Impact of respirator versus surgical masks on SARS-CoV-2 acquisition in healthcare workers: a prospective multicentre cohort.

BACKGROUND There is insufficient evidence regarding the role of respirators in the prevention of SARS-CoV-2 infection. We analysed the impact of filtering facepiece class 2 (FFP2) versus surgical masks on the risk of SARS-CoV-2 acquisition among Swiss healthcare workers (HCW). METHODS Our prospective multicentre cohort enrolled HCW from June to August 2020. Participants were asked about COVID-19 risk exposures/behaviours, including preferentially worn mask type when caring for COVID-19 patients outside of aerosol-generating procedures. The impact of FFP2 on (1) self-reported SARS-CoV-2-positive nasopharyngeal PCR/rapid antigen tests captured during weekly surveys, and (2) SARS-CoV-2 seroconversion between baseline and January/February 2021 was assessed. RESULTS We enrolled 3259 participants from nine healthcare institutions, whereof 716 (22%) preferentially used FFP2. Among these, 81/716 (11%) reported a SARS-CoV-2-positive swab, compared to 352/2543 (14%) surgical mask users; seroconversion was documented in 85/656 (13%) FFP2 and 426/2255 (19%) surgical mask users. Adjusted for baseline characteristics, COVID-19 exposure, and risk behaviour, FFP2 use was non-significantly associated with decreased risk for SARS-CoV-2-positive swab (adjusted hazard ratio [aHR] 0.8, 95% CI 0.6-1.0) and seroconversion (adjusted odds ratio [aOR] 0.7, 95% CI 0.5-1.0); household exposure was the strongest risk factor (aHR 10.1, 95% CI 7.5-13.5; aOR 5.0, 95% CI 3.9-6.5). In subgroup analysis, FFP2 use was clearly protective among those with frequent (> 20 patients) COVID-19 exposure (aHR 0.7 for positive swab, 95% CI 0.5-0.8; aOR 0.6 for seroconversion, 95% CI 0.4-1.0). CONCLUSIONS Respirators compared to surgical masks may convey additional protection from SARS-CoV-2 for HCW with frequent exposure to COVID-19 patients

Loss-of-function of the long non-coding RNA A830019P07Rik in mice does not affect insulin expression and secretion.

Long non-coding RNAs (lncRNAs) contribute to diverse cellular functions and the dysregulation of their expression or function can contribute to diseases, including diabetes. The contributions of lncRNAs to β-cell development, function and survival has been extensively studied in vitro. However, very little is currently known on the in vivo roles of lncRNAs in the regulation of glucose and insulin homeostasis. Here we investigated the impact of loss-of-function in mice of the lncRNA A830019P07Rik, hereafter P07Rik, which was previously reported to be associated with reduced plasma insulin levels. Compared with wild-type littermates, male and female P07Rik mutant mice did not show any defect in glycaemia and plasma insulin levels in both fed and fasted state. Furthermore, P07Rik mutant mice displayed similar glucose and insulin levels in response to an intra-peritoneal glucose tolerance test. Ex vivo, islets from mutant P07Rik released similar amount of insulin in response to increased glucose concentration as wildtype littermates. In contrast with previous reports, our characterization of P07Rik mouse mutants revealed that loss of function of this lncRNA does not affect glucose and insulin homeostasis in mice

Involvement of 4E-BP1 in the protection induced by HDLs on pancreatic beta cells.

High-density lipoproteins (HDLs) protect pancreatic beta cells against apoptosis. This property might relate to the increased risk to develop diabetes in patients with low HDL blood levels. The mechanisms by which HDLs protect beta cells are poorly characterized however. Here we used a transcriptomic approach to identify genes differentially modulated by HDLs in beta cells subjected to apoptotic stimuli. The transcript encoding 4E-BP1 was up-regulated by serum starvation and HDLs blocked this increase. 4E-BP1 inhibits cap-dependent translation in its non- or hypo-phosphorylated state but it looses this ability when hyper-phosphorylated. At the protein level, 4E-BP1 was also up-regulated in response to starvation and IL1beta and this was blunted by HDLs. While an ectopic increase of 4E-BP1 expression induced beta cell death, silencing 4E-BP1 increase with shRNAs inhibited the apoptotic-inducing capacities of starvation. HDLs can therefore protect beta cells by blocking 4E-BP1 protein expression but this is not the sole protective mechanism activated by HDLs. Indeed, HDLs blocked apoptosis induced by ER stress with no associated decrease in total 4E-BP1 induction. Although, HDLs favored the phosphorylation, and hence the inactivation of 4E-BP1 in these conditions, this appeared not to be required for HDL protection. Our results indicate that HDLs can protect beta cells through modulation of 4E-BP1 depending on the type of stress stimuli