection, during light and dark phases, using cortical electrodes implanted through stereotaxic surgery. Open field and elevated-plus maze tests were performed in the day after treatment was ended, for evaluation of behavioral effects. Results In the light phase of the acute sleep recording, paradoxical sleep was significantly decreased in COCCLN rats, compared to CTRL animals. Paradoxical sleep onset latency was significantly increased in COC and COCCLN groups, compared to CTRL rats. In the dark phase, paradoxical sleep was significantly increased in these same groups, compared to controls. Regarding behavioral tests, COCCLN rats presented a reduction in peripheral squares crossed in open field, and a decrease in the number of risk assessment episodes in the elevated-plus maze. Conclusion Cocaine and clonazepam association caused a significant impact in paradoxical sleep in rats. These results suggest that sleep impairment is a possible outcome from this substance combination. Behavioral test results suggest increase in impulsivity and decrease in exploratory behavior. These effects might indicate appearance of withdrawal symptoms after treatment ceased. Support (If Any) Our studies are supported by Associação Fundo de Incentivo à Pesquisa (AFIP) and Conselho Nacional de Desenvolvimento Científico Tecnológico (CNPq - Grant #133397/2017-3); J.C.F.G., S.T. and M.L.A. received CNPq fellowships.

Introduction Sleep disorders are associated with various human pathologies and interfere with biological processes essential for health and quality of life. On the other hand, cancer is one of the most common diseases worldwide with an average of 1,500 deaths per day in the USA. Is there a factor common to both sleep disorders and cancer that serves to link these conditions? Discussion It is a normal process for cellular metabolism to produce reactive oxidant series (ROS). However, when the production of ROS overcomes the antioxidant capacity of the cell to eliminate these products, the resulting state is called oxidative stress. Oxidative DNA damage may participate in ROS-induced carcinogenesis. Moreover, ROS are also produced in the sleep deprivation process. The aim of this article is to review pathways and mechanisms that may point to oxidative stress as a link between sleep deprivation and cancer.

Since the beginning of the COVID-19 pandemic, older adults have been found to be a highly vulnerable group, with a higher prevalence of severe cases and negative outcomes. Research has focused on the reasons why older adults are at greater risk; Sleep-related factors have been suggested as one possible explanation for this. An individual’s sleep pattern undergoes significant changes over the course of their life. In older adults a specific sleep profile can be observed, one characterized by advanced sleep timing, a morningness preference, longer sleep-onset latency, shorter overall sleep duration, increased sleep fragmentation, reduced slow-wave sleep and, increased wake time after sleep onset. Additionally, an increased prevalence of sleep disorders can be observed, such as obstructive sleep apnea and insomnia. Previous research has already linked sleep disorders (especially sleep apnea) with COVID-19, but few studies have focused specifically on the older population. We believe that the intrinsic sleep patterns of older adults, and the prevalence of sleep disorders in this population, may be important factors that could explain why they are at a greater risk of negative COVID-19 outcomes. In this review, we discuss the relationship between sleep and COVID-19 among older adults, focusing on three different aspects: (1) Sleep-related issues that might increase the likelihood of getting infected by SARS-COV-2; (2) Sleep disturbances that might increase the predisposition to worse COVID-19 prognosis and outcomes; and (3) COVID-19-related aspects affecting community-dwelling older adults, such as social isolation, quarantine, and home confinement, among others, that might impact sleep.

Poor sleep is a risk factor for falling among older adults. This study aimed to investigate whether poor sleep quality and excessive daytime sleepiness in older people was associated with fear of falling. Participants aged 60 years or older were interviewed, with those who did not have preserved cognitive skills being excluded. Data on age, gender, body mass index, alcohol consumption, mental status, depression, excessive daytime sleepiness, sleep quality, comorbidities and fear of falling were collected. Univariate and multivariate linear regression were conducted. The logistic regression assessed the association between daytime sleepiness and fear of falling. The odds of an older adult being afraid of falling was 3 times higher among those with excessive daytime sleepiness, in comparison to those with no excessive daytime sleepiness. The higher the daytime sleepiness, the greater the fear of falling. Health professionals should be aware of older patients’ sleepiness because it can increase fear of falling and influence their treatment.

According to the criteria of the International Classification of Sleep Disorders (ICSD-3), it is estimated that the prevalence of insomnia in the general population varies between 6.6% and 12%. Insomnia is a sleep disturbance related to a reduction in the quality or quantity of satisfactory sleep. Among the available treatments, there are both pharmacological and non-pharmacological approaches. One recent possible non-pharmacological approach that has been suggested is based on the use of probiotics and the gut-brain axis. There has been increasing scientific focus on this area because of the suggested importance of enteric microbiota in relation to many aspects of health. It has been proposed that probiotics can be used to interact with the intestinal environment to benefit individuals suffering from a variety of conditions. In relation to sleep, some studies have indicated that gamma-amino butyric acid (GABA) produced by the intestinal microbiota may influence the central nervous system (CNS) through the vagus nerve and have an influence on sleep. In this sense, Lactobacillus is one of the major GABA producing bacteria in the gut microbiota. Our hypothesis is that supplementation with Lactobacillus as a probiotic might improve sleep pattern and quality, acting as an ally in the treatment of insomnia. In the present study, a search was conducted in Pubmed and Google Scholar databases, looking for articles with themes related to probiotics, intestinal microbiota and sleep. No clinical trials were found that evaluated the effect of probiotics for sleep disorders in humans.Conclusions • Research and clinical use of probiotics have been growing due to their health benefits in several areas. In addition, the use of probiotics for sleep and emotional disorders, such as insomnia, stress, anxiety and depression, is gaining space. This way, future research can help developing complementary treatments for people with insomnia and other sleep disorders.

Rapid eye movements (REM) sleep density is the parameter proposed to explain the variability in the amount of eye movements during REM sleep. Alterations in REM sleep density have been proposed as a screening criterion for individuals with depression and other mental health conditions, but its accuracy has not been properly evaluated. The lack of consensus and the variability of the methods used to score it reduces the external validity of the results, hindering an adequate analysis of its diagnostic accuracy and clinical applicability. This scoping review aimed to identify and quantify the methods used to score REM sleep density, describing their main characteristics. A literature search was conducted in PubMed, Scopus, PsycInfo, and Web of Science. Only studies with objective measures for REM sleep density analysis in individuals with depression were considered eligible. The final sample comprised 57 articles, covering 64 analyses of REM sleep density. The relative frequency methods were the predominant measurement parameter for analyzing REM sleep density across studies. The most frequently adopted REM estimation unit was the number of REM events followed by mini-epochs containing REM. The most common unit of measurement were frequency/time measures. The results demonstrate that there is no consistency in the methods used to calculate REM sleep density in the literature, and a high percentage of studies do not describe their methods in sufficient detail. The most used method was the number of REM episodes per minute of REM sleep, but its use is neither unanimous nor consensual. The methodological inconsistencies and omissions among studies limit the replicability, comparability, and clinical applicability of REM sleep density. Future guidelines should discuss and include a specific methodology for the scoring of REM sleep density, so it can be consensually implemented in clinical services and research.