Mapping Science Based on Research Content Similarity

Maps of science representing the structure of science help us understand science and technology development. Thus, research in scientometrics has developed techniques for analyzing research activities and for measuring their relationships; however, navigating the recent scientific landscape is still challenging, since conventional inter-citation and co-citation analysis has difficulty in applying to recently published articles and ongoing projects. Therefore, to characterize what is being attempted in the current scientific landscape, this article proposes a content-based method of locating research articles/projects in a multi-dimensional space using word/paragraph embedding. Specifically, for addressing an unclustered problem, we introduced cluster vectors based on the information entropies of technical concepts. The experimental results showed that our method formed a clustered map from approx. 300 k IEEE articles and NSF projects from 2012 to 2016. Finally, we confirmed that formation of specific research areas can be captured as changes in the network structure

Hepatic inflammation facilitates transcription-associated mutagenesis via AID activity and enhances liver tumorigenesis.

First published online: May 12, 2015Chronic inflammation triggers the aberrant expression of a DNA mutator enzyme, activation-induced cytidine deaminase (AID), and contributes to tumorigenesis through the accumulation of genetic aberrations. To gain further insight into the inflammation-mediated genotoxic events required for carcinogenesis, we examined the role of chronic inflammation in the emergence of genetic aberrations in the liver with constitutive AID expression. Treatment with thioacetamide (TAA) at low-dose concentrations caused minimal hepatic inflammation in both wild-type (WT) and AID transgenic (Tg) mice. None of the WT mice with low-dose TAA administration or AID Tg mice without hepatic inflammation developed cancers in their liver tissues over the 6 month study period. In contrast, all the AID Tg mice with TAA treatment developed multiple macroscopic hepatocellular carcinomas during the same observation period. Whole exome sequencing and additional deep-sequencing analyses revealed the enhanced accumulation of somatic mutations in various genes, including dual specificity phosphatase 6 (Dusp6), early growth response 1 (Egr1) and inhibitor of DNA binding 2 (Id2), which are putative tumor suppressors, in AID-expressing liver with TAA-mediated hepatic inflammation. Microarray and quantitative reverse transcription-polymerase chain reaction analyses showed the transcriptional upregulation of various genes including Dusp6, Egr1 and Id2 under hepatic inflammatory conditions. Together, these findings suggest that inflammation-mediated transcriptional upregulation of target genes, including putative tumor suppressor genes, enhances the opportunity for inflamed cells to acquire somatic mutations and contributes to the acceleration of tumorigenesis in the inflamed liver tissues