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  1. Güvenir M, Otlu B, Tunc E, Aktas E, Suer K
    Malays J Med Sci, 2018 Mar;25(2):40-49.
    PMID: 30918454 DOI: 10.21315/mjms2018.25.2.5
    Background: Stenotrophomonas maltophilia is a non-fermentative gram-negative bacillus which is widely recognised as an important nosocomial pathogen causing pneumonia, blood-stream, wound and urinary tract infections, particularly in immunosuppressed patients. The aim of this study was to evaluate a nosocomial outbreak of by S. maltophilia in an intensive care unit of a tertiary hospital and evaluate unexpected multiclonality.

    Methods: A total of 11 isolates from respiratory cultures in intensive care unit of a 24 bed tertiary hospital obtained over a one months period and one isolate obtained from the nebuliser during environmental screening were investigated. The bacteria were identified by Phoenix 100 system. The clonal relatedness was evaluated by PFGE and semi-automated repetitive sequence-based PCR. Genotyping tests were repeated for 10 serial subcultures.

    Results: PFGE and DiversiLab yielded 10 genotypic profiles for 12 isolates. Four to eight different genotypes were observed from 10 subcultures of the same isolate.

    Conclusion: We conclude that, high genetic diversity and supposed multiclonal appearance of the outbreak isolates may be due to changing profiles during subcultures most probably depending on hypermutation.

  2. Yildiz I, Sagliker Y, Demirhan O, Tunc E, Inandiklioglu N, Tasdemir D, et al.
    J Ren Nutr, 2012 Jan;22(1):157-61.
    PMID: 22200434 DOI: 10.1053/j.jrn.2011.10.030
    Hypotheses explaining pathogenesis of secondary hyperparathyroidism (SH) in late and severe CKD as a unique entity called Sagliker syndrome (SS) are still unclear. This international study contains 60 patients from Turkey, India, Malaysia, China, Romania, Egypt, Tunisia, Taiwan, Mexico, Algeria, Poland, Russia, and Iran. We examined patients and first degree relatives for cytogenetic chromosomal abnormalities, calcium sensing receptor (Ca SR) genes in exons 2 and 3 abnormalities and GNAS1 genes mutations in exons 1, 4, 5, 7, 10, 13. Our syndrome could be a new syndrome in between SH, CKD, and hereditary bone dystrophies. We could not find chromosomal abnormalities in cytogenetics and on Ca SR gene exons 2 and 3. Interestingly, we did find promising missense mutations on the GNAS1 gene exons 1, 4, 10, 4. We finally thought that those catastrophic bone diseases were severe SH and its late treatments due to monetary deficiencies and iatrogenic mistreatments not started as early as possible. This was a sine qua non humanity task. Those brand new striking GNAS1 genes missense mutations have to be considered from now on for the genesis of SS.
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