ObjectiveThis study is to document the clinical characteristics and improvement in management of acute myocardial infarction (AMI) in Chinese population.ResultsThis study included 64,654 patients (23,805 patients in 2011, 40,849 patients in 2013), of which STEMI and NSTEMI account for 85.09% and 14.91%, respectively. From 2011 to 2013, significant improvement has been achieved in the recanalization rate of PCI (96.01% vs. 98.63%, P < 0.001) and in-hospital deaths (4.52% vs. 3.55%, P = 0.038). Although the time of door-to-balloon and the duration of PCI were satisfactorily controlled within 90min and 60min, respectively, the onset-to-FMC time (≈3.5h) and door-to-thrombolysis time (≈1.1h) limited the efficiency of management. The total cost of medical care showed no increase from 2011 to 2013, but the patient's paid Portion decreased from 20.33% to 13.96%.Materials and MethodsThe AMI patients admitted in the general hospitals in 2011 and 2013 were retrospectively analyzed according to the data reported to the Single Disease Quality Control Information Systemissued by Chinese Hospital Association.ConclusionCompared to the Western countries, STEMI accounted for a larger portion of AMI, and the AMI management in China basically meets the standards of the quality control of guidelines. With improvement of management, there was no increase in the total medical cost, while the patient's paid portion was actually reduced. In future, improvement of transportation strategy and the public medical education are recommended to shorten the onset-to-FMC time to further improve the outcome of AMI patients.

An expression of the extropy of a mixed system's lifetime was given firstly. Based on this expression, two mixed systems with same signature but with different components were compared. It was shown that the extropy of lifetime of a mixed system equals to that of its dual system if the lifetimes of the components have symmetric probability density function. Moreover, some bounds of the extropy of lifetimes of mixed systems were obtained and the concept of Jensen–extropy (JE) divergence of mixed systems was proposed. The JE divergence is non-negative and it can be used as an alternative information criteria for comparing mixed systems with homogeneous components. To illustrate the applications of JE divergence, some examples are addressed at the end of this paper.

IntroductionUlcerative 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.MethodsDextran 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.ResultsThe 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-1β, 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.ConclusionApigenin 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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