Large expert-curated database for benchmarking document similarity detection in biomedical literature search

Document recommendation systems for locating relevant literature have mostly relied on methods developed a decade ago. This is largely due to the lack of a large offline gold-standard benchmark of relevant documents that cover a variety of research fields such that newly developed literature search techniques can be compared, improved and translated into practice. To overcome this bottleneck, we have established the RElevant LIterature SearcH consortium consisting of more than 1500 scientists from 84 countries, who have collectively annotated the relevance of over 180 000 PubMed-listed articles with regard to their respective seed (input) article/s. The majority of annotations were contributed by highly experienced, original authors of the seed articles. The collected data cover 76% of all unique PubMed Medical Subject Headings descriptors. No systematic biases were observed across different experience levels, research fields or time spent on annotations. More importantly, annotations of the same document pairs contributed by different scientists were highly concordant. We further show that the three representative baseline methods used to generate recommended articles for evaluation (Okapi Best Matching 25, Term Frequency-Inverse Document Frequency and PubMed Related Articles) had similar overall performances. Additionally, we found that these methods each tend to produce distinct collections of recommended articles, suggesting that a hybrid method may be required to completely capture all relevant articles. The established database server located at https://relishdb.ict.griffith.edu.au is freely available for the downloading of annotation data and the blind testing of new methods. We expect that this benchmark will be useful for stimulating the development of new powerful techniques for title and title/abstract-based search engines for relevant articles in biomedical research.Peer reviewe

Genomic and genome-wide association of susceptibility to radiation-induced fibrotic lung disease in mice.

Background and Purpose: To identify genes which influence the fibrotic response to thoracic cavity radiotherapy, we combined a genome wide single nucleotide polymorphism (SNP) association evaluation of inbred strain response with prior linkage and gene expression data. Material and Methods: Mice were exposed to 18 Gy whole thorax irradiation and survival, bronchoalveolar cell differential, and histological alveolitis and fibrosis phenotypes were determined. Association analyses were completed with 1.8 million SNPs in single markers and haplotypes. Results: Nine strains developed significant fibrosis and 11 strains succumbed to alveolitis only or alveolitis with minimal fibrosis. Post irradiation survival time (p<0.001) and bronchoalveolar lavage neutrophil percent (p=0.055) were correlated with extent of alveolitis and were not significantly correlated with fibrosis. Genome wide SNP analysis identified 10 loci as significantly associated with radiation-induced fibrotic lung disease (p<8.41 x10-6; by permutation test), with the most significant SNP within a conserved non-coding region downstream of cell adhesion molecule 1 (Cadm1). (...) Conclusions: Combining genomic approaches identified variation within specific genes which function in the tissue response to injury as associated with fibrosis following thoracic irradiation in mice

Osteopenia in Cftr-deltaF508 mice

AbstractBackgroundMice with the cystic fibrosis transmembrane conductance regulator (Cftr) gene knocked out develop osteopenia. To determine whether this phenotype is present in cystic fibrosis mouse models with the ΔF508 Cftr mutation we assessed the femora of adult FVB/N Cftrtm1Eur and C57BL/6 Cftrtm1Kth mice.MethodsBone disease, relative to littermate controls, was measured using histology, densitometry and quantitative imaging.ResultsC57BL/6 Cftrtm1Kth mice had shorter femurs and bones of lower volume due to thinner trabeculae, compared to wild type littermates. FVB/N Cftrtm1Eur mice also presented a lower bone volume which was due to significantly fewer trabeculae in this strain. Osteoblast and osteoclast numbers did not differ between CF and controls, for either of FVB/N Cftrtm1Eur or C57BL/6 Cftrtm1Kth mice. The bone architecture of FVB/N Cftrtm1Eur mice did not significantly differ from that of C57BL/6 Cftrtm1Kth mice.ConclusionsAn osteopenic bone disease is evident in adult ΔF508-Cftr cystic fibrosis mouse models