RESUMEN
Healthcare professionals are standing against the widespread use of e-cigarettes among the population, especially young adults. E-cigarettes are generally introduced, especially via social media platforms, as a safer alternative to conventional cigarette smoking. The aim of this study was to measure the prevalence of e-cigarette use among healthcare professions students at the University of Jordan, as well as to explore their knowledge and attitudes toward the use of e-cigarettes. An anonymous Google-Form®-based cross-sectional questionnaire was presented to potential participants at the University of Jordan. Students' responses were analyzed using SPSS® 23.0 software. A total of 679 online surveys were completed. About 37.4% of students reported using e-cigarettes at least once in their lifetime and about 20% of students were current e-cigarette users. The multivariate analysis showed that the factors associated with E-cigarette smoking are being male, having mothers, siblings, or friends using e-cigarettes, having easy access to e-cigarettes, and having social media as the main source of knowledge regarding e-cigarettes. The relatively high acceptance level and use of e-cigarettes among health professions students should be an alarming sign to decision-makers to give more attention to legislation that controls tobacco products including e-cigarette selling and advertising.
RESUMEN
Recent studies implicate the Cyr61, CTGF, Nov (CCN) matricellular signaling protein family as emerging players in vascular biology, with NOV (alias CCN3) as an important regulator of vascular homeostasis. Herein, we examined the role of CCN3 in the pathogenesis of atherosclerosis. In response to a 15-week high-fat diet feeding, CCN3-deficient mice on the atherosclerosis-prone Apoe-/- background developed increased aortic lipid-rich plaques compared to control Apoe-/- mice, a result that was observed in the absence of alterations in plasma lipid content. To address the cellular contributor(s) responsible for the atherosclerotic phenotype, we performed bone marrow transplantation experiments. Transplantation of Apoe; Ccn3 double-knockout bone marrow into Apoe-/- mice resulted in an increase of atherosclerotic plaque burden, whereas transplantation of Apoe-/- marrow to Apoe; Ccn3 double-knockout mice caused a reduction of atherosclerosis. These results indicate that CCN3 deficiency, specifically in the bone marrow, plays a major role in the development of atherosclerosis. Mechanistically, cell-based studies in isolated peritoneal macrophages demonstrated that CCN3 deficiency leads to an increase of lipid uptake and foam cell formation, an effect potentially attributed to the increased expression of scavenger receptors CD36 and SRA1, key factors involved in lipoprotein uptake. These results suggest that bone marrow-derived CCN3 is an essential regulator of atherosclerosis and point to a novel role of CCN3 in modulating lipid accumulation within macrophages.