COVID‐19: Facemasks, healthcare policies and risk factors in the crucial initial months of a global pandemic

Previous pandemics have shown that facemask use becomes highly popular in public settings due to fear of the disease spreading. There is, however, a lack of strong scientific evidence that facemasks can significantly reduce the spread of respiratory diseases and as such, most governing policies do not mandate these coverings. There is a stark contrast between the policies and acceptance of facemasks across different geographies. In this work, several data sources have been thoroughly analysed to elucidate how viral diseases are transmitted and spread with particular emphasis on the novel SARS‐CoV‐2 virus which is causing an outbreak of COVID‐19. The different types of facemasks and respirators are also explained, the nature of their design and their efficacy is also examined. Several key factors which have been hypothesised to contribute to the spread of viral infections are elaborated in detail including the effect of temperature and humidity, public transportation systems, population density, socio‐economics and sociology. In this work, data are analysed to explain how the disease is spread, how facemasks function and the differences in the number of initial cases based on several contributing factors to the spread of disease. There are also some dangers in automatically recommending community facemask wearing, such as a reduction in the immune system functionality from the reduced exposure to microbes and the disposal issues which result from the large‐scale use of such materials. The questions of whether facemasks are useful in a community setting or if they divert valuable material away from critical healthcare providers are discussed

Increased leptin concentrations correlate with increased concentrations of inflammatory markers in morbidly obese individuals

OBJECTIVE: To study whether an increase of plasma leptin concentrations, as observed in the case of increased body weight, is associated with an inflammatory state. SUBJECTS: Sixty-three healthy subjects with body mass index (BMI) ranging from 20 to 61 kg/m2. MEASUREMENTS: Plasma concentrations of leptin, the inflammatory parameter soluble TNF-alpha receptors (TNFR55 and TNFR75), the acute phase proteins lipopolysaccharide binding protein (LBP), serum amyloid A (SAA), alpha-acid glycoprotein (AGP), C-reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1) and the anti-inflammatory soluble Interleukin-1 decoy receptor (sIL-1RII) were measured. RESULTS: As expected, BMI correlated significantly with leptin (r=0.823, P <0.001), but also with all acute phase proteins, both soluble TNF receptors and PAI concentrations. After correction for BMI and sex, no significant correlation between leptin and the acute phase proteins was seen. Interestingly, however, leptin strongly correlated with both TNF receptors (r=0.523, P <0.001 for TNFR55 and r=0.438, P <0.001 for TNFR75). CONCLUSIONS: This study shows the development of a pro-inflammatory state with increasing body weight. The BMI independent relationship between leptin and both soluble TNF-receptors is consistent with a regulatory role for leptin in the inflammatory state in morbidly obese subject