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Results from clinical studies are often subject to the risk of bias (deviation from the truth, systematic error). Therefore, a critical appraisal of studies provides a useful strategy in evidence-based healthcare to safeguard against wrong decisions and resulting in overtreatment or undertreatment. This article explains the frequently encountered types of bias, differentiates between them and provides strategies for avoidance of systematic errors. In addition, the two established Cochrane tools with which the risk of bias can be assessed in randomized and non-randomized studies are presented. To highlight the most important components of these tools for bias assessment, examples of randomization, confounding, blinding, completeness of data and selective reporting are provided. Finally, it is shown that bias should not be confused with other study limitations, such as external validity and imprecision.People with intellectual disability (ID) have a high vulnerability to develop mental health problems. The prevalence of mental disorders is higher than in the general population and, in addition, adults with ID often show behavioral problems that imply a need for psychiatric psychotherapeutic care. In view of the impairments of intellectual functioning, impaired adaptive behavioral skills and physical illnesses, the needs of this target group are usually complex and require particular expertise. A number of specific assessment instruments are available for target group-specific diagnostics to collate the cognitive performance and emotional development as well as for psychopathological symptoms and behavioral disorders. To improve the accuracy of diagnosis in the ID population, existing alternatives to DSM or ICD should be applied especially to adults with moderate or severe ID. Guidelines for psychopharmacotherapy and adapted user guides for psychotherapeutic treatment provide support in the context of target group-specific treatment.OBJECTIVE To prospectively compare the prevalence and frequency of subchondral bone marrow edema (BME) in the lumbar facet joints of low back pain patients and healthy subjects. MATERIALS AND METHODS Lumbar magnetic resonance imaging (MRI) examinations were performed on 55 asymptomatic participants (18 men; age range 21-63; mean 36 ± 12 years; body mass index (BMI) range 16-31; mean 22.6 ± 3.2 kg/m2) and 79 low back pain patients (36 men; age range 18-77; mean 47 ± 14 years; BMI range 18-40; mean 27.8 ± 4.4 kg/m2). In both groups, facet joint subchondral BME signal was evaluated using T2-weighted STIR imaging, and facet joint osteoarthritis was characterized as mild, moderate, and severe. RESULTS The BME signal was found in seven asymptomatic participants (12.7%) and 28 low back pain patients (35.4%) (P = 0.003). A significant portion of the patients (15.2%) presented more than one BME signal (P = 0.011). By pooling the ten facet joints of all subjects in each group, a significant difference in osteoarthritis grade distribution was observed between the two groups (P  less then  0.001). When adjusted for low back pain status, age, BMI, Modic type 1, disk herniation, and facet joint osteoarthritis maximal grade, only the latter was significantly associated with the facet joint BME signal (P  less then  0.001). Temsirolimus CONCLUSION Despite the higher prevalence and frequency of the BME signal in facet joints of low back pain patients compared to that in healthy subjects, the signal was found to be associated with the severity of the patients' osteoarthritis and not with their low back pain status.Hesperidin (HD), a bioflavonoid, has been shown to exert hepatoprotective effects. Our aim is to investigate the possible protective effects of HD against methotrexate (MTX) hepatotoxicity in adult male Sprague-Dawley (SD) rats that were divided into four groups (10 rats/each) and were exposed to MTX with or without HD co-administration for consecutive 28 days. The results showed that HD significantly ameliorated MTX-induced increase in liver enzymes and histopathological changes. Hepatic oxidative stress was suppressed by HD, as evidenced by the decrease in malondialdehyde (MDA), with a concomitant increase in total antioxidant activity (TAC), catalase (CAT), and glutathione (GSH) levels. Moreover, co-administration of HD with MTX remarkably upregulated the expression of Nrf2 and HO-1 compared with the MTX group. By the decrease in nuclear factor-kB (NF-κB) pathway and tumor necrosis factor α (TNF-α), HD obviously attenuated inflammatory response in MTX-lesioned livers. Likewise, the downregulation of P53 by HD could explain its antiapoptotic effects as indicated by increase BCl2 and the significant decrease of caspase-9 mRNA expression as compared with the MTX group. Thus, these findings revealed the hepatoprotective nature of HD against MTX hepatotoxicity by attenuating the pro-inflammatory and apoptotic mediators and improving antioxidant aptitude.Oral tumor microenvironment is characterized by chronic inflammation signified with infiltrating leukocytes and soluble mediators which cause immune suppression. However, how immunosuppressive cells like myeloid-derived suppressor cells (MDSCs) maintain the immunosuppressive tumor microenvironment and influence T cell function in oral squamous cell carcinoma (OSCC) patients remains poorly understood. In the present study, we found that percentages of MDSCs were higher in oral cancer patients compared to healthy individuals and correlated with cancer stage. Monocytic MDSCs (M-MDSCs) were prevalent in the periphery, while granulocytic/polymorphonuclear subset dominated the tumor compartment. M-MDSCs suppressed the lymphocyte proliferation and decreased the CD3-ζ (zeta) chain expression and interferon gamma production. The percentage of M-MDSCs in peripheral blood correlated inversely with CD3-ζ chain expression in T cells of these patients. Interleukin 6 (IL-6)-induced phosphorylated STAT3-regulated programmed cell death ligand 1, CCAAT/enhancer-binding proteins alpha and beta and Interleukin 10 expression in MDSCs. Temsirolimus MDSCs inhibited TGF-β-driven generation of induced regulatory T cells in vitro. M-MDSCs secreted interleukins IL-6, IL-1β, IL-23 and PGE2 and facilitated T-helper 17 (Th17) cell differentiation which utilizes nitric oxide synthase and cyclooxygenase 2 enzyme activity. Interestingly, OSCC patients showed increased levels of Th17 cells in peripheral blood and tumor tissue. Thus, increased frequency of MDSCs, Th17 cells and decreased expression of CD3-ζ chain portray T cell tolerance and chronic inflammatory state facilitating tumor growth.