Evidence map›Paper›PMID 26603341›Full record

ArticleScientific reports2015

Phenotypic and genomic comparisons of highly vancomycin-resistant Staphylococcus aureus strains developed from multiple clinical MRSA strains by in vitro mutagenesis.

Kenichi Ishii, Fumiaki Tabuchi, Miki Matsuo, Keita Tatsuno, Tomoaki Sato, Mitsuhiro Okazaki, Hiroshi Hamamoto, Yasuhiko Matsumoto, Chikara Kaito, Tetsuji Aoyagi and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Knockout ofJournal of bacteriology · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Kenichi IshiiLaboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Fumiaki TabuchiLaboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Miki MatsuoDepartment of Bacteriology, Faculty of Medicine, Juntendo University, Tokyo, Japan.
Keita TatsunoDepartment of Infection Control and Prevention, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Tomoaki SatoDepartment of Infection Control and Prevention, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Mitsuhiro OkazakiDepartment of Medical Technology, School of Health Sciences, Tokyo University of Technology, Tokyo, Japan.
Hiroshi HamamotoLaboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Yasuhiko MatsumotoLaboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Chikara KaitoLaboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Tetsuji AoyagiDepartment of Infection Control and Laboratory Diagnostics, Internal Medicine, Tohoku University Graduate School of Medicine, Tokyo, Japan.
Keiichi HiramatsuDepartment of Bacteriology, Faculty of Medicine, Juntendo University, Tokyo, Japan.
Mitsuo KakuDepartment of Infection Control and Laboratory Diagnostics, Internal Medicine, Tohoku University Graduate School of Medicine, Tokyo, Japan.
Kyoji MoriyaDepartment of Infection Control and Prevention, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Kazuhisa SekimizuLaboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of vancomycin (VCM) resistance in Staphylococcus aureus threatens global health. Studies of the VCM-resistance mechanism and alternative therapeutic strategies are urgently needed. We mutagenized S. aureus laboratory strains and methicillin-resistant S. aureus (MRSA) with ethyl methanesulfonate, and isolated mutants that exhibited high resistance to VCM (minimum inhibitory concentration = 32 μg/ml). These VCM-resistant strains were sensitive to linezolid and rifampicin, and partly to arbekacin and daptomycin. Beta-lactams had synergistic effects with VCM against these mutants. VCM-resistant strains exhibited a 2-fold increase in the cell wall thickness. Several genes were commonly mutated among the highly VCM-resistant mutants. These findings suggest that MRSA has a potential to develop high VCM resistance with cell wall thickening by the accumulation of mutations.

Indexed as

GenomicsAnti-Bacterial AgentsCell WallDNA, BacterialEthyl MethanesulfonateHumansMethicillin-Resistant Staphylococcus aureusMicrobial Sensitivity TestsMicroscopy, Electron, TransmissionMutagenesisMutagensPhenotypeSequence Analysis, DNAStaphylococcal InfectionsStaphylococcus aureusVancomycinAnti-Bacterial AgentsDNA, BacterialEthyl MethanesulfonateMutagensVancomycin

Identifiers

PMID26603341
PMCPMC4658547

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.