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001). DEX (n = 36) versus NO-DEX (n = 36) group showed longer N2 stage [68.9% (57.5-80.9) versus 49.5% [35.7-61.4]; p  less then  0.0003]; longer Total Sleep Time [6.5 h (5.7-7.7) versus 3.4 h (1.8-4.9); p  less then  0.0001, and higher Sleep Efficiency [84.2% (71.3-92.6) versus 47.7% (23.4-60.9); p  less then  0.0001]; shorter N1 (percentage of Total Sleep Time) [10.5% (7.8-20.0) and 38.8% (25.6-50.3); p  less then  0.0001]; longer N3 stage [13.6% (1.9-23.3) versus 4.3% (0.4-14.0); p = 0.058]; fewer Cortical Arousals [15 episodes/hour (8.1-24.6) versus 48.7 episodes/hour (29.7-80.4); p  less then  0.0001]. The questionnaire showed better values in DEX-group in all explored items (p  less then  0.0001). CONCLUSIONS Abnormal sleep is common in intensive care unit patients who have not received sedation. Dexmedetomidine, titrated to reach an appropriate sedation level, may optimize sleep duration and architecture. OBJECTIVE To assess the independent and combined effects of night sleep duration and sleep quality on depressive symptoms. METHODS A total of 28,202 participants (11,236 males and 16,966 females) aged 18-79 years from the Henan Rural Cohort were included in this study. Night sleep duration and sleep quality were defined by the Pittsburgh Sleep Quality Index (PSQI). Logistic regression and restricted cubic splines were applied to evaluate the association of night sleep duration and sleep quality with depressive symptoms. RESULTS A U-shaped dose-response relationship between night sleep duration and depressive symptoms along with a J-shaped relationship between sleep quality and depressive symptoms were observed. Compared with reference group (7- less then 8 h), shorter sleep duration ( less then 6 h) and longer sleep duration (≥10 h) were associated with increased risk of depressive symptoms in males (short sleep Odds Ratio (OR) = 1.84, 95% confidence interval (CI), 1.34-2.52; long sleep OR = 1.56, 95% CI, 1.01-2.42) and females (short sleep OR = 2.19, 95% CI, 1.77-2.70; long sleep OR = 1.51, 95% CI, 1.10-2.10). Compared with good sleepers, poor sleepers had 4.23-fold (95% CI3.54-5.06) and 3.87-fold (95% CI 3.41-4.40) increased odds of depressive symptoms in males and females. Furthermore, participants with longer night sleep duration (≥10 h) and poorer sleep quality had the strongest effect on depressive symptoms (males OR = 6.64, 95% CI, 3.21-13.74; females OR = 7.76, 95% CI, 5.00-12.02). CONCLUSIONS Extreme night sleep duration and poor sleep quality were independently and combinedly related to elevated depressive symptoms, suggesting that keeping optimal night sleep duration and good sleep quality maybe benefit for maintaining mental health. TRIAL REGISTRATION Chinese Clinical Trial Register. Registration number ChiCTR-OOC-15006699. OBJECTIVES To investigate the relationship between the lesion location and post-stroke restless legs syndrome (RLS). METHODS A total of 376 patients with acute cerebral infarction were recruited from Tangshan Gongren Hospital, Department of Neurology between May 2016 and May 2017, all of whom were evaluated for RLS. Established RLS was diagnosed according to the criteria of the International Restless Legs Syndrome Study Group (IRLSSG) in 2012. Neurological functions were assessed according to the National Institutes of Health Stroke Scale (NIHSS). The lesion location was evaluated with magnetic resonance imaging (MRI). learn more The associations between the lesion location and post-stroke RLS were then analyzed by logistic regression. RESULTS A total of 49 patients (13.03%) had RLS. The multivariate logistic regression model adjusting for post-stroke RLS risk factors including gender, age, history of hypertension, history of diabetes, history of stroke, smoking, drinking, body mass index (BMI), NIHSS, hemoglobin, platelet and homocysteine determined that body of caudate nucleus and pontine were significantly associated with post-stroke RLS with odds ratio (OR) of 26.26 (95% confidence interval (CI) 9.41-73.28,p  less then  0.001) and OR of 4.37 (95% CI 1.24-15.34, p = 0.021). The stepwise logistic regression model with temporal lobe, parietal lobe, occipital lobe, frontal lobe, callosum, body of caudate nucleus, thalamus, lenticulo capsule, corona radiata, centrum semi-ovale and pontine as potential predictors yielded a predictor mode. The stepwise logistic regression predictor mode indicated that body of caudate nucleus and pontine predicted post-stroke RLS with similar OR to multivariate models of 23.61 (95% CI 9.53-58.51, p  less then  0.001) and 4.46 (95% CI 1.38-14.4, p = 0.012). CONCLUSIONS The ischemic infarcts located in body of caudate nucleus, pontine are significantly associated with post-stroke RLS. Body of caudate nucleus acute infarcts may play a role in the development of post-stroke RLS. INTRODUCTION Immune-related hepatitis (ir-hepatitis) is a common side-effect of checkpoint inhibitors (CPIs). Here, we characterise ir-hepatitis in a large cohort of patients with metastatic melanoma (MM) treated with CPIs and describe potential risk factors and efficacy of medical management. METHODS The retrospective study included a large cohort of patients with MM treated with CPIs between 2010 and 2019. Patients were retrieved from the national Danish Metastatic Melanoma Database. RESULTS Five hundred twenty one patients were included. Ir-hepatitis was found in 6.8% of patients. Combination therapy was associated with a significantly greater risk than monotherapy. Of all patients, 34.9% with hepatitis had a different hepatitis grading, when based on either alanine transaminase (ALT) or aspartate transaminase (AST) levels. Of all patients, 72.1% with hepatitis received steroid treatment, and two patients received additional second-line immunosuppressants. Of all patients, 35.5% experienced hepatitis relapse during steroid tapering. Of all patients, 18.6% and 25% of patients with grade ≥2 and ≥ III3, respectively, developed hepatitis within 7 days after finishing an antibiotic treatment for infection. Patients (62.5%) who received a cumulative dose of >4000 mg steroid experienced cancer progression, compared with 22.7% of patients treated with less then 4000 mg. CONCLUSION Several observations of clinical importance were made. Infection and antibiotic treatment during CPIs could be a possible risk factor for developing ir-hepatitis. Severity of ir-hepatitis is potentially underestimated in a significant number of patients, if only one liver enzyme is measured. The role of second-line immunosuppressants needs to be further investigated because of the high risk of hepatitis relapse during steroid tapering and the potential negative impact of cumulative steroid dose on response to CPIs.