Financial threat, hardship and distress predict depression, anxiety and stress among the unemployed youths: a Bangladeshi multi-cities study

Introduction: Unemployment has a contributory role in the development of mental health problems and in Bangladesh there is increasing unemployment, particularly among youth. Consequently, the present study investigated depression, anxiety, and stress among recent graduates in a multi-city study across the country. Methods: A cross-sectional study was conducted among 988 Bangladeshi graduate jobseekers in six major cities of the country between August to November 2019. The measures included socio-demographics and life-style factors, study and job-related information, Economic Hardship Questionnaire, Financial Threat Scale, Financial Well-Being Scale, and Depression Anxiety Stress Scale-21. Results: Depression, anxiety and stress rates among the present sample were 81.1% (n=801), 61.5% (n=608) and 64.8% (n=640) respectively. Factors related to gender, age, socio-economic conditions, educational background, lack of extra-curricular activities, and high screen activity were significant risk factors of depression, anxiety, and stress. Structural equation modeling indicated that (while controlling for age, daily time spent on sleep study, and social media use), financial threat was moderately positively related to depression, anxiety, and stress. Financial hardship was weakly positively associated with depression, anxiety, and stress, whereas financial wellbeing was weakly negatively associated with depression, anxiety, and stress. Limitations: Due to the nature of the present study (i.e., cross-sectional study) and sampling method (i.e., convenience sampling), determining causality between the variables is not possible. Conclusions: The present results emphasized the important detrimental role of financial troubles on young people's mental health by showing that financial problems among unemployed youth predict elevated psychiatric distress in both men and women

Treatment of OPG-deficient mice with WP9QY, a RANKL-binding peptide, recovers alveolar bone loss by suppressing osteoclastogenesis and enhancing osteoblastogenesis.

Osteoblasts express two key molecules for osteoclast differentiation, receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG), a soluble decoy receptor for RANKL. RANKL induces osteoclastogenesis, while OPG inhibits it by blocking the binding of RANKL to RANK, a cellular receptor of RANKL. OPG-deficient (OPG–/–) mice exhibit severe alveolar bone loss with enhanced bone resorption. WP9QY (W9) peptide binds to RANKL and blocks RANKL-induced osteoclastogenesis. W9 is also reported to stimulate bone formation in vivo. Here, we show that treatment with W9 restores alveolar bone loss in OPG–/–mice by suppressing osteoclastogenesis and enhancing osteoblastogenesis. Administration of W9 or risedronate, a bisphosphonate, to OPG–/–mice significantly decreased the osteoclast number in the alveolar bone. Interestingly, treatment with W9, but not risedronate, enhanced Wnt/β-catenin signaling and induced alveolar bone formation in OPG–/–mice. Expression of sclerostin, an inhibitor of Wnt/β-catenin signaling, was significantly lower in tibiae of OPG–/–mice than in wild-type mice. Treatment with risedronate recovered sclerostin expression in OPG–/–mice, while W9 treatment further suppressed sclerostin expression. Histomorphometric analysis confirmed that bone formation-related parameters in OPG–/–mice, such as osteoblast number, osteoblast surface and osteoid surface, were increased by W9 administration but not by risedronate administration. These results suggest that treatment of OPG–/–mice with W9 suppressed osteoclastogenesis by inhibiting RANKL signaling and enhanced osteoblastogenesis by attenuating sclerostin expression in the alveolar bone. Taken together, W9 may be a useful drug to prevent alveolar bone loss in periodontitis