Thermal degradation of plastics is a promising technology for addressing the waste management issues of landfill disposal, while obtaining useful products. Primary thermal degradation of polymers usually yields a large quantity of high molecular weight compounds with a limited applicability, making necessary a secondary degradation to improve the product quality. In this study, pyrolysis vapors from waste high density polyethylene (HDPE) were subjected to secondary degradation by varying the temperature and vapor residence time (VRT) in the reaction zone of a new two-stage micropyrolysis reactor (TSMR) attached to a commercial micropyrolysis unit. Temperature and VRT variations showed a strong effect on the product distribution, with low temperature (625 °C) and short VRT (1.4 s) producing a wide range of gases and liquid products and with high temperature (675 °C) and long VRT (5.6 s) producing mostly hydrocarbon gases and mono- and polyaromatics. The results showed a good agreement with previously reported product distributions for larger-scale pyrolysis reactors and were well explained by known degradation mechanisms.
The hydrolytic degradation of poly(lactic acid) (PLA) devices has previously been reported as size dependent for devices such as plates, microspheres, and films between 2 and 0.3 mm in thickness or diameter. In this study, the effect of fiber diameter on the degradation characteristics of PLA fiber of two diameters, 32 mm (PLA32) and 118 mm (PLA118), aged at 40, 60, and 80 C with 100% relative humidity, was investigated. Additionally, both PLA32 and PLA118 were aged at 40 and 60 C under nitrogen purge. The degradation of the fibers was evaluated based on changes in the total weight, crystallinity, and molecular weight of the samples. Both diameters exhibited similar total weight loss, crystallinity, and molecular weight loss profiles under each set of degradation conditions. Two models for the change in molecular weight were compared: a first order model and an autocatalytic model. For the obtained data, both models provided a reasonable fit of the molecular weight data. Based on the rate constants obtained for each model, the activation energy for PLA degradation was calculated (26.3 kcal mol 21 for the first order model and 22.4 kcal mol 21 for the autocatalytic model). The activation energies obtained were close to other values reported in the literature for PLA hydrolysis.
When bacterial pathogens enter the gut, they encounter a complex milieu of signaling molecules and metabolites produced by host and microbial cells or derived from external sources such as the diet. This metabolomic landscape varies throughout the gut, thus establishing a biogeographical gradient of signals that may be sensed by pathogens and resident bacteria alike. Enteric bacterial pathogens have evolved elaborate mechanisms to appropriately regulate their virulence programs, which involves sensing and responding to many of these gut metabolites to facilitate successful gut colonization. Long chain fatty acids (LCFAs) represent major constituents of the gut metabolome that can impact bacterial functions. LCFAs serve as important nutrient sources for all cellular organisms and can function as signaling molecules that regulate bacterial metabolism, physiology, and behaviors. Moreover, in several enteric pathogens, including Salmonella enterica, Listeria monocytogenes, Vibrio cholerae, and enterohemorrhagic Escherichia coli, LCFA sensing results in the transcriptional repression of virulence through two general mechanisms. First, some LCFAs function as allosteric inhibitors that decrease the DNA binding affinities of transcriptional activators of virulence genes. Second, some LCFAs also modulate the activation of histidine kinase receptors, which alters downstream intracellular signaling networks to repress virulence. This mini-review will summarize recent studies that have investigated the molecular mechanisms by which different LCFA derivatives modulate the virulence of enteric pathogens, while also highlighting important gaps in the field regarding the roles of LCFAs as determinants of infection and disease.
The trillions of microorganisms inhabiting the human gut are intricately linked to human health. At the species abundance level, correlational studies have connected specific bacterial taxa to various diseases. While the abundances of these bacteria in the gut serve as good indicators for disease progression, understanding the functional metabolites they produce is critical to decipher how these microbes influence human health. Here, we leverage multi-omics big data analysis to directly establish a negative correlation between sulfonolipid (SoL) biosynthesis in the human gut microbiome and inflammatory bowel disease (IBD). We experimentally validate this informatic correlation in a mouse model of IBD, showing that SoLs are produced in higher abundance in non-IBD mice compared to IBD mice. We determine that SoLs consistently contribute to the immunoregulatory activity of SoL-producing human gut commensal strains. We further reveal that sulfobacin A (SoL A), a representative member of SoLs, primarily mediates its dual immunomodulatory activity through Toll-like receptor 4 (TLR4). We also demonstrate that SoL A interacts with TLR4 via direct binding to myeloid differentiation factor 2 and that SoL A competes with the natural ligand, lipopolysaccharide, for binding. Together, these results suggest that SoLs mediate a protective effect against IBD through TLR4 signaling and also showcase a widely applicable informatics-based approach to directly linking the biosynthesis of functional metabolites to human health.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.