Music-based therapeutic interventions for medical school students with emotional regulation and mental health: a pre-post cohort study.

Purpose: Depression and anxiety are prevalent mental health challenges among college students. Music therapy has shown effectiveness in addressing depressive symptoms and enhancing psychosomatic functioning. This study aimed to evaluate the effectiveness of a 4-step structured music therapy program in improving mood and reducing symptoms of depression and anxiety among medical school students. Materials and methods: The self-controlled study involved 45 medical school students (21 men and 24 women) aged 18-24 years to examine the prevalence of depression and anxiety, common mental health issues among medical school students. Participants underwent psychological assessment using the Symptom Checklist-90 (SCL-90), Self-Rating Anxiety Scale (SAS), and Self-Rating Depression Scale (SDS). An 8-week music therapy intervention, comprising four steps-sociality, interaction, music lessons, and creative expression-was administered. Results: Before-intervention, 55.6% and 15.6% students were identified as suffering from depression and anxiety respectively. Post-intervention, significant reductions in psychological distress, particularly in the Global Severity Index (GSI) and Positive Symptom Total (PST) on the SCL-90 scale, were observed (P < 0.05). Male students exhibited notable improvements in various psychological symptoms compared to females. Junior grade students demonstrated greater improvements, and clinical medicine students exhibited significant enhancements in specific areas post-intervention. Conclusion: The structured music therapy program showed promising results in improving mood and regulating emotions among medical school students. Music therapy holds potential as a holistic approach to address mental health challenges in this demographic.

Identification of early derangements of coagulation, hematological and biochemical profiles in patients with acute pancreatitis.

BACKGROUND: Acute pancreatitis (AP) is a severe disease involving various pathological processes. We aimed to use rapid -thromboelastography (r-TEG) combined with conventional coagulation assays (CCAs) and other laboratory tests, to identify early derangements in coagulation, hematological, and biochemical profiles in patients with AP. METHODS: We enrolled 177 patients diagnosed with AP and 121 controls. Blood samples were analyzed using r-TEG, CCAs, and hematological and biochemical tests within 2 h of patient admission. All testing parameters were compared between the patients and the controls. Pearson's correlation coefficient was used to determine the correlation between the parameters among the patients. Logistic regression analysis was performed to evaluate the effects of the variables (demographic, coagulation, hematological and biochemical) on AP. RESULTS: Using r-TEG and CCAs, we observed differences in coagulation parameters between the patients with AP and the controls. The r-TEG results showed a pro-coagulant state and increased platelet activation in AP patients. Pearson's correlation analysis showed that inflammatory indicators were strongly correlated with coagulation/platelets in the pathological process of AP. Logistic regression analysis revealed that age, K, neutrophil (NEUT), triglyceride (TG) and blood amylase (AMY) were significantly associated with the development of AP. CONCLUSION: Coagulation profile and platelet play essential roles in the pathogenesis of AP. Pro-coagulant state and increased platelet activation in patients with AP were demonstrated using r-TEG. The r-TEG parameter K, age, NEUT, TG, and AMY may be used as potential indicators of AP.

Comparison between thromboelastography and conventional coagulation assays in patients with deep vein thrombosis.

BACKGROUND: Conventional coagulation assays (CCAs) are of limited value in the assessment of coagulation status in patients with deep vein thrombosis (DVT). We aimed to compare thromboelastography (TEG) and CCAs in identifying DVT and evaluating coagulation status in DVT patients. METHODS: Sixty-six patients diagnosed with DVT and forty healthy controls were enrolled. Blood samples were collected within 4 h of patients' admission to hospital before any operation and tested by TEG and CCAs. TEG and CCA parameters were compared between DVT patients and controls. The ability of each parameter in identifying DVT was assessed. Pearson's correlation was used to determine the correlation between TEG and CCA parameters among the study population. RESULTS: TEG showed significant differences between DVT patients and controls, indicating a hypercoagulable tendency in patients suffering from DVT. In contrast, no significant difference regarding CCAs was observed between the DVT and control group. Furthermore, TEG displayed a better capacity in identifying DVT than CCAs. In addition, Pearson's correlation analysis showed TEG and CCA parameters had few correlations. CONCLUSION: TEG has advantages in identifying DVT and detecting hypercoagulability, and provides a better insight in evaluating coagulation status in patients with DVT than CCAs.

The FGL2 prothrombinase contributes to the pathological process of experimental pulmonary hypertension.

In situ thrombus formation is one of the major pathological features of pulmonary hypertension (PH). The mechanism of in situ thrombosis has not been clearly identified. Fibrinogen-like protein 2 (FGL2) prothrombinase is an immune coagulant that can cleave prothrombin to thrombin, which then converts fibrinogen into fibrin. This mechanism triggers in situ thrombus formation directly, bypassing both the intrinsic and extrinsic coagulation pathways. FGL2 prothrombinase is mainly expressed in endothelial cells and mediates multiple pathological processes. This implies that it may also play a role in PH. In this study, we examined the expression of FGL2 in idiopathic pulmonary arterial hypertension (IPAH) patients, and in monocrotaline-induced rat and hypoxia-induced mouse PH models. Fgl2-/- mice were used to evaluate the development of PH and explore associated pathological changes. These included in situ thrombosis, vascular remodeling, and endothelial apoptosis. Following these analyses, we examined possible signaling pathways downstream of FGL2 in PH. We show FGL2 is upregulated in pulmonary vascular endothelium in human IPAH and in two animal PH models. Genetic knockout of Fgl2 limited the development of PH, indicated by decreased in situ thrombus formation, less vascular remodeling, and reduced endothelial dysfunction. In addition, loss of FGL2 downregulated PAR1 (proteinase-activated receptor 1) expression and decreased the overactivation and consumption of platelets in hypoxia-induced PH. These results indicate FGL2 participate in the development of PH and loss of FGL2 could attenuate PH by reducing in situ thrombosis and suppressing PAR1 signaling. Thus we provide evidence that suggests FGL2 prothrombinase presents a potential therapeutic target for clinical treatment of PH.NEW & NOTEWORTHY This is the first study to demonstrate that fibrinogen-like protein 2 (FGL2) participates in the pathological progression of pulmonary hypertension (PH) in human idiopathic pulmonary arterial hypertension, a monocrotaline rat PH model, and a hypoxia mouse PH model. Genetic knockout of Fgl2 significantly limited the development of PH indicated by reduced in situ thrombosis, vascular remodeling, and endothelial dysfunction, and suppressed PAR1 (proteinase-activated receptor 1) signaling and overactivation of platelets on PH. These results suggest FGL2 presents a potential therapeutic target for clinical treatment of PH.