Insufficient sleep on weekdays has become a societal norm, and studies have shown that sleep deprivation increases the risk of depression. Although individuals often resort to weekend catch-up sleep (CUS) as a compensatory measure, the present evidence supporting its efficacy in mitigating the risk of depression is limited. This article attempts to explore the relationship between CUS and depression. In this study, a total of 5510 participants were included, characterized into two groups: nondepressed (n =5051) and depressed (n =459), with data extracted from the National Health and Nutrition Examination Survey (NHANES). Compared with people without CUS, those practicing CUS exhibited a significantly lower risk of depression (OR =0.81, P =0.048). In subgroup analysis, this reduction effect was only observed in males (OR =0.70, 95% CI 0.05 to 0.99, P =0.04), middle-aged (>40, ≤ 60) (OR: 0.57, 95% CI: 0.40 to 0.81, P =0.002), married or living with parents (OR: 0.61, 95% CI: 0.44 to 0.86, P =0.004), groups with three or more family members (OR: 0.69, 95% CI: 0.52 to 0.93, P =0.01), and individuals without alcohol intake (OR: 0.24,95% CI: 0.09 to 0.67, P =0.006). Therefore, in the realm of depression treatment, doctors may consider advising patients to get adequate sleep on weekends as part of their overall treatment plan. At the same time, individuals can also choose weekend sleep as a proactive strategy for regulating their psychological status.

Background:Osteoarthritis (OA) is a leading cause of disability, affecting millions worldwide. Emerging evidence suggests that sleep behaviors, particularly weekend catch-up sleep (WCS), may influence OA risk, though research on this association is limited.Methods:Data from the National Health and Nutrition Examination Survey (NHANES) 2017-2020 were analyzed, including 7,059 adults aged 20 and older. Weighted logistic regression models adjusted for demographic and lifestyle factors were used to examine the relationship between WCS and OA.Results:Among the participants, those with short (OR = 0.85, 95% CI 0.75-0.95), moderate (OR = 0.78, 95% CI 0.69-0.89), and long (OR = 0.80, 95% CI 0.71-0.90) WCS durations demonstrated a significantly lower prevalence of OA compared to those without WCS. The protective effect of WCS was consistent across all adjusted models. Subgroup analyses showed that this inverse association was robust across various age groups, genders, races, education levels, marital statuses, poverty income ratios (PIR), and workday sleep durations.Conclusions:This study found that weekend catch-up sleep is inversely associated with the prevalence of osteoarthritis. Adequate weekend catch-up sleep may play a role in reducing the risk of OA. These findings suggest that improving sleep patterns could be a potential strategy for OA prevention.

Objective Previous studies have reported contradictory findings regarding the relationship between obstructive sleep apnea (OSA) and abnormal brain morphology. Furthermore, the causal relationship between OSA and brain morphology has not been clearly established. The aim of this study was to utilize Mendelian randomization (MR) analysis to investigate the impact of obstructive sleep apnea (OSA) on brain morphology and determine its potential causal relationship. Methods Firstly, the inverse-variance weighted (IVW) method was employed to assess the causal effects of OSA on cortical surface area and brain structure volume. Additionally, two additional MR methods, namely weighted median and MR-Egger, were used to supplement the results from IVW. Subsequently, a reverse MR analysis was conducted to determine the direction of causality. Furthermore, sensitivity analyses were performed including Cochrane's Q test, MR-Egger intercept test, MR-PRESSO global test, and leave-one-out analysis. Results The results of the study showed that OSA patients had a tendency towards decreased cortical surface area and hippocampal volume in the precuneus region compared to individuals without OSA, while the superior temporal cortical surface area showed an increase. The results from the weighted median and MR-Egger analyses were consistent with those from the IVW analysis. Sensitivity tests confirmed the reliability of the causal estimates. Conclusions This study provides preliminary evidence of an association between OSA and brain structure using large-scale genome-wide association data. The results demonstrate that OSA is associated with changes in brain structure. Therefore, individuals with OSA should be vigilant about the risks of related diseases due to alterations in brain tissue.

Epilepsy is a group of enduring neurological disorder characterized by spontaneous and recurrent seizures with heterogeneous etiology, clinical expression, severity, and prognosis. Growing body of research investigates that epileptic seizures are originated from neuronal synchronized and excessive electrical activity. However, the underlying molecular mechanisms of epileptogenesis have not yet been fully elucidated and 30% of epileptic patients still are resistant to the currently available pharmacological treatments with recurrent seizures throughout life. Over the past two decades years accumulated evidences provide strong support to the hypothesis that neuroinflammation, including microglia and astrocytes activation, a cascade of inflammatory mediator releasing, and peripheral immune cells infiltration from blood into brain, is associated with epileptogenesis. Meanwhile, an increasing body of preclinical researches reveal that the anti-inflammatory therapeutics targeting crucial inflammatory components are effective and promising in the treatment of epilepsy. The aim of the present study is to highlight the current understanding of the potential neuroinflammatory mechanisms in epileptogenesis and the potential therapeutic targets against epileptic seizures.

Objective:Restoration of blood circulation within "time window" is the principal treating goal for treating acute ischemic stroke.Previous studies revealed that delayed recanalization might cause serious ischemia/reperfusion injury.However,plenty of evidences showed delayed recanalization improved neurological outcomes in acute ischemic stroke.This study aims to explore the role of delayed recanalization on blood-brain barrier(BBB)in the penumbra(surrounding ischemic core)and neurological outcomes after middle cerebral artery occlusion(MCAO).Methods:Recanalization was performed on the 3rd day after MCAO.BBB disruption was tested by Western blotting,Evans blue dye,and immunofluorescence staining.Infarct volume and neurological outcomes were evaluated on the 7th day after MCAO.The expression of fibroblast growth factor 21(FGF21),fibroblast growth factor receptor 1(FGFR1),phosphatidylinositol-3-kinase(PI3K),and serine/threonine kinase(Akt)in the penumbra were observed by immunofluorescence staining and/or Western blotting.Results:The extraversion of Evans blue,IgG,and albumin increased surrounding ischemic core after MCAO,but significantly decreased after recanalization.The expression of Claudin-5,Occludin,and zona occludens 1(ZO-1)decreased surrounding ischemic core after MCAO,but significantly increased after recanalization.Infarct volume reduced and neurological outcomes improved following recanalization(on the 7th day after MCAO).The expressions of Claudin-5,Occludin,and ZO-1 decreased surrounding ischemic core following MCAO,which were up-regulated corresponding to the increases of FGF21,p-FGFR1,PI3K,and p-Akt after recanalization.Intra-cerebroventricular injection of FGFR1 inhibitor SU5402 down-regulated the expression of PI3K,p-Akt,Occludin,Claudin-5,and ZO-1 in the penumbra,which weakened the beneficial effects of recanalization on neurological outcomes after MCAO.Conclusion:Delayed recanalization on the 3rd day after MCAO increases endogenous FGF21 in the penumbra and activates FGFR1/PI3K/Akt pathway,which attenuates BBB disruption in the penumbra and improves neurobehavior in MCAO rats.

Background: Temozolomide (TMZ) is generally applied for glioma treatment, while drug resistance of TMZ limits its therapeutic efficacy. Mannose exerts evident anti-tumor effect. We intended to investigate whether mannose enhanced TMZ sensitivity to glioma and examined the underlying mechanism. Methods: MTT and clone formation assays were performed to detect cell viability and proliferation. Cell apoptosis was measured by flow cytometry. The protein and gene expression levels were detected by Western blot and qRT-PCR assays. Xenograft glioma model was established to explore the influence of mannose in vivo. Results: Mannose inhibited glioma cell growth, which was facilitated by knockdown of phosphomannose isomerase (PMI) while reversed by overexpression of PMI. Mannose enhanced the sensitivity of glioma cells to TMZ, indicated by the further inhibited cell viability and colony formation and the aggravated cell apoptosis, which was reversed by overexpression of O6-methylguanine DNA methyltransferase (MGMT). Furthermore, mannose and TMZ inhibited MGMT expression and Wnt/beta-catenin activation. Moreover, activating Wnt/beta-catenin pathway blocked anti-proliferative effect induced by mannose and TMZ, which was further suppressed by overexpressed MGMT. Mannose inhibited glioma growth, suppressed Ki67 and downregulated MGMT and beta-catenin in vivo. Conclusion: Mannose inhibited MGMT to enhance sensitivity of glioma cells to TMZ, with Wnt/beta-catenin pathway involvement. Our data suggested that mannose could be an innovative agent to improve glioma treatment, particularly in TMZ-resistant glioma with high MGMT.

Epilepsy is a common neurological disease that is not always controlled, and the ketogenic diet shows good antiepileptic effects drug-resistant epilepsy or seizures caused by specific metabolic defects via regulating the metabolism. The brain is a vital organ with high metabolic demands, and epileptic foci tend to exhibit high metabolic characteristics. Accordingly, there has been growing interest in the relationship between brain metabolism and epilepsy in recent years. To date, several new antiepileptic therapies targeting metabolic pathways have been proposed (i.e., inhibiting glycolysis, targeting lactate dehydrogenase, and dietary therapy). Promising strategies to treat epilepsy via modulating the brain's metabolism could be expected, while a lack of thorough understanding of the role of brain metabolism in the control of epilepsy remains. Herein, this review aims to provide insight into the state of the art concerning the brain's metabolic patterns and their association with epilepsy. Regulation of neuronal excitation via metabolic pathways and antiepileptic therapies targeting metabolic pathways are emphasized, which could provide a better understanding of the role of metabolism in epilepsy and could reveal potential therapeutic targets.

目的 分析性早熟住院患儿的临床资料,提高对该疾病的认识及诊治水平.方法 回顾2014年1月至2018年12月湘雅三医院26例性早熟住院患儿的一般资料、检验、检查及治疗情况,并比较中枢性及外周性性早熟患儿的指标.结果 性早熟患儿的平均就诊年龄6.14岁,从发现第二性征到就诊的平均时间为5.20个月.中枢性性早熟绝大部分为特发性,鞍区磁共振阳性发现率低.外周性性早熟病因有卵巢颗粒细胞瘤或滤泡囊肿、生殖细胞瘤、肾上腺瘤、先天性肾上腺增生.女性中枢性性早熟患儿促黄体生成素(LH)和促卵泡刺激素(FSH)基础平均水平为0.79 IU/L及3.86 IU/L,雌激素平均66.58 pmol/L.促性腺激素释放激素(GnRH)刺激后,LH峰值平均12.55 IU/L,LH峰/FSH峰平均0.96.促甲状腺激素(TSH)、甲状旁腺素(PTH)和生长激素(GH)正常,25羟维生素D3水平偏低.较中枢性性早熟,外周性性早熟患儿的性激素水平显著升高,促性腺激素水平显著减低.结论 性早熟受关注不够,基础LH测定及GnRH刺激试验对筛查及诊断、鉴别儿童性早熟意义重大,而维生素D不足可能与中枢性性早熟有关.