Fairness in online vehicle-cargo matching: An intuitionistic fuzzy set theory and tripartite evolutionary game approach

This paper explores the concept of fairness and equitable matching in an on-line vehicle-cargo matching setting, addressing the varying degrees of satisfaction experienced by shippers and carriers. Relevant indicators for shippers and carriers in the on-line matching process are categorized as attributes, expectations, and reliability, which are subsequent quantified to form satisfaction indicators. Employing the intuitionistic fuzzy set theory, we devise a transformed vehicle-cargo matching optimization model by combining the fuzzy set's membership, non-membership, and uncertainty information. Through an adaptive interactive algorithm, the matching scheme with fairness concerns is solved using CPLEX. The effectiveness of the proposed matching mechanism in securing high levels of satisfaction is established by comparison with three benchmark methods. To further investigate the impact of considering fairness in vehicle-cargo matching, a shipper-carrier-platform tripartite evolutionary game framework is developed under the waiting response time cost (WRTC) sharing mechanism. Simulation results show that with fairness concerns in vehicle-cargo matching, all stakeholders are better off: The platform achieves positive revenue growth, and shippers and carriers receive positive subsidy. This study offers both theoretical insights and practical guidance for the long-term and stable operation of the on-line freight stowage industry.Comment: 36 pages, 15 figure

Differentiation-inducing and anti-proliferative activities of isoliquiritigenin and all-trans-retinoic acid on B16F0 melanoma cells: Mechanisms profiling by RNA-seq

Melanoma is a cancer that arises from melanocytes, specialized pigmented cells that are found predominantly in the skin. The incidence of malignant melanoma has significantly increased over the last decade. With the development of therapy, the survival rate of some kind of cancer has been improved greatly. But the treatment of melanoma remains unsatisfactory. Much of melanoma's resistance to traditional chemotherapy is believed to arise intrinsically, by virtue of potent growth and cell survival-promoting genetic alteration. Therefore, significant attention has recently been focused on differentiation, therapy, as well as differentiation inducer compounds. In previous study, we found isoliquiritigenin (ISL), a natural product extracted from licorice, could induce B16F0 melanoma cell differentiation. Here we investigated the transcriptional response of melanoma differentiation process induced by ISL and all-trans-retinoic acid (RA). Results showed that 390 genes involves in 201 biochemical pathways were differentially expressed in ISL treatment and 304 genes in 193 pathways in RA treatment. Differential expressed genes (DGEs, fold-change (FC) >= 10) with the function of anti-proliferative and differentiation inducing indicated a loss of grade malignancy characteristic. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated glutathione metabolism, glycolysis/gluconeogenesis and pentose phosphate pathway were the top three relative pathway perturbed by ISL, and mitogen-activated protein kinase (MAPK) signaling pathway was the most important pathway in RA treatment. In the analysis of hierarchical clustering of DEGs, we discovered 72 DEGs involved in the process of drug action. We thought Cited1, Tgm2, Xaf1, Cd59a, Fbxo2, Adh7 may have critical role in the differentiation of melanoma. The evidence displayed herein confirms the critical role of reactive oxygen species (ROS) in melanoma pathobiology and provides evidence for future targets in the development of next-generation biomarkers and therapeutics. (C) 2016 Elsevier B.V. All rights reserved

Modulation of platelet-derived microparticles to adhesion and motility of human rheumatoid arthritis fibroblast-like synoviocytes.

Platelet-derived microparticles (PMPs) are closely associated with disease activity in rheumatoid arthritis (RA) and contribute to the inflammatory process. Rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) play important roles in the progression of joint destruction. The aim of this study is to demonstrate whether PMPs affect the adhesion and motility of RA-FLSs. Our data indicated that PMPs promoted migration, invasion and adhesion to extracellular matrix (ECM) of RA-FLSs. Further study showed that PMPs up-regulated the expression of matrix metalloproteinase-1 (MMP1) and increased the level of phosphorylation of NF-κB (p-NF-κB) and Erk (p-Erk) in RA-FLSs. These results suggest that PMPs promote RA-FLSs adhesion and motility presumably by increasing MMP1 via activating Erk-mediated NF-κB pathway

Effects of PMPs on gene expression of RA-FLSs.

<p>(A) The clustering analysis compared the differences of gene expression between the group without (A6647) and with 50 μg/ml (A6648) PMPs: Red region, genes up-regulated in RA-FLSs. Green region, genes down-regulated in RA-FLSs. (B) Top 10 differential genes of pathway enrichment analysis are listed. (C) Relative mRNA levels of MMP1 and MMP2 of RA-FLSs after treated with PMPs were measured by RT-qPCR and GAPDH was used as an equal loading control. (*<i>p</i> < 0.05 vs. 0 μg/ml PMPs). (D) Protein levels of MMP1 and MMP2 were detected by western blot and normalized to GAPDH. (E) Quantification of protein levels was shown (*<i>p</i> < 0.05 vs. 0 μg/ml PMPs).</p

Effects of PMPs on adhesion of RA-FLSs.

<p>RA-FLSs were seeded onto the collagen I- (a), fibronectin- (b) or matrigel- (c) coated 96-well culture plates, respectively, and incubated at 37°C for 45 min. The CCK-8 assays were conducted to quantify the number of the adhesive cells by absorbance at 450 nm, and performed in six wells from four independent experiments. (*<i>p <</i> 0.05 vs. 0 μg/ml PMPs).</p

Effects of PMPs on the expression and activation of Erk and Akt in RA-FLSs.

<p>(A and B) Protein levels of p-Erk, Erk, Akt and p-Akt were analyzed from PMPs-treated RA-FLSs with corresponding antibodies. Quantification analysis was shown and expressed as fold-change. (*p < 0.05 vs. 0 μg/ml PMPs) (C) Quantification of the migration assay of RA-FLSs with PMPs and PD98059 was shown. (*<i>p <</i> 0.05 vs. PMPs) (D and E) Western blotting was performed to detect Erk, p-Erk, IκB, p- IκB, NF-κB and p- NF-κB of RA-FLSs after treated with PMPs and PD98059. (*<i>p</i> < 0.05 vs. PMPs) (F)RT-qPCR was conducted to detect the expression of MMP1 in RA-FLSs after treated with PMPs and PD98059. (*<i>p</i> < 0.05 vs. PMPs).</p

Verification of PMPs by flow cytometry.

<p>PMPs were isolated from platelet-rich plasma and stained with PE-labeled anti-CD41.The events in P2 were PMPs, which were compared to 0.82 μm standard microspheres.</p

Effects of PMPs on the expression and activation of IκB and NF-κB in RA-FLSs.

<p>(A and B) Western blotting was performed to detect the expression of p-IκB, IκB, NF-κB and p-NF-κB of RA-FLSs after treated with PMPs. The quantification was expressed as fold-change of 0μg/ml PMPs. (*<i>p</i> < 0.05 vs. 0 μg/ml PMPs) (C) Quantification of the migration assay of RA-FLSs treated with PMPs and JSH-23 was shown. (*<i>p <</i> 0.05 vs. PMPs) (D and E) After treated with PMPs and JSH-23, the expression of p-IκB, IκB, p-NF-κB and NF-κB of RA-FLSs were detected by western blot. (*<i>p</i> < 0.05 vs. PMPs) (F) After treated with PMPs and JSH-23, the expression of MMP1 was detected by RT-qPCR. (*<i>p</i> < 0.05 vs. PMPs).</p