OBJECTIVES We sought to identify and consider methodological issues that may have limited or confounded investigations into links between depression and acute coronary syndrome (ACS) events. METHODS We reviewed salient research studies to identify such issues.  https://www.selleckchem.com/products/MG132.html  RESULTS Against previous conclusions, we found that lifetime depression is unlikely to have any primary ACS impact, while we clarify that 'incident depression' (depression commencing at variable periods around the time of the ACS event) appears to confer a greater risk than non-incident depression. As the time periods of incident depressions are likely to have quite differing causes, evaluating any consolidated risk period appears unwise. It remains unclear whether it is 'depression' that provides the risk for ACS events or a higher order factor. Variable use of depression measures and failure to evaluate depressive sub-types have further limited clarification. The response by ACS patients to antidepressant medication appears limited, and it remains to be determined whether exposure to an antidepressant might be a contributing factor. Finally, studies may have focused on an excessively refined association, and neglected to recognise that depression is associated with a wide range of vascular events, suggesting that a broader conceptual model may be required. LIMITATIONS The authors have considered only a limited set of studies in preparing this review, with the critique relying at times on subjective interpretation. CONCLUSIONS After decades of research pursuing links between depression and ACS events explanatory links remain obscure, presumably reflecting a range of methodological issues that we have discussed in this paper . BACKGROUND Background Depressive disorders account for almost half of all Disability Adjusted Life Years caused by psychiatric disorders but efficacy of pharmacological interventions to prevent depressive disorders is not known. We aimed to assess efficacy of pharmacological treatments in prevention of depression. METHODS We searched PubMed, Psych Info, EMBASE, and CINHAL from 1980 to January 2020 and bibliographies of relevant systematic reviews. We selected randomised controlled trials (RCTs) that used a pharmacological intervention to prevent the onset of the new depressive episode in adult population. Study selection, data extraction and reporting was done following PRISMA guidelines. Data were pooled using random-effects meta-analysis. RESULTS 28 trials (2745 participants) were included in meta-analysis. Antidepressants (22 studies), Selenium, Hormone Replacement Therapy Omega-3 fatty acids and Melatonin were used to prevent depression, mostly in physical conditions associated with high risk of depression. All pharmacological interventions [pooled Odds Ratios (OR) 0.37 CI (0.25-0.54)], and antidepressants (OR 0.29, 95% CI 0.18, 0.46) were significantly more effective than placebo in preventing depression. Antidepressants were significantly better than placebo in trials that had low risk of bias (n = 16; OR 0.43 [0.30, 0.60]), in preventing post stroke depression (OR = 0.16, 95% CI 0.05, 0.55) and depression associated with Hepatitis C (OR = 0.56, 95% CI 0.31, 1.02). Limitations include small number of studies focussed only on high risk conditions and short follow up in most studies. CONCLUSIONS Prevention of depression may be possible in patients who have high-risk conditions such as stroke but the strategy requires complete risk and benefits analysis before it can be considered for clinical practice. V.PURPOSE To update the prevalence of depression in the US and identify whether misperception exists in depression assessed by self-report versus validated tools administered by trained professionals. METHODS We extracted data on sociodemographic characteristics, lifestyle factors, medical conditions, depressive symptoms, and self-reported depressive feeling from National Health and Nutrition Examination Survey (NHANES) study 2015-2018. We calculated the weighted prevalence and 95% CI of depressive symptoms assessed by a validated tool PHQ-9 (score≥10) and self-reported depression respectively. Then, we performed multivariable logistic regressions to identify their sociodemographic and lifestyle correlates. Finally, we calculated the agreement between PHQ-9 assessed depressive symptoms and self-reported depressive feeling to examine possible misperception. RESULTS The present analysis included a total of 10,257 adults (Weighted N = 215,964,374) aged 20 years and older. Prevalence of depressive symptoms (PHQ-9 score ≥10) were 8.0% from 2015 to 2018 in the US. 19.7% and 11.3% adults reported feeling depressed at least once a month and at least once a week, respectively. Depressive experience was largely misperceived in the US (Kappa agreement = 50.98%, Cohen's Kappa = 0.16, p  less then  0.001). Particularly, an estimated 1.1 million US adults had depressive symptoms but never felt being depressed. Several consistent demographic and behavioral correlates were identified across the two measures, namely age, sex, race/ethnicity, poverty and sitting time. CONCLUSIONS A high prevalence of depression was found, and misperception of depression exists among the US adult population. Our findings highlight an urgent need for health professionals to reduce the burden of depression with considering patients' socioeconomic status and lifestyle factors. BACKGROUND Bipolar depression (BDD) and major depressive disorder (MDD) are two diseases both characterized by depressed mood and diminished interest or pleasure. Recent neuroimaging studies have implicated the thalamo-cortical circuit in mood disorders, and the present study aimed to map thalamo-cortical connectivity to explore the dissociable and common abnormalities between bipolar and major depression in this circuit. METHOD Applying resting-state functional magnetic resonance imaging (fMRI), we mapped the thalamo-cortical circuit using a fine-grained thalamic atlas with 8 sub-regions bilaterally in 38 BDD patients, 42 MDD patients and 39 healthy controls (HCs). Correlation analysis was then performed between thalamo-cortical connectivity and clinical variables. RESULT The findings showed that both patient groups exhibited prefronto-thalamo-cerebellar and sensorimotor-thalamic hypoconnectivity, while the abnormalities in MDD were more extensive. Particularly, MDD group showed decreased thalamic connectivity with the salience network including the insula, anterior cingulate cortex (ACC), and striatum.