A New Type of Quartz Smog Chamber: Design and Characterization.

Since the 1960s, many indoor and outdoor smog chambers have been developed worldwide. However, most of them are made of Teflon films, which have relatively high background contaminations due to the wall effect. We developed the world's first medium-size quartz chamber (10 m3), which is jointed with 32 pieces of 5 mm thick polished quartz glasses and a stainless-steel frame. Characterizations show that this chamber exhibits excellent performance in terms of relative humidity (RH) (2-80%) and temperature (15-30 ± 1 °C) control, mixing efficiency of the reactants (6-8 min), light transmittance (>90% above 290 nm), and wall loss of pollutants. The wall loss rates of the gas-phase pollutants are on the order of 10-4 min-1 at 298 K under dry conditions. It is 0.08 h-1 for 100-500 nm particles, significantly lower than those of Teflon chambers. The photolysis rate of NO2 (JNO2) is automatically adjustable to simulate the diurnal variation of solar irradiation from 0 to 0.40 min-1. The inner surface of the chamber can be repeatedly washed with deionized water, resulting in low background contaminations. Both experiments (toluene-NOx and α-pinene-ozone systems) and box model demonstrate that this new quartz chamber can provide high-quality data for investigating SOA and O3 formation in the atmosphere.

Novel Fluorescence Method for Determination of Spatial Interparticle Distance in Polymer Nanocomposites.

Interparticle distance (ID) is generally used for spatial evaluation on the dispersion of nanofillers in polymer nanocomposites (PNCs) in order to gain in-depth insight into fundamental understanding of reinforcement and structure-property correlation. However, currently available methods mainly rely on two-dimensional observation technologies or simulation methods. Herein, using layered double hydroxides (LDHs) in low-density polyethylene (LDPE) as a model matrix, we developed a novel spatial ID determination method through a post labeling fluorescent imaging technique. The spatial ID of LDH nanofillers was achieved by a MATLAB program based on the 3D coordinates of LDH nanofillers in PNCs. The spatial ID data indicated the varied dispersion states of LDH nanofillers from "random", "even", to "clustered" in PNCs. More importantly, the so-called exceptional performances of PNCs at high loading of LDH nanofillers can be reasonably explained in combination with the mechanical studies. This proposed approach could undoubtedly provide valuable information in elucidating the structure-property correlation in PNCs. We believe that this work would be a guide to design advanced PNC materials.

Three-dimensional direct visualization of silica dispersion in polymer-based composites.

The uniform dispersion of silica fillers or other neutral fillers in the polymer matrix is significant for fabricating high-performance polymer-based composites. However, there is a long-standing challenge to provide a comprehensive, wide-area and real 3D distribution map to achieve direct visualization for the dispersion state of neutral silica. Herein, we propose a novel strategy for modifying silica fillers with commercial fluorophores to form fluorescent fillers in a standard manner. Through fluorescence imaging technology, we successfully observed the 2D-planar and 3D-spatial dispersion states of silica fillers in the polymer matrix. This success not only provides a visualized evaluation method for the spatial dispersion of an oxide filler, but also offers great potential in the further establishment of industrialized standards for the polymer-based composite industry.

Evolution of organic carbon during COVID-19 lockdown period: Possible contribution of nocturnal chemistry.

Carbonaceous aerosol is one of the main components of atmospheric particulate matter, which is of great significance due to its role in climate change, earth's radiation balance, visibility, and human health. In this work, carbonaceous aerosols were measured in Shijiazhuang and Beijing using the OC/EC analyzer from December 1, 2019 to March 15, 2020, which covered the Coronavirus Disease 2019 (COVID-19) pandemic. The observed results show that the gas-phase pollutants, such as NO, NO2, and aerosol-phase pollutants (Primary Organic Compounds, POC) from anthropogenic emissions, were significantly reduced during the lockdown period due to limited human activities in North China Plain (NCP). However, the atmospheric oxidation capacity (Ox/CO) shows a significantly increase during the lockdown period. Meanwhile, additional sources of nighttime Secondary Organic Carbon (SOC), Secondary Organic Aerosol (SOA), and babs, BrC(370 nm) are observed and ascribed to the nocturnal chemistry related to NO3 radical. The Potential Source Contribution Function (PSCF) analysis indicates that the southeast areas of the NCP region contributed more to the SOC during the lockdown period than the normal period. Our results highlight the importance of regional nocturnal chemistry in SOA formation.

The impact of ammonium on the distillation of organic carbon in PM2.5.

Thermal desorption coupled with different detectors is an important analysis method for ambient carbonaceous aerosols. However, it is unclear how the compounds coexisting in both the gas and particle phases affect carbonaceous aerosol concentrations and measurements during thermal desorption. We observed matrix effects leading to a redistribution of different OC fractions (OC1 to OC4) during the thermal desorption process. These factors led to the formation of OC with low volatility (OC4), mainly from high-volatility OC (OC1 and OC2). Laboratory studies further indicated that ammonium promotes such matrix effects by transforming OC in the particle phase. Therefore, in addition to providing insights into the chemical evolution of OC during haze events, we argue that thermal-desorption-based OC measurements should be used with caution, which is an important step towards a more accurate measurement of OC in the ambient atmosphere.

Silencing of functional p53 attenuates NAFLD by promoting HMGB1-related autophagy induction.

BACKGROUND AND AIM: Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease worldwide, but its pathogenesis remains imprecisely understood and requires further clarification. Recently, the tumor suppressor p53 has received growing attention for its role in metabolic diseases. In this study, we performed in vivo and in vitro experiments to identify the contribution of p53-autophagy regulation to NAFLD. METHODS: Livers from wild-type and p53 knockout mice as well as p53-functional HepG2 cells and p53-dysfunctional Huh7 cells were examined for autophagy status and HMGB1 translocation. In vivo and in vitro NAFLD models were established, and steatosis was detected. In the cell models, autophagy status and steatosis were examined by p53 and/or HMGB1 silencing. RESULTS: First, the silencing of p53 could induce autophagy both in vivo and in vitro. In addition, p53 knockout attenuated high-fat diet-induced NAFLD in mice. Similarly, knockdown of p53 could alleviate palmitate-induced lipid accumulation in cell models. Furthermore, high mobility group box 1 (HMGB1) was proven to contribute to the effect of silencing p53 on alleviating NAFLD in vitro as an autophagy regulator. CONCLUSION: The anti-NAFLD effect of functional p53 silencing is associated with the HMGB1-mediated induction of autophagy.

Inhibition of Histone Deacetylation by MS-275 Alleviates Colitis by Activating the Vitamin D Receptor.

BACKGROUND: Ulcerative colitis [UC] is a common chronic inflammatory bowel disease without curative treatment. METHODS: We conducted gene set enrichment analysis to explore potential therapeutic agents for UC. Human colon tissue samples were collected to test H3 acetylation in UC. Both in vivo and in vitro colitis models were constructed to verify the role and mechanism of H3 acetylation modification in UC. Intestine-specific vitamin D receptor [VDR]-/- mice and VD [vitamin D]-deficient diet-fed mice were used to explore downstream molecular mechanisms accordingly. RESULTS: According to the Connectivity Map database, MS-275 [class I histone deacetylase inhibitor] was the top-ranked agent, indicating the potential importance of histone acetylation in the pathogenesis of UC. We then found that histone H3 acetylation was significantly lower in the colon epithelium of UC patients and negatively associated with disease severity. MS-275 treatment inhibited histone H3 deacetylation, subsequently attenuating nuclear factor kappa B [NF-κB]-induced inflammation, reducing cellular apoptosis, maintaining epithelial barrier function, and thereby reducing colitis activity in a mouse model of colitis. We also identified VDR as be a downstream effector of MS-275. The curative effect of MS-275 on colitis was abolished in VDR-/- mice and in VD-deficient diet-fed mice and VDR directly targeted p65. In UC patients, histone H3 acetylation, VDR and zonulin-1 expression showed similar downregulation patterns and were negatively associated with disease severity. CONCLUSIONS: We demonstrate that MS-275 inhibits histone deacetylation and alleviates colitis by ameliorating inflammation, reducing apoptosis, and maintaining intestinal epithelial barrier via VDR, providing new strategies for UC treatment.

LB100 ameliorates nonalcoholic fatty liver disease via the AMPK/Sirt1 pathway.

BACKGROUND: It is well known that nonalcoholic fatty liver disease (NAFLD) is associated with insulin resistance (IR). LB100, a serine/threonine protein phosphatase 2A (PP2A) inhibitor, is closely related to IR. However, there is little data regarding its direct influence on NAFLD. AIM: To elucidate the effect and underlying mechanism of LB100 in NAFLD. METHODS: After 10 wk of high fat diet (HFD) feeding, male C57BL/6 mice were injected intraperitoneally with vehicle or LB100 for an additional 6 wk (three times a week). The L02 cell line was treated with LB100 and free fatty acids (FFAs) for 24 h. Hematoxylin and eosin and oil red O staining were performed for histological examination. Western blot analysis was used to detect the protein expression of Sirtuin 1 (Sirt1), total and phosphorylated AMP-activated protein kinase α (AMPKα), and the proteins involved in lipogenesis and fatty acid oxidation. The mRNA levels were determined by qPCR. Pharmacological inhibition of AMPK was performed to further examine the exact mechanism of LB100 in NAFLD. RESULTS: LB100 significantly ameliorated HFD-induced obesity, hepatic lipid accumulation and hepatic injury in mice. In addition, LB100 significantly downregulated the protein levels of acetyl-CoA carboxylase, sterol regulatory element-binding protein 1 and its lipogenesis target genes, including stearoyl-CoA desaturase-1 and fatty acid synthase, and upregulated the levels of proteins involved in fatty acid ß-oxidation, such as peroxisome proliferator-activated receptor α (PPARα), peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), carnitine palmitoyltransferase 1α, acyl-CoA oxidase 1 and uncoupling protein 2, as well as the upstream mediators Sirt1 and AMPKα in the livers of HFD-fed mice. In vitro, LB100 alleviated FFA-induced lipid accumulation in L02 cells through the AMPK/Sirt1 signaling pathway. Further studies showed that the curative effect of LB100 on lipid accumulation was abolished by inhibiting AMPKα in L02 cells. CONCLUSION: PP2A inhibition by LB100 significantly ameliorates hepatic steatosis by regulating hepatic lipogenesis and fatty acid oxidation via the AMPK/Sirt1 pathway. LB100 may be a potential therapeutic agent for NAFLD.

CYP3A suppression during diet-induced nonalcoholic fatty liver disease is independent of PXR regulation.

Cytochrome P450 3A (CYP3A) activity is inhibited, and its expression is suppressed during many diseases, including nonalcoholic fatty liver disease (NAFLD). However, the mechanism is controversial. Here, we report that PXR may not take part in the downregulation of CYP3A during NAFLD. Hepatic CYP3A11 (major subtype of mouse CYP3A) mRNA and protein expression was significantly decreased in both mice fed a high-fat diet (HFD) for 8 weeks and palmitate (PA)-treated mouse primary hepatocytes. Similarly, in HepG2 cells, PA treatment significantly suppressed the CYP3A4 (major subtype of human CYP3A) mRNA level and promoter transcription activity. However, Western blotting analysis found an induction of PXR nuclear translocation during NAFLD in both in vivo and in vitro models. Moreover, immunofluorescence determination also found nuclear translocation effect of PXR by PA stimulation in HepG2 cells. In addition, the siRNA knockdown of PXR did not affect the suppressive effects of PA on the CYP3A4 promoter transcription activity and mRNA levels in HepG2 cells. Similarly, PXR knockdown also did not affect the suppressive effects of PA on CYP3A11 mRNA and protein expression levels in mouse primary hepatoctyes. Taken together, the results showed that the suppressive effect of CYP3A transcription was independent of PXR regulation.

Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver disease via the Sirt1/AMPK and NF-κB signaling pathways.

BACKGROUND: Allyl isothiocyanate (AITC), a classic anti-inflammatory and antitumorigenic agent, was recently identified as a potential treatment for obesity and insulin resistance. However, little is known about its direct impact on the liver. AIM: To investigate the effect and underlying mechanism of AITC in nonalcoholic fatty liver disease (commonly referred to as NAFLD). METHODS: To establish a mouse and cellular model of NAFLD, C57BL/6 mice were fed a high fat diet (HFD) for 8 wk, and AML-12 cells were treated with 200 µM palmitate acid for 24 h. For AITC treatment, mice were administered AITC (100 mg/kg/d) orally and AML-12 cells were treated with AITC (20 µmol/L). RESULTS: AITC significantly ameliorated HFD-induced weight gain, hepatic lipid accumulation and inflammation in vivo. Furthermore, serum alanine aminotransferase and aspartate aminotransferase levels were markedly reduced in AITC-treated mice. Mechanistically, AITC significantly downregulated the protein levels of sterol regulatory element-binding protein 1 (SREBP1) and its lipogenesis target genes and upregulated the levels of proteins involved in fatty acid ß-oxidation, as well as the upstream mediators Sirtuin 1 (Sirt1) and AMP-activated protein kinase α (AMPKα), in the livers of HFD-fed mice. AITC also attenuated the nuclear factor kappa B (NF-κB) signaling pathway. Consistently, AITC relieved palmitate acid-induced lipid accumulation and inflammation in AML-12 cells in vitro through the Sirt1/AMPK and NF-κB signaling pathways. Importantly, further studies showed that the curative effect of AITC on lipid accumulation was abolished by siRNA-mediated knockdown of either Sirt1 or AMPKα in AML-12 cells. CONCLUSION: AITC significantly ameliorates hepatic steatosis and inflammation by activating the Sirt1/AMPK pathway and inhibiting the NF-κB pathway. Therefore, AITC is a potential therapeutic agent for NAFLD.