A Novel Multi-agent Formation Control Law With Collision Avoidance

In this paper a stable formation control law that simultaneously ensures collision avoidance has been proposed.It is assumed that the communication graph is undirected and connected.The proposed formation control law is a combination of the consensus term and the collision avoidance term(CAT).The first order consensus term is derived for the proposed model,while ensuring the Lyapunov stability.The consensus term creates and maintains the desired formation shape,while the CAT avoids the collision.During the collision avoidance,the potential function based CAT makes the agents repel from each other.This unrestricted repelling magnitude cannot ensure the graph connectivity at the time of collision avoidance.Hence we have proposed a formation control law,which ensures this connectivity even during the collision avoidance.This is achieved by the proposed novel adaptive potential function.The potential function adapts itself,with the online tuning of the critical variable associated with it.The tuning has been done based on the lower bound of the critical variable,which is derived from the proposed connectivity property.The efficacy of the proposed scheme has been validated using simulations done based on formations of six and thirty-two agents respectively.

Synergistic effects of methyl 2-cyano-3,11-dioxo-18beta-olean-1,-12-dien-30-oate and erlotinib on erlotinib-resistant non-small cell lung cancer cells

Non-small cell lung cancer(NSCLC)is often characterized by an underlying mutation in the epidermal growth factor receptor(EGFR),contributing to aggressive metastatic disease.Methyl 2-cyano-3,11-dioxo-18 beta-olean-1,12-dien-30-oate(CDODA-Me),a glycyrrhetinic acid derivative,reportedly improves the therapeutic response to erlotinib(ERL),an EGFR tyrosine kinase inhibitor.In the present study,we performed a series of studies to demonstrate the efficacy of CDODA-Me(2μM)in sensitizing HCC827 R(ERL-resistant)cells to ERL.Herein,we first established the selectivity of ERL-induced drug resistance in the HCC827 R cells,which was sensitized when ERL was combined with CDODA-Me(2μM),shifting the IC50 from 23.48μM to 5.46μM.Subsequently,whole transcriptomic microarray expression data demonstrated that the combination of ERL+CDODA-Me elicited 210 downregulated genes(0.44%of the whole transcriptome(WT))and 174 upregulated genes(0.36%of the WT),of which approximately 80%were unique to the ERL+CDODA-Me group.Synergistic effects centered on losses to cell cycle progression transcripts,a reduction of minichromosome maintenance complex components(MCM2-7),all key components of the Cdc45·MCM2-7 GINS(CMG)complex,and replicative helicases;these effects were tantamount to the upregulation of processes associated with the nuclear factor erythroid 2 like 2 translational response to oxidative stress,including sulfiredoxin 1,heme oxygenase 1,and stress-induced growth inhibitor 1.Collectively,these findings indicate that the synergistic therapeutic effects of ERL+CDODA-Me on resistant NSCLC cells are mediated via the inhibition of mitosis and induction of oxidative stress.