Design and Optimisation of a Microwave Reactor for Kilo-Scale Polymer Synthesis

Current industrial production of polymer resins is generally undertaken in large multi-tonne stirred tank reactors. These are characterised by relatively slow heating and cooling cycles, resulting in long vessel cycle times and extended production campaigns. In this work we present a design for a hybrid microwave/oil jacket proof of concept system capable of producing up to 4.1 kg of polymer resin per batch. By exploiting rapid volumetric heating effects of microwave energy at 2.45GHz, we have optimised the synthetic regime, such that a 3.7 kg batch of polyester resin pre-polymer can be made in only 8 hours 20 minutes, with higher molecular weight (Mn 2,100) compared to the conventional process taking 22 hours 15 minutes (Mn 1,200), yielding an increase in synthesis rate of at least 265. The increase in polymer molecular weight also suggests a higher conversion was achieved over a shorter time scale

Design and optimisation of a microwave reactor for kilo-scale polymer synthesis

Current industrial production of polymer resins is generally undertaken in large multi-tonne stirred tank reactors. These are characterised by relatively slow heating and cooling cycles, resulting in long vessel cycle times and extended production campaigns. In this work we present a design for a hybrid microwave/oil jacket proof of concept system capable of producing up to 4.1?kg of polymer resin per batch. By exploiting rapid volumetric heating effects of microwave energy at 2.45?GHz, we have optimised the synthetic regime, such that a 3.7?kg batch of polyester resin pre-polymer can be made in only 8?h 20?min, with higher molecular weight (Mn 2100) compared to the conventional process taking 22?h 15?min (Mn 1200), yielding an increase in synthesis rate of at least 265%. The increase in polymer molecular weight also suggests a higher conversion was achieved over a shorter time scale

Indoor airborne particle sources and semi-volatile partitioning effect of outdoor fine PM in offices

To date, few studies have focused on PM air quality in offices, despite the fact that a lot of people spend many working hours a day in such offices. The aim of the present study is to investigate PM1 and PM2.5 in offices in Milan (Northern Italy) and in the air outside those offices. The PM samples were analyzed to determine the entity of certain compounds with possible direct or indirect adverse effects on human health: PAHs, BpA, and water soluble inorganic ions. A good correlation between outdoor and indoor PM mass concentrations emerged (R2 w0.87). The maximum I/O concentration ratiowas 0.92, suggesting that the indoor PM levelwas always lower than the outdoor level. The average infiltration factor, FINF,was 0.55, showing that about a half of the outdoor PMhad come indoors. The indoor-generated particles, Cig, had values ranging from 0 to 4.4 mg m3 (<25% of the indoor PM), showing that PM indoor sources had only made a limited contribution to total indoor PM. The results of the indoor-to-outdoor comparisons for the aforementioned chemical compounds demonstrate that the offices were characterized by the absence of effective indoor sources of particulatebound PAHs and inorganic ions, whereas Cig was around 58% of the indoor concentration for BpA. Our analysis of the FINF data pointed to the presence of a volatilization effect from PM for semi-volatile compounds like ammonium nitrate and 4- or 5-ring PAHs, which affected the measurement of their FINF. We propose the introduction of a new and simple parameter, called volatilization correction, to take account of this effect

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease