Objective: The objective of this study was to explore the evolution footprints of simulated driving research in the past 20 years through rigorous and systematic bibliometric analysis, to provide insights regarding when and where the research was performed and by whom and how the mainstream content evolved over the years.
Methods: The analysis began with data retrieval in Web of Science with defined search terms related to simulated driving. BibExcel and CiteSpace were employed to conduct the performance analysis and co-citation network analysis; that is, probe of the performance of institutes, journals, authors, and research hotspots.
Results: A total of 3,766 documents were filtered out and presented an exponential growth from 1997 to 2016. The United States contributed the most publications as well as international collaborations followed by Germany and China. In addition, several universities in The Netherlands and the United States dominated the list of contributing institutes. The leading journals were in transportation and ergonomics. The leading researchers were also recognized among the 8,721 contributing authors, such as J. D. Lee, D. L. Fisher, J. H. Kim, and K. A. Brookhuis. Finally, the co-citation analysis illuminated the evolution of simulated driving research that covered the following topics roughly in chronological order: task-induced stress, drivers with neurological disorders, alertness and sleepiness while driving, trust toward driving assistance systems, driver distraction, the effect of drug use, the validity of simulators, and automated driving.
Conclusions: This article employed bibliometric tools to probe the contributing countries, institutes, journals, authors, and mainstream hotspots of simulated driving research in the past 20 years. A systematic bibliometric analysis of this field will help researchers realize the panorama of global simulated driving and establish future research directions. 相似文献
Fine particulatematter (PM2.5) is associated with increased risks of Alzheimer’s disease (AD),yet the toxicologicalmechanisms of PM2.5 promoting AD remain unclear. In this study,wildtype
and APP/PS1 transgenic mice (AD mice) were exposed to either filtered air (FA) or PM2.5 for eight weeks with a real-world exposure system in Taiyuan, China (mean PM2.5 concentration
in the cage was 61 μg/m3). We found that PM2.5 exposure could remarkably aggravate AD mice’s ethological and brain ultrastructural damage, along with the elevation of the pro-inflammatory cytokines (IL-6 and TNF-α), Aβ-42 and AChE levels and the decline of ChAT levels in the brains. Based on high-throughput sequencing results, some differentially expressed (DE) mRNAs and DE miRNAs in the brains of AD mice after PM2.5 exposure were screened.Using RT-qPCR, seven DEmiRNAs (mmu-miR-193b-5p, 122b-5p, 466h-3p, 10b-5p, 1895, 384–5p, and 6412) and six genes (Pcdhgb8, Unc13b, Robo3, Prph, Pter, and Tbata)
were evidenced the and verified. Two miRNA-target gene pairs (miR-125b-Pcdhgb8 pair and miR-466h-3p-IL-17Rα/TGF-βR2/Aβ-42/AChE pairs) were demonstrated that they were more
related to PM2.5-induced brain injury. Results of Gene Ontology (GO) pathways and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways predicted that synaptic and postsynaptic
regulation, axon guidance, Wnt, MAPK, and mTOR pathways might be the possible regulatory mechanisms associated with pathological response. These revealed that PM2.5-
elevated pro-inflammatory cytokine levels and PM2.5-altered neurotransmitter levels in AD mice could be the important causes of brain damage and proposed the promising miRNA
andmRNA biomarkers and potentialmiRNA-mRNA interaction networks of PM2.5-promoted AD. 相似文献