86, 95% CI 1.98-7.54) and having insomnia (P less then 0.001, OR = 4.76, 95% CI 2.99-7.56) were associated with higher risk of depression. QOL was significantly lower in physical (F (1,632) = 35.421, P less then 0.001), psychological (F (1,632) = 20.777, P less then 0.001), social (F (1,632) = 8.169, P less then 0.001) and environmental domains (F (1,632) = 11.861, P less then 0.001) in those with depression. Conclusion Depression was common in older nursing home residents especially those living in the high-altitude region. Considering the negative impact of depression on QOL and functional outcomes, routine screening and timely treatment of depression should be implemented in this population.Background Depression, anxiety, and disordered sleep are some common symptoms associated with sub-optimal mental health. During the COVID-19 pandemic, mental health issues have grown increasingly more prevalent in the population. Due to social distancing and other limitations during the pandemic, there is a need for home-based, flexible interventions that can improve mental health. The Yoga of Immortals (YOI) mobile application provides a structured intervention that can be used on any mobile device and applied from the user's home.  https://www.selleckchem.com/products/atn-161.html  Methods A total of 1,505 participants were enrolled in the study and used the YOI app for an 8-week period. Participants were asked to fill out three questionnaires The Patient Health Questionnaire, 8 items (PHQ-8), the Generalized Anxiety Disorder questionnaire (GAD-7) and the Insomnia Severity Index (ISI). These three items were completed by 1,297 participants a total of four times before starting YOI, two more times during use, and a fourth time after the 8-week usage period. Changes in PHQ8, GAD7 and ISI in participants were compared to a control group, who did not use the YOI app but completed all questionnaires (590 controls finished all questionnaires). Results Participants reported significant decreases in depression and anxiety-related symptoms. Compared to baseline, PHQ-8 scores decreased 50% on average after the 8-week period. GAD-7 scores also decreased by 40-50% on average, and ISI scores decreased by 50%. These changes were significantly greater (p less then 0.05) than that observed in the control group. Participants who reported a previous diagnosis of depression and generalized anxiety reported significantly larger decreases in PHQ-8 and GAD-7 as compared to participants with no prior diagnosis (p less then 0.05). Conclusions Regular use of the YOI intervention over an 8-week period led to significant decreases in symptoms of both depression and anxiety, as well as alleviation of insomnia.N6-methyladenosine (m6A), the most abundant RNA modification in eukaryotes, plays a pivotal role in regulating many cellular and biological processes. Aberrant m6A modification has recently been involved in carcinogenesis in various cancers, including pancreatic cancer. Pancreatic cancer is one of the deadliest cancers. It is a heterogeneous malignant disease characterized by a plethora of diverse genetic and epigenetic events. Increasing evidence suggests that dysregulation of m6A regulatory factors, such as methyltransferases, demethylases, and m6A-binding proteins, profoundly affects the development and progression of pancreatic cancer. In addition, m6A regulators and m6A target transcripts may be promising early diagnostic and prognostic cancer biomarkers, as well as therapeutic targets. In this review, we highlight the biological functions and mechanisms of m6A in pancreatic cancer and discuss the potential of m6A modification in clinical applications.MicroRNAs (miRNAs) play a critical role in regulating various biological processes, such as cell differentiation and immune modulation by binding to their target genes. miR-223 is a miRNA with important functions and has been widely investigated in recent years. Under certain physiological conditions, miR-223 is regulated by different transcription factors, including sirtuin1 (Sirt1), PU.1 and Mef2c, and its biological functions are mediated through changes in its cellular or tissue expression. This review paper summarizes miR-223 biosynthesis and its regulatory role in the differentiation of granulocytes, dendritic cells (DCs) and lymphocytes, macrophage polarization, and endothelial and epithelial inflammation. In addition, it describes the molecular mechanisms of miR-223 in regulating lung inflammation, rheumatoid arthritis, enteritis, neuroinflammation and mastitis to provide insights into the existing molecular regulatory networks and therapies for inflammatory diseases in humans and animals.Pulmonary fibrosis develops when myofibroblasts and extracellular matrix excessively accumulate in the injured lung, but what drives fibrosis is not fully understood. Glycolysis has been linked to cell growth and proliferation, and several studies have shown enhanced glycolysis promotes pulmonary fibrosis. However, detailed studies describing this switch remain limited. Here, we identified that TGF-β1 effectively increased the expression of circHIPK3 in lung fibroblasts, and circHIPK3 inhibition attenuated the activation, proliferation, and glycolysis of fibroblasts in vitro. Dual-luciferase reporter gene assays, RNA immunoprecipitation (RIP), and RNA pull-down assays showed that circHIPK3 could function as a sponge of miR-30a-3p and inhibit its expression. Furthermore, FOXK2, a driver transcription factor of glycolysis, was identified to be a direct target of miR-30a-3p. Mechanistically, circHIPK3 could enhance the expression of FOXK2 via sponging miR-30a-3p, thereby facilitating fibroblast glycolysis and activation. Besides, miR-30a-3p overexpression or FOXK2 knockdown blocked fibroblast activation induced by TGF-β1 and abrogated the profibrotic effects of circHIPK3. Moreover, circHIPK3 and miR-30a-3p were also dysregulated in fibrotic murine lung tissues induced by silica. Adeno-associated virus (AAV)-mediated circHIPK3 silence or miR-30a-3p overexpression alleviated silica-induced pulmonary fibrosis in vivo. In conclusion, our results identified circHIPK3/miR-30a-3p/FOXK2 regulatory pathway as an important glycolysis cascade in pulmonary fibrosis.