Search

An open source software (Aerosol and Air Quality Research Lab-Aerosol Dynamics Model, AAQRL-ADM) used for aerosol dynamics simulations is developed by including four models: discrete, discrete-sectional, method of moments, and modal. First, the mathematical description of these models as well as the effects of aerosol dynamics available in the software are reviewed, and a modal model is developed to use multiple modes to represent particle size spectrum. Second, the design of a working principle and user graphical interface (GUI) of AAQRL-ADM is described. Third, the models in AAQRL-ADM are validated by investigating the evolution of particle size distribution (PSD) in considering the effects of coagulation, condensation, and nucleation. Next, the trade-off between simulation accuracy and numerical efficiency is discussed for all of the four models, and a guide to choosing the appropriate aerosol dynamic model in practical simulation is presented. Finally, discrete-sectional, moment, and modal models are used to investigate the particle size distribution in a furnace aerosol reactor along a streamline, coupled with the velocity and temperature profiles. AAQRL-ADM is provided free of charge for the use of public researchers. Copyright © 2020 American Association for Aerosol Research [ABSTRACT FROM AUTHOR]

While there are several computational studies on differential mobility analyzers (DMA), there is none for high flow DMA to classify nanoparticles less than 3 nm. A specific design of a high flow DMA, a half mini DMA, is investigated to predict its performance through numerical modeling in the incompressible flow regime. The governing equations for flow field, electric field and aerosol transport are solved using COMSOL 5.3. The transfer function of the half mini DMA is compared with that of a nano DMA (TSI 3085). The results show that both the height of the transfer function and resolution (R) of the half mini DMA are much better than those of nano DMA in sub-2 nm particle size range. Finally, the transfer function of half mini DMA is evaluated for different values of aerosol flow rate to the sheath flow rate (q/Q). Comparison of the simulated transfer function with existing models from Knutson-Whitby and Stolzenburg is also elucidated. It is found that the former model overestimates the resolution; whereas the latter is close to the simulation results for q/Q above 0.067. This work provides a useful method to study the flow regimes and transfer function of a high flow DMA. Copyright © 2018 American Association for Aerosol Research [ABSTRACT FROM AUTHOR]

Brown fat generates heat through uncoupled respiration, protecting against hypothermia and obesity. Adult humans have brown fat, but the amounts and activities are substantially decreased in obesity, by unknown mechanisms. Here we show that elevated micro RNA 34a (miR-34a) in obesity inhibits fat browning in part by suppressing the browning activators fibroblast growth factor 21 (FGF21) and SIRT1. Lentivirus-mediated down regulation of miR-34a inmice with diet-induced obesity reduced adiposity, improved serum profiles, increased the mitochondrial DNA copy number, and increased oxidative function in adipose tissue in both BALB/c and C57BL/6mice. Remarkably, down regulation of miR-34a increased coexpression of the beige fat-specific marker CD137 and the browning marker UCP1 in all types of white fat, including visceral fat, and promoted additional browning in brown fat. Mechanistically, down regulation ofmiR-34a increased expression of the FGF21 receptor components, FGFR1 and βKL, and also that of SIRT1, resulting in FGF21/SIRT1-dependent deacetylation of PGC-1α and induction of the browning genes Ucp1, Pgc-1α, and Prdm16. Importantly, anti-miR-34a-mediated beneficial effects, including decreased adiposity, are likely from multiple tissues, since down regulation of miR-34a also improves hepatic FGF21 signaling and lipid oxidation. This study identifies miR-34a as an inhibitor of beige and brown fat formation, providing a potential target for treating obesity-related diseases. [ABSTRACT FROM AUTHOR]

Innate γδ T cells play critical roles in mucosal immunity such as regulating intestinal epithelial homeostasis. In addition, γδ T cells are significantly increased in the inflamed mucosa of patients with ulcerative colitis. However, γδ T cells are a heterogeneous population. IL-17-producing versus IFNγ-producing γδ T cells play differential roles in different disease settings. Therefore, dissecting the exact role of different subsets of γδ T cells in colitis is essential for understanding colitis immunopathogenesis. In the current study, we found that TCR δ-deficient mice had a more severe dextran sodium sulfate (DSS)-induced colitis that was reduced upon reconstitution of γδT17 cells but not IFNγ-producing γδ T cells. Immunophenotyping of the cellular infiltrate upon DSS-induced colitis showed a reduced infiltration of Gr-1+CD11b+myeloid cells into the sites of inflammation in mice lacking γδT17 cells. Further experiments demonstrated that IL-17, IL-18, and chemokine CXCL5 were critical in Gr-1+CD11b+myeloid cell recruitment.In vitroT cell suppressive assay indicated that this Gr-1+CD11b+population was immunosuppressive. Depletion of Gr-1+CD11b+myeloid cells resulted in an increase severity of DSS-induced colitis. Our study elucidates a new immune pathway involving γδT17-dependent recruitment of Gr-1+CD11b+myeloid cells to the site of colitis inflammation important in the protection of colitis initiation and progression. [ABSTRACT FROM PUBLISHER]