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• A more direct relationship between expected performance (EP) and network reliability is presented. • An improved d -MC additive algorithm is proposed to compute EP. • An EP optimization model is developed under the cost constraint, along with an efficient solution method. In this paper, a logistics network is modeled as a cost-related multi-distribution multi-state flow network (CMMFN) where each arc is featured with more than one capacity distribution and each capacity distribution corresponds to a specific cost. Expected performance (EP) that represents the probability-weighted average delivery capacity can serve as a comprehensive measurement of the operational quality of a logistics network. A more direct relationship between EP and network reliability is constructed, and then an improved d -minimal cut (d -MC) additive algorithm is presented to compute EP. Moreover, an EP optimization model is developed subject to a given cost. To facilitate the solution of the EP optimization model, a concept of critical cost vector is defined and a method, called CCV method, is put forth to find all critical cost vectors. Finally, an efficient algorithm integrating the improved d -MC algorithm with the CCV method is proposed for the EP model. An illustration of the proposed model and methods is given through an example; moreover, their applications are demonstrated via a case study. [ABSTRACT FROM AUTHOR]

• This study proposes a new maintenance cost integrated reliability index to measure multi-state flow network (MFN). • This study considers a more general case that an MFN is restored from a degraded state to an expected state. • This study presents an efficient method to evaluate the maintenance cost integrated reliability of an MFN. In this study, every edge of a multi-state flow network (MFN), in addition to multiple capacities, are endowed with a maintenance cost. The existing studies measure the maintenance cost integrated reliability index of an MFN with an assumption that all edges are maintained to restore the network from a degraded state to the largest state, and in contrast, this study takes one step further to consider a more general case that the network is restored from a degraded state to an expected state (including but not limited to the largest state). This study proposes a method to simultaneously evaluate the index MR (d , D , T) , defined as the probability that a network can be restored from a degraded state of capacity level below d to an expected state of capacity level not less than D and the maintenance cost is within a limit T , and the index UR d defined as the probability that network is in a degraded state. The maintenance cost integrated reliability R (d , D , T) is then calculated, which is the ratio of MR (d , D , T) to UR d denoting the ability of an MFN to restore from a failure state to an expected state under the limited maintenance cost. Numerical examples are presented to demonstrate the reliability index R (d , D , T). [ABSTRACT FROM AUTHOR]

• Oridonin, as well as MCC950 and CY-09, inhibits the NLRP3 inflammasome response. • Oridonin, found in traditional Chinese medicine, shows anti-inflammatory property in mice MI model. • Oridonin treatment reduces myocardial fibrosis and preserves cardiac function after MI. Myocardial infarction (MI) triggers a strong inflammatory response that is associated with myocardial fibrosis and cardiac remodeling. Interleukin (IL)-1β and IL-18 are key players in this response and are controlled by NLRP3-inflammatory bodies. Oridonin is a newly reported NLRP3 inhibitor with strong anti-inflammatory activity. We hypothesized that the covalent NLRP3 inhibitor Oridonin could reduce IL-1β and IL-18 expression and ameliorate myocardial fibrosis after myocardial infarction in mice, improve poor heart remodeling, and preserve heart function. Male C57BL/6 mice were subjected to left coronary artery ligation to induce MI and then treated with Oridonin (1, 3, or 6 mg/kg), MCC950 (10 mg/kg), CY-09 (5 mg/kg) or saline three times a week for two weeks. Four weeks after MI, cardiac function and myocardial fibrosis were assessed. In addition, myocardial expressions of inflammatory factors and fibrotic markers were analyzed by western blot, immunofluorescence, enzyme-linked immunosorbent assay, and quantitative real-time polymerase chain reaction. Oridonin treatment preserved left ventricular ejection fraction and fractional shortening, and markedly limited the myocardial infarct size in treated mice. The myocardial fibrosis was lower in the 1 mg/kg group (15.98 ± 1.64)%, 3 mg/kg group (17.39 ± 2.45)%, and 6 mg/kg group (16.76 ± 3.06)% compared to the control group (23.38 ± 1.65)%. Moreover, similar with the results of Oridonin, MCC950 and CY-09 also preserved cardiac function and reduced myocardial fibrosis. The expression levels of NLRP3, IL-1β and IL-18 were decreased in the Oridonin treatment group compared to non-treated group. In addition, myocardial macrophage and neutrophil influxes were attenuated in the Oridonin treated group. The covalent NLRP3-inflammasome inhibitor Oridonin reduces myocardial fibrosis and preserves cardiac function in a mouse MI model, which indicates potential therapeutic effect of Oridonin on acute MI patients. [ABSTRACT FROM AUTHOR]