Mental distress links with physical activities, sedentary lifestyle, social support, and sleep problems: A Syrian population cross-sectional study

BackgroundMental diseases are very widespread and difficult to treat, affecting around 12% of the global population in 2019. Since social interaction is crucial to human existence and loneliness has been proven to be a significant predictor of depressive symptoms, it stands to reason that social connection problems would also contribute to depression. Physical inactivity seems to weaken and aggravate insulin tolerance alterations, glucose homeostasis, and plasma triglyceride levels, thereby influencing one's mood and happiness. This suggests that physical inactivity may be a significant risk factor for mental illness. This research contributes to our understanding of the mental health situation in Syria by exploring associations between a set of measurable characteristics that may be adjusted.MethodsAn online quantitative cross-sectional study was conducted between March and April 2022 in Syria, using a structured questionnaire that assesses data on behaviors of health, health in general, wellbeing, and adult population quality of life.ResultsAmong 1,224 respondents (371 men and 853 women), women have shown higher levels of mental distress, sleep issues, low engagement in structured activities, and a difficult work environment than men. Women experiencing mental anguish have reported being more sedentary, participating in less scheduled activities, and receiving less social support.ConclusionsThere are observable connections between high sedentary time and women experiencing mental distress. The mental health of Syrian women in distress was associated with a lack of participation in both organized activities and physical exercise in their free time. Furthermore, sleep issues and financial troubles were seen in persons with mental diseases of both males and females

Thrombocytopenia in Patients With Chronic Hepatitis C: A Possible Role of HCV on Platelet Progenitor Cell Maturation

A total of 30 patients with chronic hepatitis C (HCV) thrombocytopenia (TP) and 20 healthy controls were studied. Both groups were subjected to complete medical history, clinical examination in addition to assessment of hepatitis markers: level of thrombopoietin (Tpo), Geimsa-stained bone marrow smears, and in vitro short-term megakaryocytic progenitors culture (CFU-MK). Serum Tpo level was significantly elevated in patients with TP HCV. Short-term CFU-MK showed an evident depression in the colony-forming unit-megakaryocyte (CFU-meg). There is a positive correlation between the number of CFU-meg and the platelet count and between serum Tpo level and prothrombin time, transaminase, albumin, and the Child Pugh score of liver disease; a negative correlation between serum Tpo level and the number of CFU-meg and between serum Tpo level and the platelet count. Thus, the level of Tpo could be an indicator of intact functional response of the hepatocytes

Metformin Protects against Diabetic Cardiomyopathy: An Association between Desmin–Sarcomere Injury and the iNOS/mTOR/TIMP-1 Fibrosis Axis

The intermediate filament protein desmin is essential for maintaining the structural integrity of sarcomeres, the fundamental unit of cardiac muscle. Diabetes mellitus (DM) can cause desmin to become dysregulated, following episodes of nitrosative stress, through the activation of the iNOS/mTOR/TIMP-1 pathway, thereby stimulating collagen deposition in the myocardium. In this study, type 2 diabetes mellitus (T2DM) was induced in rats. One group of animals was pre-treated with metformin (200 mg/kg) prior to diabetes induction and subsequently kept on metformin until sacrifice at week 12. Cardiac injuries developed in the diabetic rats as demonstrated by a significant (p p < 0.0001) correlation between desmin tissue levels/sarcomere damage and glycated hemoglobin, heart rate, iNOS, mTOR, and fibrosis was observed. These findings demonstrate an association between damage of the cardiac contractile unit—desmin and sarcomere—and the iNOS/mTOR/TIMP-1/collagen axis of fibrosis in T2DM-induced cardiomyopathy, with metformin exhibiting beneficial cardiovascular pleiotropic effects

Lipopolysaccharide induces acute lung injury and alveolar haemorrhage in association with the cytokine storm, coagulopathy and AT1R/JAK/STAT augmentation in a rat model that mimics moderate and severe Covid-19 pathology.

Progress in the study of Covid-19 disease in rodents has been hampered by the lack of angiotensin-converting enzyme 2 (ACE2; virus entry route to the target cell) affinities for the virus spike proteins across species. Therefore, we sought to determine whether a modified protocol of lipopolysaccharide (LPS)-induced acute respiratory distress syndrome in rats can mimic both cell signalling pathways as well as severe disease phenotypes of Covid-19 disease. Rats were injected via intratracheal (IT) instillation with either 15 mg/kg of LPS (model group) or saline (control group) before being killed after 3 days. A severe acute respiratory syndrome (SARS)-like effect was observed in the model group as demonstrated by the development of a "cytokine storm" (>2.7 fold increase in blood levels of IL-6, IL-17A, GM-CSF, and TNF-α), high blood ferritin, demonstrable coagulopathy, including elevated D-dimer (approximately 10-fold increase), PAI-1, PT, and APTT (p 4 fold increase). Chest imaging revealed bilateral small patchy opacities of the lungs. Severe lung injury was noted by the presence of both, alveolar collapse and haemorrhage, desquamation of epithelial cells in the airway lumen, infiltration of inflammatory cells (CD45+ leukocytes), widespread thickening of the interalveolar septa, and ultrastructural alterations similar to Covid-19. Thus, these findings demonstrate that IT injection of 15 mg/kg LPS into rats, induced an AT1R/JAK/STAT-mediated cytokine storm with resultant pneumonia and coagulopathy that was commensurate with moderate and severe Covid-19 disease noted in humans