Environmental factors of obesity before and after COVID-19 pandemic: a review.

In past decades the prevalence of overweight and obesity had grown rapidly. There are numerous factors contributing to this unfavorable change in people's health. This review article investigates the environmental factors which may play a role in the prevalence of overweight and obesity and additionally the novel factors which appeared after the beginning of the COVID-19 pandemic, which caused the increase in BMI during the lockdown period.

Eagle's Syndrome as a Cause of Discomfort and the Subjective Presence of a Foreign Body in the Throat.

Eagle syndrome consists of symptoms resulting from the elongation and excessive calcification of the styloid process of the temporal bone and calcification of the ligaments associated with this process. The main symptoms of this syndrome are the feeling of a foreign body in the throat, dysphagia and pain localized in the temporomandibular region, neck and ear. The authors describe the case report of a previously healthy 39-year-old Caucasian male that complained of discomfort and foreign body sensation in his throat.

HDL induces NO-dependent vasorelaxation via the lysophospholipid receptor S1P3.

HDL is a major atheroprotective factor, but the mechanisms underlying this effect are still obscure. HDL binding to scavenger receptor-BI has been shown to activate eNOS, although the responsible HDL entities and signaling pathways have remained enigmatic. Here we show that HDL stimulates NO release in human endothelial cells and induces vasodilation in isolated aortae via intracellular Ca2+ mobilization and Akt-mediated eNOS phosphorylation.

Suppression of endothelial cell apoptosis by high density lipoproteins (HDL) and HDL-associated lysosphingolipids.

Apoptotic cell death following injury of vascular endothelium is assumed to play an important role in the pathogenesis of atherosclerosis. In this report, we demonstrate that high density lipoproteins (HDL), a major anti-atherogenic lipoprotein fraction, protect endothelial cells against growth factor deprivation-induced apoptosis. HDL blocked the mitochondrial pathway of apoptosis by inhibiting dissipation of mitochondrial potential (Deltapsi(m)), generation of reactive oxygen species, and release of cytochrome c into the cytoplasm.

Activation of phosphatidylinositol-specific phospholipase C by HDL-associated lysosphingolipid. Involvement in mitogenesis but not in cholesterol efflux.

Our earlier studies demonstrated that high-density lipoproteins (HDLs) stimulate multiple signaling pathways, including activation of phosphatidylcholine-specific phospholipases C and D (PC-PLs) and phosphatidylinositol-specific phospholipase C (PI-PLC). However, only activation of PC-PLs was linked to the HDL-induced cholesterol efflux. In the study presented here, the role of HDL-induced PI-PLC activation was studied.