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Sestrin2 (SESN2), a highly conserved stress-responsive protein, can be triggered by various noxious stimuli, such as hypoxia, DNA damage, oxidative stress, endoplasmic reticulum (ER) stress, and inflammation. Multiple transcription factors regulate SESN2 expression, including hypoxia-inducible factor 1 (HIF-1), p53, nuclear factor E2-related factor 2 (Nrf2), activating transcription factor 4 (ATF4), ATF6, etc. Upon induction, SESN2 generally leads to activation of adenosine monophosphate-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin complex 1 (mTORC1). To maintain cellular homeostasis, SESN2 and its downstream molecules directly scavenge reactive oxygen species or indirectly influence the expression patterns of key genes associated with redox, macroautophagy, mitophagy, ER stress, apoptosis, protein synthesis, and inflammation. In liver diseases including acute liver injury, fatty liver diseases, hepatic fibrosis, and hepatocellular carcinoma (HCC), SESN2 is abnormally expressed and correlated with disease progression. In NAFLD, SESN2 helps with postponing disease progression through balancing glycolipid metabolism and macroautophagy (lipophagy), and rectifying oxidative damage and ER stress. During hepatic fibrosis, SESN2 represses HSCs activation and intrahepatic inflammation, hindering the occurrence and progress of fibrogenesis. However, the role of SESN2 in HCC is controversial due to its paradoxical pro-autophagic and anti-apoptotic effects. In conclusion, this review summarizes the biological functions of SESN2 in hypoxia, genotoxic stress, oxidative stress, ER stress, and inflammation, and specifically emphasizes the pathophysiological significance of SESN2 in liver diseases, aiming to providing a comprehensive understanding for SESN2 as a potential therapeutic target in liver diseases.

Vehicular emissions have become a primary anthropogenic source of urban atmospheric volatile halogenated hydrocarbons (VHCs) with the rapid increase of vehicle population, while characteristics of the VHC emissions from different vehicles were rarely systematically investigated. In this study, the on-road tailpipe emissions were sampled from seven in-use vehicles, including two light-duty gasoline vehicles (LDGV), three light-duty diesel trucks (LDDT), one heavy-duty diesel truck (HDDT), and a liquefied petroleum gas-electric hybrid bus (LPGB), using a portable emission measurement system (PEMS) combined with summa canisters, and 35 individual VHC species were identified by a gas chromatography mass spectrometry detector (GC-MSD). Results showed that VHC emissions under urban driving conditions were much higher than those on the suburban roads and highways. The VHC emission factors of LDGV were 1.2 ± 0.34 mg/km and 3.6 ± 1.5, 6.8 ± 0.89, and 1.6 ± 0.28 mg/km for LDDT, HDDT, and LPGB, respectively. For the LDGV, chlorobenzene, 1,2-dichloroethane, and hexachlorobutadiene were the top three VHC species. 1,2-Dichloroethane, trichloromethane, and methyl chloride were the main VHC constituents in the LDDT. Chlorobenzene was the most abundant VOC species for the HDDT, followed by 1,2-dichloroethane and 1,4-dichlorobenzene. The major species for LPGB were 1,2,4-trichlorobenzene, carbon tetrachloride, and benzyl chloride. The major tailpipe VHC species obtained in this study were partial consistent with previous studies with different test methods. The results provide an initial evaluation of the tailpipe VHC emissions, which may provide experimental data support for the refined source apportionment of atmospheric VHCs and the control of vehicular VHCs.

A surge in the size of the automobile population has caused vehicular emissions to become a major source of urban atmospheric pollution. Elevating standards is an effective method of controlling vehicular emissions and improving air quality. Light-duty vehicles are the major contributors to HC and CO emissions as they constitute a large proportion of all vehicles. Consequently, controlling light-duty vehicular emissions has been the primary means of air pollution prevention in China. This paper first reviews the progress of emission control standards in mainland China. Second, it analyzes features of the China 6 emissions standards, namely the continuation of European standards, the harmony of global technology regulations, and fusion with the standards of the USA. This is followed by a description and discussion of the status of research on mainstream after-treatment technologies such as the gasoline particulate filter, lean-NOx trap, and selective catalytic reduction. Finally, this study argues that the technical routes for implementing three-way catalysts, gasoline particulate filters, and onboard refueling vapor recovery in gasoline vehicles and diesel oxidation catalysts, diesel particulate filters, and selective catalyst reduction in diesel vehicles meet China 6 standards. Moreover, onboard diagnostics-based control of light vehicle emissions is introduced, and the development directions of vehicle gasoline (the reduction in sulfur, olefin, and aromatic content and vapor pressure control in summer) and vehicle diesel (an increase in the Cetane number and reduction in the forecasted polycyclic aromatic content) are discussed. State-of-the-art outlook for light-duty vehicle emission control standards in China

Hepatocyte senescence is a key event participating in the progression of alcoholic liver disease. Autophagy is a critical biological process that controls cell fates by affecting cell behaviors like senescence. Pterostilbene is a natural compound with hepatoprotective potential; however, its implication for alcoholic liver disease was not understood. This study was aimed to investigate the therapeutic effect of pterostilbene on alcoholic liver disease and elucidate the potential mechanism. Our results showed that pterostilbene alleviated ethanol-triggered hepatocyte damage and senescence. Intriguingly, pterostilbene decreased the protein abundance of cellular communication network factor 1 (CCN1) in ethanol-exposed hepatocytes, which was essential for pterostilbene to execute its anti-senescent function. In vivo studies verified the anti-senescent effect of pterostilbene on hepatocytes of alcohol-intoxicated mice. Pterostilbene also relieved senescence-associated secretory phenotype (SASP), redox imbalance, and steatosis by suppressing hepatic CCN1 expression. Mechanistically, pterostilbene-forced CCN1 reduction was dependent on posttranscriptional regulation via autophagy machinery but not transcriptional regulation. To be specific, pterostilbene restored autophagic flux in damaged hepatocytes and activated p62-mediated selective autophagy to recognize and lead CCN1 to autolysosomes for degradation. The protein abundance of Sestrin2 (SESN2), a core upstream modulator of autophagy pathway, was decreased in ethanol-administrated hepatocytes but rescued by co-treatment with pterostilbene. Induction of SESN2 protein by pterostilbene rescued ethanol-triggered autophagic dysfunction in hepatocytes, which then reduced senescence-associated markers, postponed hepatocyte senescence, and relieved alcohol-caused liver injury and inflammation. In conclusion, this work discovered a novel compound pterostilbene with therapeutic implications for alcoholic liver disease and uncover its underlying mechanism.

Ambient temperature has substantial impacts on vehicle emissions, but the impacts may differ between traditional and alcohol gasolines. The objective of this study was to investigate the effects of temperature on gaseous and particulate emissions with both traditional and alcohol gasoline. Regulated gaseous, particle mass (PM), particle number (PN) and black carbon (BC) emissions from typical passenger vehicles were separately quantified with gasoline, E10 (10% ethanol and 90% gasoline by volume) and M15 (15% methanol and 85% gasoline by volume) at both 30°C and −7°C. The particulate emissions with all fuels increased significantly with decreased temperature. The PM emissions with E10 were only 48.0%–50.7% of those with gasoline at 30°C but increased to 59.2%–79.4% at −7°C. The PM emissions with M15 were comparable to those with gasoline at 30°C, but at −7°C, the average PM emissions were higher than those with gasoline. The variation trend of PN emissions was similar to that of PM emissions with changes in the fuel and temperature. At 30°C, the BC emissions were lower with E10 and M15 than with gasoline in most cases, but E10 and M15 might emit more BC than gasoline at −7°C, especially M15. The results of the transient PN and BC emission rates show that particulate emissions were dominated mainly by those emitted during the cold-start moment. Overall, the particulate emissions with E10 and M15 were more easily affected by ambient temperature, and the advantages of E10 and M15 in controlling particulate emissions declined as the ambient temperature decreased.

Organic anion transporting polypeptides (OATPs) are important transporter proteins that are expressed at the plasma membrane of cells, where they mediate the influx of endogenous and exogenous substances including hormones, natural compounds and many clinically important drugs. OATP1A2, OATP2B1, OATP1B1 and OATP1B3 are the most important OATP isoforms and influence the pharmacokinetic performance of drugs. These OATPs are highly expressed in the kidney, intestine and liver, where they determine the distribution of drugs to these tissues. Herbal medicines are increasingly popular for their potential health benefits. Humans are also exposed to many natural compounds in fruits, vegetables and other food sources. In consequence, the consumption of herbal medicines or food sources together with a range of important drugs can result in drug-herb/food interactions via competing specific OATPs. Such interactions may lead to adverse clinical outcomes and unexpected toxicities of drug therapies. This review summarises the drug-herb/food interactions of drugs and chemicals that are present in herbal medicines and/or food in relation to human OATPs. This information can contribute to improving clinical outcomes and avoiding unexpected toxicities of drug therapies in patients.

Tailpipe emissions from light-duty gasoline vehicles usually deteriorate over time. The accumulation of engine deposits due to inadequate gasoline detergency is considered to be one of the major causes of such emission deterioration. Six in-use light-duty gasoline vehicles in Beijing were tested to investigate the impact of engine deposits on emissions of hydrocarbons (HC), carbon monoxide (CO) and nitrogen oxides (NO x ). Emissions under cold start and hot running test conditions from the six light duty vehicles were measured before and after engine deposits were removed. Results show that although individual vehicles reacted differently for each of the pollutants, elimination of engine deposits on average reduced HC emissions under hot running conditions by 29.4%, CO emissions under cold start conditions by 23.0% and CO emissions under hot running conditions by 35.5% (t < 0.05 in all cases). No pollutant emissions increased with statistical significance (t < 0.05) after the removal of engine deposits. Variations of emission changes upon removal of engine deposits were observed. Such variations are in line with previous studies, implying that the impact patterns of engine deposits on vehicle emissions may be subject to many influencing factors that are not fully understood and difficult to control under all conditions. A statistical view of the impact of engine deposits on vehicle emissions may be appropriate for evaluation of emissions reductions across a city or a country. It is necessary to maintain sufficient and effective gasoline fuel detergency in practice to keep the engines clean and in turn reduce vehicle emissions.