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1.
J Environ Sci (China) ; 127: 143-157, 2023 May.
Article in English | MEDLINE | ID: mdl-36522048

ABSTRACT

The coastal eco-city of Fuzhou in Southeastern China has experienced severe ozone (O3) episodes at times in recent years. In this study, three typical synoptic circulations types (CTs) that influenced more than 80% of O3 polluted days in Fuzhou during 2014-2019 were identified using a subjective approach. The characteristics of meteorological conditions linked to photochemical formation and transport of O3 under the three CTs were summarized. Comprehensive Air Quality Model with extensions was applied to simulate O3 episodes and to quantify O3 sources from different regions in Fuzhou. When Fuzhou was located to the west of a high-pressure system (classified as "East-ridge"), more warm southwesterly currents flowed to Fuzhou, and the effects of cross-regional transport from Guangdong province and high local production promoted the occurrence of O3 episodes. Under a uniform pressure field with a low-pressure system occurring to the east of Fuzhou (defined as "East-low"), stagnant weather conditions caused the strongest local production of O3 in the atmospheric boundary layer. Controlled by high-pressure systems over the mainland (categorized as "Inland-high"), northerly airflows enhanced the contribution of cross-regional transport to O3 in Fuzhou. The abnormal increases of the "East-ridge" and "Inland-high" were closely related to O3 pollution in Fuzhou in April and May 2018, resulting in the annual maximum number of O3 polluted days during recent years. Furthermore, the rising number of autumn O3 episodes in 2017-2019 was mainly related to the "Inland-high", indicating the aggravation of cross-regional transport and highlighting the necessity of enhanced regional collaboration and efforts in combating O3 pollution.


Subject(s)
Air Pollutants , Air Pollution , Ozone , Ozone/analysis , Air Pollutants/analysis , Photochemical Processes , Environmental Monitoring/methods , Air Pollution/analysis , Seasons , China
2.
Front Nutr ; 9: 1062961, 2022.
Article in English | MEDLINE | ID: mdl-36590200

ABSTRACT

Introduction: Ulcerative colitis (UC), a chronic non-specific colorectal inflammatory disease with unclear etiology, has long plagued human health. Gut microbiota dysbiosis destroy homeostasis of the colon, which is closely related to ulcerative colitis progress. Apigenin, a flavonoid widely present in celery, has been found to improve ulcerative colitis. However, the potential molecular mechanism of apigenin ameliorating ulcerative colitis through protecting intestinal barrier and regulating gut microbiota remains undefined. Methods: Dextran sodium sulfate (DSS)-induced colitis mouse model was conducted to evaluate the effect of apigenin on UC. Disease activity index score of mice, colon tissue pathological, cytokines analysis, intestinal tight junction proteins expression, and colonic content short-chain fatty acids (SCFAs) and 16S rRNA gene sequencing were conducted to reflect the protection of apigenin on UC. Results: The results indicated that apigenin significantly relieved the intestinal pathological injury, increased goblet cells quantity and mucin secretion, promoted anti-inflammatory cytokines IL-10 expression, and inhibited the expression of proinflammatory cytokines, TNF-α, IL-1ß, IL-6 and MPO activity of colon tissue. Apigenin increased ZO-1, claudin-1 and occludin expressions to restore the integrity of the intestinal barrier. Moreover, apigenin remodeled the disordered gut microbiota by regulating the abundance of Akkermansia, Turicibacter, Klebsiella, Romboutsia, etc., and its metabolites (SCFAs), attenuating DSS-induced colon injury. We also investigated the effect of apigenin supplementation on potential metabolic pathways of gut microbiota. Conclusion: Apigenin effectively ameliorated DSS-induced UC via balancing gut microbiome to inhibit inflammation and protect gut barrier. With low toxicity and high efficiency, apigenin might serve as a potential therapeutic strategy for the treatment of UC via regulating the interaction and mechanism between host and microorganism.

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