Energy-Efficient Multi-Trip Routing for Municipal Solid Waste Collection by Contribution-Based Adaptive Particle Swarm Optimization

Waste collection is an important part of waste management system.Transportation costs and carbon emissions can be greatly reduced by proper vehicle routing.Meanwhile,each vehicle can work again after achieving its capacity limit and unloading the waste.For this,an energy-efficient multi-trip vehicle routing model is established for municipal solid waste collection,which incorporates practical factors like the limited capacity,maximum working hours,and multiple trips of each vehicle.Considering both economy and environment,fixed costs,fuel costs,and carbon emission costs are minimized together.To solve the formulated model effectively,contribution-based adaptive particle swarm optimization is proposed.Four strategies named greedy learning,multi-operator learning,exploring learning,and exploiting learning are specifically designed with their own searching priorities.By assessing the contribution of each learning strategy during the process of evolution,an appropriate one is selected and assigned to each individual adaptively to improve the searching efficiency of the algorithm.Moreover,an improved local search operator is performed on the trips with the largest number of waste sites so that both the exploiting ability and the convergence accuracy of the algorithm are improved.Performance of the proposed algorithm is tested on ten waste collection instances,which include one real-world case derived from the Green Ring Company of Jiangbei New District,Nanjing,China,and nine synthetic instances with increasing scales generated from the commonly-used capacitated vehicle routing problem benchmark datasets.Comparisons with five state-of-the-art algorithms show that the proposed algorithm can obtain a solution with a higher accuracy for the constructed model.

Toosendanin-induced change of dopamine level detected by microdialysis in vivo at rat striatum

To investigate the effect on central nervous transmission of toosendanin (TSN), a presynaptic blocker, rat striatum was perfused in vivo with a TSN-containing artificial cere-brospinal fluid (ACSF) and the level of dopamine (DA) as well as related metabolites in the collected dialysates has been determined by a microbore HPLC with electrochemical detection (mi-crobore HPLC-ECD). The results are as follows: ( i ) TSN induced a biphasic change of DA from its basal level;( ii ) the basal contents of two metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) increased in turn and stayed at a higher level than basal control for a long period. The basal level of 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of 5-hydroxytryptamine(5-HT), had a change similar to that of HVA; (iii) after per-fusion with TSN-containing ACSF, high K+-evoked DA release was inhibited. These results show that TSN does not selectively affect acetylcholine (ACh) release, but probably acts on a common

Notch signaling inhibitor and anti-PD-L1 antibody combination therapies decelerate tumor progression in pancreatic cancer

Objective:Pancreatic cancer(PC)is a highly lethal malignancy with an immunosuppressive environment.Yet,current immune checkpoint inhibitor monotherapies have shown limited efficacy in PC,prompting the need for combination therapies.Herein,we hypothesized that combinations of Notch signaling inhibitor and anti-ligand programmed death-ligand 1(PD-L1)antibody immunotherapy would show synergistic efficacy.Methods:The baseline expression of PD-L1 and HES1 was measured in PC cell lines,single-cell RNA-seq data of PC(GSA:CRA001160),and cBioPortal databases.In an in vitro study,MIA PaCa2 and SW1990 were used to explore the mechanism between Notch signaling and PD-L1.To study the effects in vivo,a subcutaneous tumor model was established using Pan02 cells treated with either anti-PD-L1 monoclonal antibody and/or Notch inhibitor DAPT.The study performed involving human samples was approved by the Ethics Committee of Peking Union Medical College Hospital(approval No.S-K460,approval date:April 23,2018).Animal studies were approved by the Animal Research Ethics Committee of Peking Union Medical College Hospital(approval No.XHDW-2019-049,approval date:November 28,2019).Results:The Notch signaling inhibitor upregulated PD-L1 expression in PC tumor cells both in vitro and in vivo.Notch effector HES1 knockdown produced PD-L1 upregulation in both MIA PaCa2 and SW1990 cells.Combined DAPT and anti-PD-L1 antibody treatment of Pan02 subcutaneous tumor model resulted in significantly reduced tumor weights compared to that with monotherapy,as well as significantly reduced Ki67 than that in the monotherapy group and control group.Flow cytometry analysis revealed significantly increased CD8+T cell infiltration in tumors of the combination group compared with those of the monotherapy group.Conclusion:Notch signaling blockade might enhance the antitumor effect of anti-PD-L1 therapy in PC.