COVID-19 and Depression: Prevalence and Risk Factors in Youth from Maharashtra, India

Abstract Background Postpartum depression (PPD) is a common social health problem that affects not only the mother and newborn, but extends to other family members as well as various aspects of their lives. This systematic review and meta–analysis aims to identify the prevalence and risk factors of postpartum among the women in Middle East countries. Methods We searched published articles from Web of Science, EMBASE, PubMed and Cochrane electronic databases to establish study articles. Articles regarding postpartum depression prevalence and associated factors among women in the Middle East were included in this systematic review and meta–analysis. A random–effect model was used for estimation of pooled postpartum depression prevalence with a 95% confidence interval (CI) and forest plot. Presence of heterogeneity was checked by Cochran's (Q) test, and funnel plots and Egger’s statistical tests were used to assess publication bias. Results A total of 15 studies were included in this systematic review. The studies were conducted in different countries of the Middle East between 2006 and 2020, nine of the included studies were cross–sectional studies and six were cohort studies. The overall pooled estimate of the prevalence of postpartum depression in the Middle East mothers was very high 27% (95% CI 0.19–0.35). The common risk factors reported based on our review were poor economic, pregnancy associated complications, low education, unplanned pregnancy, housewife, inadequate social support from family members and the feeding by formula. Poor economic and complication during pregnancy presented a significant relationship regarding postpartum depression in meta–analysis. Conclusions The prevalence of postpartum depression in the Middle East was higher than other regions of the world. In response to this, we recommend an increase of routine screening for depression during postpartum in this area. Furthermore, it might be necessary to integrate mental health with maternal health care in clinical practice during the postpartum.

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Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

Clinical Science ◽

10.1042/cs20190999 ◽

2019 ◽

Vol 133 (22) ◽

pp. 2283-2299

Author(s):

Apabrita Ayan Das ◽

Devasmita Chakravarty ◽

Debmalya Bhunia ◽

Surajit Ghosh ◽

Prakash C. Mandal ◽

...

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Chronic Inflammation ◽

Ex Vivo ◽

Human Subjects ◽

Critical Role ◽

Atherosclerotic Cardiovascular Disease ◽

Tnf Α ◽

Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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