Objectives: Maternal depression negatively affects depression and anxiety symptoms in the offspring. This study examined the association between maternal depression and their adolescent offspring depression and anxiety, as well as the mediating role of emotional trauma in determining the association. Methods: Participants were 237 mothers (46.08±5.00 years) and their adolescent offspring (16.54±1.51 years). The participants completed the Beck Depression Inventory-II, Early Trauma Inventory Self Report-Short Form, Center for Epidemiological Studies Depression Scale for Children, and the Screen for Children’s Anxiety Related Disorders. The mediating effect of emotional trauma on offspring was explored using mediation analysis. Results: Maternal depressive symptoms were significantly correlated with adolescent offspring traumatic experiences, as well as with their depressive and anxiety symptoms. Mediation analysis results showed that emotional trauma of offspring significantly mediated the effect of maternal depression on their depressive and anxiety symptoms. Conclusion Findings indicate that maternal depression was significantly associated with depressive and anxiety symptoms in adolescent offspring, mediated by their emotional trauma. Future research is needed to investigate pathways and intervention strategies to prevent the intergenerational transmission of emotional problems.

Objectives: Maternal depression negatively affects depression and anxiety symptoms in the offspring. This study examined the association between maternal depression and their adolescent offspring depression and anxiety, as well as the mediating role of emotional trauma in determining the association. Methods: Participants were 237 mothers (46.08±5.00 years) and their adolescent offspring (16.54±1.51 years). The participants completed the Beck Depression Inventory-II, Early Trauma Inventory Self Report-Short Form, Center for Epidemiological Studies Depression Scale for Children, and the Screen for Children’s Anxiety Related Disorders. The mediating effect of emotional trauma on offspring was explored using mediation analysis. Results: Maternal depressive symptoms were significantly correlated with adolescent offspring traumatic experiences, as well as with their depressive and anxiety symptoms. Mediation analysis results showed that emotional trauma of offspring significantly mediated the effect of maternal depression on their depressive and anxiety symptoms. Conclusion Findings indicate that maternal depression was significantly associated with depressive and anxiety symptoms in adolescent offspring, mediated by their emotional trauma. Future research is needed to investigate pathways and intervention strategies to prevent the intergenerational transmission of emotional problems.

Objectives: Maternal depression negatively affects depression and anxiety symptoms in the offspring. This study examined the association between maternal depression and their adolescent offspring depression and anxiety, as well as the mediating role of emotional trauma in determining the association. Methods: Participants were 237 mothers (46.08±5.00 years) and their adolescent offspring (16.54±1.51 years). The participants completed the Beck Depression Inventory-II, Early Trauma Inventory Self Report-Short Form, Center for Epidemiological Studies Depression Scale for Children, and the Screen for Children’s Anxiety Related Disorders. The mediating effect of emotional trauma on offspring was explored using mediation analysis. Results: Maternal depressive symptoms were significantly correlated with adolescent offspring traumatic experiences, as well as with their depressive and anxiety symptoms. Mediation analysis results showed that emotional trauma of offspring significantly mediated the effect of maternal depression on their depressive and anxiety symptoms. Conclusion Findings indicate that maternal depression was significantly associated with depressive and anxiety symptoms in adolescent offspring, mediated by their emotional trauma. Future research is needed to investigate pathways and intervention strategies to prevent the intergenerational transmission of emotional problems.

Platelet-rich plasma (PRP) is a promising biomaterial rich in bioactive growth factors, offering potential as a therapeutic agent for various diseases. However, its effectiveness in central nervous system disorders like vascular dementia (VaD) remains underexplored. This study investigated the potential of PRP to mitigate VaD progression in vivo. A rat model of VaD was established via bilateral common carotid artery occlusion and hypovolemia operation. Rats were randomly assigned to receive either PRP or platelet-poor plasma (PPP)—the latter being a byproduct of PRP preparation and used as a reference standard—resulting in the groups designated as ‘operated group (OP)+PRP’ and ‘OP+PPP’, respectively. PRP or PPP (500 μl) was administered intraperitoneally on the day of the operation and postoperative days 2, 4, 6, and 8. Cognitive function was assessed using the Y-maze, Barnes maze, and passive avoidance tests. On postoperative day 8, hippocampal samples were subjected to histological and semi-quantitative analyses. OP exhibited significant memory decline compared to controls, while the ‘OP+PRP’ group showed notable improvement. Histological analysis revealed increased neuronal loss and neuroinflammation in OP hippocampi, mitigated in ‘OP+PRP’. Semi-quantitative analysis showed decreased expression of brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin receptor kinase B (TrkB) in OP, restored in ‘OP+PPP’ and further in ‘OP+PRP’. These results highlight PRP’s protective effects against VaD-induced hippocampal damage and cognitive impairment, partially attributed to BDNF/TrkB pathway upregulation.

In Harrison’s Principles of Internal Medicine, human understanding is emphasized as one of three necessary characteristics that a physician must have. Inflammation, which is caused by inflammatory inducers (inf-ids), is a fundamental feature of disease at the cellular and molecular levels. Inflammation protects the body, but excessive or prolonged inflammation can be damaging and can cause disease. Humans are repeatedly exposed to external and internal environmental factors that generate inf-ids throughout their lives. External environmental factors include microbial and non-microbial inf-ids, as well as stressors that inevitably arise during social interactions. Internal environmental factors include the adaptive physiological response that is present from birth. Inf-ids may also be produced by the four-step habit loop, which consists of a cue (e.g., stressor), emotions, routine act (adaptive response), and a reward. Immune cells in the circulatory system and in tissues may have positive and negative effects in inflammatory responses. However, low-grade inflammation may be difficult to detect. We propose a model of disease development that integrates external and internal environmental factors from the perspective of human understanding.

Background and Objectives: Metformin, a commonly used antidiabetic drug, has been reported to exhibit promising anticancer effects across various tumor types. This study investigated the effectiveness of combining metformin with radiotherapy (RT) to treat head and neck squamous cell carcinoma (HNSCC).Materials and Method In vitro experiments were conducted in which FaDu and SCC-25 cells were treated with metformin, followed by irradiation. Cell proliferation was evaluated by MTT assay, and apoptosis was assessed by staining with annexin V-fluorescein isothiocyanate/ propidium iodide, followed by flow cytometry. Western blotting was performed to evaluate changes in apoptotic markers. In vivo experiments were performed using a murine AT-84 allograft model, where tumor volume was measured and serum samples were collected to assess the level of vascular endothelial growth factor (VEGF). Results: The combination of metformin and RT significantly reduced cell proliferation in a dose- and time-dependent manner, and led to a significant increase in the apoptotic rate, accompanied by the upregulation of cleaved caspase-8 and FoxO3, and the downregulation of Bcl-2. The combination treatment also exhibited antiangiogenic effects, as shown by the reduced hypoxia-inducible factor-1 alpha level and inhibited tube formation in the endothelial cells. The combined therapy in the mouse model led to marked decrease in tumor volume and the serum VEGF level in comparison to both the control group and the RT alone. Conclusion The concurrent use of metformin and RT successfully suppressed cell proliferation, triggered apoptosis, and increased the antiangiogenic effects in HNSCC. These results support the use of metformin as an adjunct to RT for the treatment of HNSCC.