Cell block analysis showed negative staining for CD3 and positive staining for CD20 in large atypical lymphoid cells, suggesting the existence of large B-cell lymphoma. Repeat blood examination showed that the serum sIL-2R level was elevated. We decided to perform biopsy to make the final treatment decision. Histologically, the tumor demonstrated diffuse proliferation of large atypical lymphoid cells. IHC analysis showed CD3(-), CD5(+), and CD20(+). In addition, IHC analysis also showed CD79a(+), CD10(-), bcl-2(+), and cyclin D1(-). The final diagnosis was diffuse large B-cell lymphoma. DISCUSSION AND CONCLUSION Here, we present the case of a patient with ovarian malignant lymphoma that was diagnosed using cell block analysis. OBJECTIVE Bombesin-like receptor 3 (BRS3) is an orphan receptor and Brs3 knockout mice develop obesity with increased food intake and reduced resting metabolic rate and body temperature. The neuronal populations contributing to these effects were examined. METHODS We studied energy metabolism in mice with Cre-mediated recombination causing 1) loss of BRS3 selectively in SIM1- or MC4R-expressing neurons or 2) selective re-expression of BRS3 from a null background in these neurons. RESULTS The deletion of BRS3 in MC4R neurons increased body weight/adiposity, metabolic efficiency, and food intake, and reduced insulin sensitivity. BRS3 re-expression in these neurons caused partial or no reversal of these traits. However, these observations were confounded by an obesity phenotype caused by the Mc4r-Cre allele, independent of its recombinase activity. The deletion of BRS3 in SIM1 neurons increased body weight/adiposity and food intake, but not to the levels of the global null. The re-expression of BRS3 in SIM1 neurons reduced body weight/adiposity and food intake, but not to wild type levels. The deletion of BRS3 in either MC4R- or SIM1-expressing neurons affected body temperature, with re-expression in either population reversing the null phenotype. MK-5046, a BRS3 agonist, increases light phase body temperature in wild type, but not Brs3 null, mice and BRS3 re-expression in either population restored response to MK-5046. CONCLUSIONS BRS3 in both MC4R- and SIM1-expressing neurons contributes to regulation of body weight/adiposity, insulin sensitivity, food intake, and body temperature. Published by Elsevier GmbH.OBJECTIVE/BACKGROUND Sleep disturbances are very common and associated with severe complications in patients admitted to intensive care units (ICU). Commonly, sedatives like propofol or benzodiazepines have been demonstrated to increase sleep duration but worsen sleep architecture. Dexmedetomidine seems to positively affect both sleep aspects. PATIENTS/METHODS The present study aimed to investigate sleep characteristics in non-intubated patients admitted to intensive care unit. The subgroups consisted of those without sedation (NO-DEX), and those which received dexmedetomidine infusion (DEX), titrated to a Richmond Agitation-Sedation Scale target of -1/-2, were also explored. An auto-staged electroencephalographer was used to measure sleep duration and architecture. The Richard-Campbell-Sleep questionnaire was administered to all patients. RESULTS A multivariate analysis conducted in the overall population showed that dexmedetomidine infusion was the only variable independently associated with N2 increase (p  less then  0.001). 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). 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. BACKGROUND In prostate cancer (PCa), lower education level is associated with less screening, more advanced stage at diagnosis and worse survival. The aim of this study was to estimate the association between education level and treatment modality and subsequently survival. METHODS The 9255 men diagnosed with PCa in the Finnish Randomized Study of Screening for Prostate Cancer were included. Cancer stage, comorbidity, education level and primary treatment modality were extracted from the patient records, the Finnish Cancer Registry, Statistics Finland and the National Institute of Health and Welfare, and these covariates were used in logistic regression (treatment selection) and Cox regression (survival analysis). RESULTS In high-risk cancers, men with tertiary education were more likely to be treated with radical prostatectomy (odds ratio [OR] = 1.76; 95% confidence interval [CI] = 1.27-2.44) than men with primary education. Men with secondary (OR = 0.57; 95% CI = 0.38-0.84) or tertiary (OR = 0.42; 95% CI = 0.29-0.60) education were managed less frequently with mere hormonal therapy. In locally advanced cases, tertiary education was associated with more curatively aimed therapies and less hormonal therapy (OR for radical prostatectomy = 2.34; 95% CI = 1.49-3.66; OR for radiotherapy = 1.42; 95% CI = 1.09-1.85; OR for hormonal therapy = 0.45; 95% CI = 0.33-0.60). The hazard ratio for PCa death was lower in men with secondary (0.81; 95% CI = 0.69-0.95) and tertiary (0.75; 95% CI = 0.65-0.87) education than in the patients with primary education. CONCLUSIONS When controlled for the cancer risk group, comorbidity and patient’s age, low education level is independently associated with less curatively aimed treatment in men with high-risk or locally advanced PCa and subsequently worse prognosis.