LaCAM: Search-Based Algorithm for Quick Multi-Agent Pathfinding

We propose a novel complete algorithm for multi-agent pathfinding (MAPF) called lazy constraints addition search for MAPF (LaCAM). MAPF is a problem of finding collision-free paths for multiple agents on graphs and is the foundation of multi-robot coordination. LaCAM uses a two-level search to find solutions quickly, even with hundreds of agents or more. At the low-level, it searches constraints about agents' locations. At the high-level, it searches a sequence of all agents' locations, following the constraints specified by the low-level. Our exhaustive experiments reveal that LaCAM is comparable to or outperforms state-of-the-art sub-optimal MAPF algorithms in a variety of scenarios, regarding success rate, planning time, and solution quality of sum-of-costs.Comment: to be presented at AAAI-2

Engineering LaCAM∗^\ast: Towards Real-Time, Large-Scale, and Near-Optimal Multi-Agent Pathfinding

This paper addresses the challenges of real-time, large-scale, and near-optimal multi-agent pathfinding (MAPF) through enhancements to the recently proposed LaCAM* algorithm. LaCAM* is a scalable search-based algorithm that guarantees the eventual finding of optimal solutions for cumulative transition costs. While it has demonstrated remarkable planning success rates, surpassing various state-of-the-art MAPF methods, its initial solution quality is far from optimal, and its convergence speed to the optimum is slow. To overcome these limitations, this paper introduces several improvement techniques, partly drawing inspiration from other MAPF methods. We provide empirical evidence that the fusion of these techniques significantly improves the solution quality of LaCAM*, thus further pushing the boundaries of MAPF algorithms.Comment: 20 page

Fault-Tolerant Offline Multi-Agent Path Planning

We study a novel graph path planning problem for multiple agents that may crash at runtime, and block part of the workspace. In our setting, agents can detect neighboring crashed agents, and change followed paths at runtime. The objective is then to prepare a set of paths and switching rules for each agent, ensuring that all correct agents reach their destinations without collisions or deadlocks, despite unforeseen crashes of other agents. Such planning is attractive to build reliable multi-robot systems. We present problem formalization, theoretical analysis such as computational complexities, and how to solve this offline planning problem.Comment: to be presented at AAAI-2

Fibrinopeptide A release is necessary for effective B:b interactions in polymerisation of variant fibrinogens with impaired A:a interactions

Fibrin polymerisation is mediated by interactions between knobs 'A' and 'B' exposed by thrombin cleavage, and holes 'a' and 'b'. We demonstrated markedly delayed thrombin-catalysed fibrin polymerisation, through B:b interactions alone, of recombinant gamma D364H-fibrinogen with impaired hole 'a'. To determine whether recombinant variant fibrinogens with no release of fibrinopeptide A (FpA) polymerise similarly to gamma D364H-fibrinoge, we examined two variant fibrinogens with substitutions altering knob 'A', A alpha 17A- and A alpha 17C-fibrinogen. We examined thrombin- or batroxobin-catalysed fibrinopeptide release by HPLC, fibrin clot formation by turbidity and fibrin clot structure by scanning electron microscopy (SEM) and compared the results of the variants with those for gamma D364H-fibrinogen. Thrombin-catalysed FpA release of A alpha 17A-fibrinogen was substantially delayed and none observed for A alpha 17C-fibrinogen; fibrinopeptide B (FpB) release was delayed for all variants. All variant fibrinogens showed substantially impaired thrombin-catalysed polymerisation; for A alpha 17A-fibrinogen it was delayed less, and for A alpha 17C more than for gamma D364H-fibrinogen. No variants polymerised with batroxobin, which exposed only knob 'A'. The inhibition of variant fibrinogens' polymerisation was dose-dependent on the concentration of either GPRP or GHRP, and both peptides that block holes 'b'. SEM showed that the variant clots from A alpha 17A- and gamma D364H-fibrinogen had uniform, ordered fibres, thicker than normal, whereas A alpha 17C-fibrinogen formed less organised clots with shorter, thinner, and tapered ends. These results demonstrate that FpA release per se is necessary for effective B:b interactions during polymerisation of variant fibrinogens with impaired A:a interactions.ArticleTHROMBOSIS AND HAEMOSTASIS. 109(2):221-228 (2013)journal articl

Time-Independent Planning for Multiple Moving Agents

Typical Multi-agent Path Finding (MAPF) solvers assume that agents move synchronously, thus neglecting the reality gap in timing assumptions, e.g., delays caused by an imperfect execution of asynchronous moves. So far, two policies enforce a robust execution of MAPF plans taken as input: either by forcing agents to synchronize or by executing plans while preserving temporal dependencies. This paper proposes an alternative approach, called time-independent planning, which is both online and distributed. We represent reality as a transition system that changes configurations according to atomic actions of agents, and use it to generate a time-independent schedule. Empirical results in a simulated environment with stochastic delays of agents' moves support the validity of our proposal.Comment: 10 pages, 5 figures, to be presented at AAAI-21, Feb 2021, Virtual Conferenc

Nonsense-mediated mRNA decay was demonstrated in two hypofibrinogenemias caused by heterozygous nonsense mutations of FGG, Shizuoka III and Kanazawa II

We report two novel hypofibrinogenemias, Shizuoka III and Kanazawa II, which are caused by heterozygous mutations in FGG. Shizuoka III showed c.147delT and 147_149insACA in FGG exon 3 and a subsequent frameshift mutation, resulting in mature protein γ23X (native protein: γ49X), and Kanazawa II showed c.1205G>A in FGG exon 9, resulting in γ376X (native protein: γ402X). To determine whether the truncated γ-chains, γ23X and γ376X, were synthesized and participated in the assembly of fibrinogen, mutant-type cDNA vectors were transfected into Chinese hamster ovary (CHO) cells. Significant levels of mutant fibrinogen were not detected by ELISA in the culture media and cell lysates. Immunoblot analysis of cell lysates revealed that the mutant γ-chain of γ376X was observed but intact fibrinogen was not. On the other hand, mutant γ-chain was not observed in γ23X-expressing cells. To demonstrate the involvement of the mechanisms of nonsense-mediated mRNA decay (NMD), we cloned wild- and mutant-type mini-genes containing γ23 or γ376 codon and transfected these into CHO cell lines in the absence or presence of cycloheximide as an NMD inhibitor. mRNA levels were determined using real-time quantitative RT-PCR in CHO cells. In the absence of cycloheximide, levels of mRNAs transcribed from the mutant gene were lower than from the wild-type gene whereas, in the presence of cycloheximide, levels of mRNAs transcribed from the mutant gene increased dose-dependently. Finally, these results demonstrated that mRNAs containing γ23X or γ376X are degraded by the NMD system and translation of the truncated γ-chain polypeptide decrease in patients' hepatocytes, resulting in hypofibrinogenemias.ArticleTHROMBOSIS RESEARCH. 132(4):465-470 (2013)journal articl

Priority Inheritance with Backtracking for Iterative Multi-agent Path Finding

The Multi-agent Path Finding (MAPF) problem consists in all agents having to move to their own destinations while avoiding collisions. In practical applications to the problem, such as for navigation in an automated warehouse, MAPF must be solved iteratively. We present here a novel approach to iterative MAPF, that we call Priority Inheritance with Backtracking (PIBT). PIBT gives a unique priority to each agent every timestep, so that all movements are prioritized. Priority inheritance, which aims at dealing effectively with priority inversion in path adjustment within a small time window, can be applied iteratively and a backtracking protocol prevents agents from being stuck. We prove that, regardless of their number, all agents are guaranteed to reach their destination within finite time, when the environment is a graph such that all pairs of adjacent nodes belong to a simple cycle of length 3 or more (e.g., biconnected). Our implementation of PIBT can be fully decentralized without global communication. Experimental results over various scenarios confirm that PIBT is adequate both for finding paths in large environments with many agents, as well as for conveying packages in an automated warehouse.Comment: 8 pages, 2 figures, 2 tables, to be presented at IJCAI-19, Aug 2019, Maca

Nonsense-mediated mRNA decay was demonstrated in two hypofibrinogenemias caused by heterozygous nonsense mutations of FGG, Shizuoka III and Kanazawa II

We report two novel hypofibrinogenemias, Shizuoka III and Kanazawa II, which are caused by heterozygous mutations in FGG. Shizuoka III showed c.147delT and 147_149insACA in FGG exon 3 and a subsequent frameshift mutation, resulting in mature protein γ23X (native protein: γ49X), and Kanazawa II showed c.1205G>A in FGG exon 9, resulting in γ376X (native protein: γ402X). To determine whether the truncated γ-chains, γ23X and γ376X, were synthesized and participated in the assembly of fibrinogen, mutant-type cDNA vectors were transfected into Chinese hamster ovary (CHO) cells. Significant levels of mutant fibrinogen were not detected by ELISA in the culture media and cell lysates. Immunoblot analysis of cell lysates revealed that the mutant γ-chain of γ376X was observed but intact fibrinogen was not. On the other hand, mutant γ-chain was not observed in γ23X-expressing cells. To demonstrate the involvement of the mechanisms of nonsense-mediated mRNA decay (NMD), we cloned wild- and mutant-type mini-genes containing γ23 or γ376 codon and transfected these into CHO cell lines in the absence or presence of cycloheximide as an NMD inhibitor. mRNA levels were determined using real-time quantitative RT-PCR in CHO cells. In the absence of cycloheximide, levels of mRNAs transcribed from the mutant gene were lower than from the wild-type gene whereas, in the presence of cycloheximide, levels of mRNAs transcribed from the mutant gene increased dose-dependently. Finally, these results demonstrated that mRNAs containing γ23X or γ376X are degraded by the NMD system and translation of the truncated γ-chain polypeptide decrease in patients' hepatocytes, resulting in hypofibrinogenemias.ArticleTHROMBOSIS RESEARCH. 132(4):465-470 (2013)journal articl