The effects of obesity and smoking in the coronavirus disease 2019 (COVID-19) pandemic remain controversial. Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system (RAS), is the human cell receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19. ACE2 expression increases on lung alveolar epithelial cells and adipose tissue due to obesity, smoking and air pollution. A significant relationship exists between air pollution and SARS-CoV-2 infection, as more severe COVID-19 symptoms occur in smokers; comorbid conditions due to obesity or excess ectopic fat accumulation as underlying risk factors for severe COVID-19 strongly encourage the virus/ACE2 receptor-ligand interaction concept. Indeed, obesity, air pollution and smoking associated risk factors share underlying pathophysiologies that are related to the Renin-Angiotensin-System in SARS-CoV-2 infection. The aim of this review is to emphasize the mechanism of receptor-ligand interaction and its impact on the enhanced risk of death due to SARS-CoV-2 infection. Recently, the low mortality rate in patients with acute respiratory distress syndrome (ARDS) with obesity and morbid obesity is defined as

An important goal of self-assembly research is to develop a general methodology applicable to almost any material, from the smallest to the largest scales, whereby qualitatively identical results are obtained independently of initial conditions, size, shape and function of the constituents. Here, we introduce a dissipative self-assembly methodology demonstrated on a diverse spectrum of materials, from simple, passive, identical quantum dots (a few hundred atoms) that experience extreme Brownian motion, to complex, active, non-identical human cells (~10 17 atoms) with sophisticated internal dynamics. Autocatalytic growth curves of the self-assembled aggregates are shown to scale identically, and interface fluctuations of growing aggregates obey the universal Tracy-Widom law. Example applications for nanoscience and biotechnology are further provided.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently a global pandemic with unprecedented public health, economic and social impact. The development of effective mitigation strategies, therapeutics and vaccines relies on detailed genomic and biological characterization of the regional viruses. This study was carried out to isolate SARS-CoV-2 viruses circulating in Anatolia, and to investigate virus propagation in frequently-used cells and experimental animals. We obtained two SARS-CoV-2 viruses from nasopharngeal swabs of confirmed cases in Vero E6 cells, visualized the virions using atomic force and scanning electron microscopy and determined size distribution of the particles. Viral cytopathic effects on Vero E6 cells were initially observed at 72 h post-inoculation and reached 90% of the cells on the 5th day. The isolates displayed with similar infectivity titers, time course and infectious progeny yields. Genome sequencing revealed the viruses to be well-conserved, with less than 1% diversity compared to the prototype virus. The analysis of the viral genomes, along with the available 62 complete genomes from Anatolia, showed limited diversity (up to 0.2% on deduced amino acids) and no evidence of recombination. The most prominent sequence variation was observed on the spike protein, resulting in the substitution D614G, with a prevalence of 56.2%. The isolates produced non-fatal infection in the transgenic type I interferon knockout (IFNAR −/- ) mice, with varying neutralizing antibody titers. Hyperemia, regional consolidation and subpleural air accumulation was observed on necropsy, with similar histopathological and immunohistochemistry findings in the lungs, heart, stomach, intestines, liver, spleen and kidneys. Peak viral loads were detected in the lungs, with virus RNA present in the kidneys, jejunum, liver, spleen and heart. In conclusion, we characterized two local isolates, investigated in vitro growth dynamics in Vero E6 cells and identified IFNAR−/− mice as a potential animal model for SARS-CoV-2 experiments.

Obesity and metabolic syndrome is a multisystemic disorder, that is characterized by excess caloric intake and spillover lipotoxicity caused by ectopic lipid accumulation in non-adipose tissues. Low grade chronic inflammation and insulin resistance are the hallmarks of the disorder, which further aggravate the condition. Gut microbiota constitutes an indispensible part of human superorganism's energy harvesting apparatus. The dynamic composition of microbiota changes with age, life style and host metabolic background. The wealth of genetic repertoire provided by these microorganism enables to extend host's substrate processing and harvesting capability. Some of these compounds including short chain fatty acids and indole act as signalling molecules on mammalian cells and modulate their behaviour. Nonetheless, this symbiotic style of interaction is restrained by immune system. The role of chronic low grade inflammation in metabolic syndrome is well established. Treg cells are the key players that sense and reshape the composition of microbiota. In this regard, any disturbance in Treg functionality may aggravate the inflammation and shift the symbiotic balance towards dysbiosis, which is characterized by autoimmunity and insulin resistance. Thus, immune system is responsible for the modulation of host and microbiota metabolisms and Treg cells act as a bridge in between.