Background Emergence of coronavirus disease 2019 (COVID-19) forced the worldwide higher educational institutes to adopt distance learning mode. Further, remote electronic exams (E−exams) were considered as mode of assessment. Objectives : This cross-sectional study evaluated the students' experience of remote E-exams during the COVID-19 pandemic among Medical Sciences students in Jordan. Materials and Methods: A survey of 29 questions was prepared on Google forms and distributed among students at Faculties of Medical Sciences (Medicine, Dentistry, Pharmacy, Nursing and Applied Medical Sciences) at Jordan University of Science and Technology. The questions include students' demographics, stress experience, and factors contributing to stress as well as behavioral changes related to remote E-exams. Responses were analyzed using descriptive, cross tabulation and Chi-square tests. Results: Among 1019 respondents, 32% reported more stress with remote E-exams. This was associated with academic major and gender. Among students with more stress during remote E-exams, the exam duration, mode of questions navigation and technical problems (exam platform and internet connectivity) appeared as the main factors related to stress in 78%, 76% and >60%, respectively. Other factors include concern regarding the teaching methods, exam environment and students' dishonesty. Remote E-exams had negative impact on students' dietary habits (increase consumption of caffeine and high energy drinks, high sugar food, fast food), sleep (reduction in sleeping hours, more consumption of insomnia medications), physical activity (less exercises) and smoking habits (increase). Conclusion : Results suggested a negative impact of E-exams on students within Medical Faculties. Robust exam platform and remote mock E-exams are recommended to reduce students' potential stress. A stress-free environment is very essential to encourage students to adopt remote E-exams, particularly if the pandemic will take longer. Various awareness programs about students' habits related to dietary, sleep quality, physical activity and smoking are highly valuable for students’ health benefits. This is of particular importance since the current students at Faculties of Medical Sciences are the future health care providers.

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Cysteinyl leukotrienes (cys-LTs), LTC4, LTD4, LTE4 are potent inflammatory lipid mediators that act through two distinct G-protein-coupled receptors, CysLT1R and CysLT2R. Although cys-LTs are shown to induce vascular leakage and atherosclerosis, the molecular mechanism by which cys-LTs modulate endothelial function is not known. Here, we show that cys-LTs (LTC4 and LTD4) induce robust calcium influx in human umbilical vein endothelial cells (HUVECs) through CysLT2R, but not CysLT1R. Further, cys-LT treatment induced endothelial cell (EC) contraction leading to monolayer disruption via CysLT2R/Rho kinase dependent pathway. Furthermore, stimulation with cys-LTs potentiated TNFα-induced VCAM-1 expression and leukocyte recruitment to ECs through CysLT2R. In contrast, we found that both LTC4 and LTD4 stimulated EC proliferation through CysLT1R. Taken together, these results suggest that cys-LTs induce endothelial inflammation and proliferation via CysLT2R/Rho kinase and CysLT1R/Erk dependent pathways, respectively, which play critical role in the etiology of cardiovascular diseases such as atherosclerosis and myocardial infarction.

Contributions of mechanical signals to airway remodeling during asthma are poorly understood. Transient receptor potential vanilloid 4 (TRPV4), a mechanosensitive ion channel, has been implicated in cardiac and pulmonary fibrosis; however, its role in asthma remains elusive. Employing a -induced asthma model, we report here that TRPV4-knockout mice were protected from-induced airway remodeling. Furthermore, lung fibroblasts that were isolated from TRPV4-knockout mice showed diminished differentiation potential compared with wild-type mice. Fibroblasts from asthmatic lung exhibited increased TRPV4 activity and enhanced differentiation potential compared with normal human lung fibroblasts. Of interest, TGF-β1 treatment enhanced TRPV4 activation in a PI3K-dependent manner in normal human lung fibroblasts Mechanistically, TRPV4 modulated matrix remodeling in the lung 2 distinct but dependent pathways: one enhances matrix deposition by fibrotic gene activation, whereas the other slows down matrix degradation by increased plasminogen activator inhibitor 1. Of importance, both pathways are regulated by Rho/myocardin-related transcription factor-A and contribute to fibroblast differentiation and matrix remodeling in the lung. Thus, our results support a unique role for TRPV4 in -induced airway remodeling and warrant further studies in humans for it to be used as a novel therapeutic target in the treatment of asthma.-Gombedza, F., Kondeti, V., Al-Azzam, N., Koppes, S., Duah, E., Patil, P., Hexter, M., Phillips, D., Thodeti, C. K., Paruchuri, S. Mechanosensitive transient receptor potential vanilloid 4 regulates-induced airway remodeling 2 distinct pathways modulating matrix synthesis and degradation.

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