AI Article Synopsis

  • A study analyzed 290 meningococcal isolates from Japan between 2003 and 2020 to assess their susceptibility to eight antibiotics, including penicillin and ciprofloxacin.
  • Most isolates were found susceptible to chloramphenicol, ceftriaxone, meropenem, minocycline, and rifampicin, while two isolates were resistant to azithromycin and some were resistant or intermediate to penicillin and ciprofloxacin.
  • Genetic analysis revealed that around 40% of penicillin-resistant isolates belonged to unique Japanese strains, indicating that resistance traits appear to be spread clonally rather than through gene transfer from other bacteria.

Article Abstract

Although we previously reported that some meningococcal isolates in Japan were resistant to penicillin (PCG) and ciprofloxacin (CIP), the antibiotic susceptibilities of isolates obtained in Japan remained unclear. In the present study, 290 . isolates in Japan between 2003 and 2020 were examined for the sensitivities to eight antibiotics (azithromycin, ceftriaxone, ciprofloxacin, chloramphenicol, meropenem, minocycline, penicillin, and rifampicin). All isolates were susceptible to chloramphenicol, ceftriaxone, meropenem, minocycline, and rifampicin while two were resistant to azithromycin. Penicillin- and ciprofloxacin-resistant and -intermediate isolates (PCG, CIP, PCG and CIP, respectively) were also identified. Based on our previous findings from whole genome sequence analysis, approximately 40% of PCG were associated with ST-11026 and cc2057 meningococci, both of which were unique to Japan. Moreover, the majority of ST-11026 meningococci were CIP or CIP. Sensitivities to PCG and CIP were closely associated with genetic features, which indicated that, at least for Japanese meningococcal isolates, PCG or CIP would be less likely to be horizontally conferred from other neisserial genomes by transferring of the genes responsible ( and genes, respectively), but rather that ancestral strains conferring PCG or CIP phenotypes clonally disseminated in Japan.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10648979PMC
http://dx.doi.org/10.1128/aac.00744-23DOI Listing

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Article Synopsis
  • A study analyzed 290 meningococcal isolates from Japan between 2003 and 2020 to assess their susceptibility to eight antibiotics, including penicillin and ciprofloxacin.
  • Most isolates were found susceptible to chloramphenicol, ceftriaxone, meropenem, minocycline, and rifampicin, while two isolates were resistant to azithromycin and some were resistant or intermediate to penicillin and ciprofloxacin.
  • Genetic analysis revealed that around 40% of penicillin-resistant isolates belonged to unique Japanese strains, indicating that resistance traits appear to be spread clonally rather than through gene transfer from other bacteria.
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Enhancer of zeste homolog 2 depletion induces cellular senescence via histone demethylation along the INK4/ARF locus.

Int J Biochem Cell Biol

August 2015

Department of Gastrointestinal Surgery II, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Wuhan, Hubei Province 430022, People's Republic of China. Electronic address:

Polycomb group proteins are epigenetic transcriptional repressors that function through recognition and modification of histone methylation and chromatin structure. As a member of PcG proteins, enhancer of zeste homolog 2 (EZH2) targets cell cycle regulatory proteins which govern cell cycle progression and cellular senescence. In previous work, we reported that EZH2 depletion functionally induced cellular senescence in human gastric cancer cells with mutant p53.

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Three global assays, the Calibrated Automated Thrombogram (CAT), the ProC Global (PCG), and the Coagulation Inhibitor Potential (CIP) were performed in frozen plasma samples from 24 normal controls and 24 patients with inherited thrombophilia. Six patients had inherited antithrombin (AT) deficiency; 18 patients had abnormalities in the protein C/S anticoagulant system (protein C deficiency (n=3), protein S deficiency (n=10), homozygous FV Leiden mutation (n=5)). Nine of these twenty four patients carried additionally the heterozygous FV Leiden mutation.

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