Sleep plays an important role in maintaining neuronal circuitry, signalling and helps maintain overall health and wellbeing. Sleep deprivation (SD) disturbs the circadian physiology and exerts a negative impact on brain and behavioural functions. SD impairs the cellular clearance of misfolded neurotoxin proteins like α-synuclein, amyloid-β, and tau which are involved in major neurodegenerative diseases like Alzheimer's disease and Parkinson's disease. In addition, SD is also shown to affect the glymphatic system, a glial-dependent metabolic waste clearance pathway, causing accumulation of misfolded faulty proteins in synaptic compartments resulting in cognitive decline. Also, SD affects the immunological and redox system resulting in neuroinflammation and oxidative stress. Hence, it is important to understand the molecular and biochemical alterations that are the causative factors leading to these pathophysiological effects on the neuronal system. This review is an attempt in this direction. It provides up-to-date information on the alterations in the key processes, pathways, and proteins that are negatively affected by SD and become reasons for neurological disorders over a prolonged period of time, if left unattended.Endometrial cancer is one of the most common malignant tumors, lowering the quality of life among women worldwide. Autophagy plays dual roles in these malignancies. To search for prognostic markers for endometrial cancer, we mined The Cancer Genome Atlas and the Human Autophagy Database for information on endometrial cancer and autophagy-related genes and identified five autophagy-related long noncoding RNAs (lncRNAs) (LINC01871, SCARNA9, SOS1-IT1, AL161618.1, and FIRRE). Based on these autophagy-related lncRNAs, samples were divided into high-risk and low-risk groups. Survival analysis showed that the survival rate of the high-risk group was significantly lower than that of the low-risk group. Univariate and multivariate independent prognostic analyses showed that patients' age, pathological grade, and FIGO stage were all risk factors for poor prognosis. A clinical correlation analysis of the relationship between the five autophagy-related lncRNAs and patients' age, pathological grade, and FIGO stage was als serve as novel therapeutic targets and biomarkers. Many doctors ignored the possibility that there is still a spinal cord compression (SCC) need for decompression after atlantoaxial reduction. https://www.selleckchem.com/products/zotatifin.html Reduction can be achieved on kinematic magnetic resonance imaging (MRI); thus, we want to analyze the role of kinematic MRI in reducible atlantoaxial dislocation and make a preoperative decision whether to perform decompression. 36 patients with atlantoaxial reduction on preoperative kinematic MRI in extension postures were enrolled retrospectively. Grouping was based on the condition of SCC after atlantoaxial reduction preoperatively. Group A patients with SCC after atlantoaxial reduction on dynamic cervical MRI were treated with C1 laminectomy for decompression and atlantoaxial fixation. Group B patients with no significant SCC, according to dynamic MRI, underwent only atlantoaxial fixation. Clinical outcomes were evaluated using JOA score for spinal cord function. Radiological outcomes were assessed by measuring spinal cord diameter on MRI. The mean follow-up time was 17.1 months. Postoperative JOA score and percentage of SCC in both groups were significantly better than its preoperative score. There were no significant statistical differences in the JOA score at 12 months after surgery and the JOA improvement rate between two groups. All patients in the two groups had a lower percentage of SCC on preoperative extension MRI, compared with neutral MRI. No significant statistical differences in the spinal decompression improvement rate were observed between the two groups. Decompression should be performed in patients who still have significant SCC on preoperative kinematic MRI. Kinematic MRI could be used to assess SCC and decide whether to perform decompression preoperatively. Decompression should be performed in patients who still have significant SCC on preoperative kinematic MRI. Kinematic MRI could be used to assess SCC and decide whether to perform decompression preoperatively. DNA methylation plays a vital role in prognosis prediction of cancers. In this study, we aimed to identify novel DNA methylation site biomarkers and create an efficient methylated site model for predicting survival in kidney renal papillary cell carcinoma (KIRP). DNA methylation and gene expression profile data were downloaded from The Cancer Genome Atlas (TCGA) database and the Gene Expression Omnibus (GEO) database. Differential methylated genes (DMGs) and differential expression genes (DEGs) were identified and then searched for the hub genes. Cox proportional hazards regression was applied to identify DNA methylated site biomarkers from the hub genes. Kaplan-Meier survival and ROC analyses were used to validate the effective prognostic ability of the methylation gene site biomarker. The biomarker sites were validated in the GEO cohorts. The GO and KEGG annotation was done to explore the biological function of DNA methylated site signature. Nine DMGs with opposite expression patterns containing 47 mel rate and guiding tailored therapy for KIRP patients. Our study demonstrated that the methylated gene site signature might be a powerful prognostic tool for evaluating survival rate and guiding tailored therapy for KIRP patients. Associations between iodine intake and thyroid nodules (TNs) were not consistent. We aimed to illustrate the relationship between urinary iodine concentration (UIC) and TNs. A total of 12,698 participants were enrolled in analysis. All of the participants filled out questionnaires and underwent physical examinations, laboratory tests, and thyroid ultrasonography. UIC, serum thyrotropin (TSH), thyroid peroxidase antibodies (TPOAb), and thyroglobulin antibodies (TgAb) were measured in the central laboratory. The prevalence of TNs was 16.00%, and the median UIC was 206.1  g/L. TNs and UIC were negatively related when UIC was less than 527  g/L (adjusted OR = 0.87; 95% CI, 0.80, 0.94), and the relationship between UIC and TNs was not statistically significant when UIC was greater than 527  g/L (adjusted OR = 1.25; 95% CI, 0.98, 1.60). In women, UIC was negatively associated with risk for TNs (adjusted OR 0.95; 95% CI, 0.91, 0.99). The relationship between TNs and UIC differed between men and women. The risk of TNs decreased with the elevation of UIC in men when UIC was lower than 527  g/L, while UIC and the presence of TNs were negatively correlated in women.