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윤재석,김소영,윤경식,신희정,정호상,정혜주,김영훈,신지순,차혜진,한경문,현승하,이택형,박혜경,김형수 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.12
Astemizole, a non-sedating histamine H1 receptorblocker, is widely known to cause cardiac arrhythmia,which prolongs the QT interval. However, the precisemolecular mechanism involved in antihistamine-inducedcardiovascular adverse effects other than hERG channelinhibition is still unclear. In this study, we used DNAmicroarray analysis to detect the mechanisms involved inlife-threatening adverse effects caused by astemizole. Ratprimary cardiomyocytes were treated with various concentrationsof astemizole for 24 h and the correspondingcell lysates were analyzed using a DNA microarray. Astemizole altered the expression profiles of genesinvolved in calcium transport/signaling. Using qRT-PCRanalysis, we demonstrated that, among those genes, p21(Cdc42/Rac)-activated kinase 1 (pak1) mRNA was downregulatedby treatment with terfenadine and astemizole. Astemizole also reduced pak1 protein levels in rat cardiomyocytes. In addition, astemizole decreased pak1mRNA and protein levels in H9c2 cells and induced anincrease in cell surface area (hypertrophy) and cytotoxicity. Fingolimod hydrochloride (FTY720), a pak1 activator,inhibited astemizole-induced hypertrophy and cytotoxicityin H9c2 cells. These results suggest that antihistamine-inducedcardiac adverse effects are associated with pak1expression and function.
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A Case of Drug-Induced Hepatitis due to Bortezomib in Multiple Myeloma
김영원,민창기,김가영,이수현,정윤영,양승하,이승은,박경신 대한면역학회 2012 Immune Network Vol.12 No.3
We report on a case of severe hepatotoxicity in a 52-year-old male with multiple myeloma (MM) who had received bortezomib therapy. At patient presentation, liver enzymes were normal, but started to markedly increase 3 days after the patient’s second dose of bortezomib was administered, when free kappa light chains were noticeably reduced in the serum. After discontinuation of bortezomib, liver enzymes recovered gradually to baseline. Then, the patient was started on a thalidomide-containing regimen, which he was able to tolerate well. The patient achieved complete remission prior to autologous stem cell transplantation (ASCT). The patient underwent ASCT without occurrence of further liver toxicity. We report on a case of severe hepatotoxicity in a 52-year-old male with multiple myeloma (MM) who had received bortezomib therapy. At patient presentation, liver enzymes were normal, but started to markedly increase 3 days after the patient’s second dose of bortezomib was administered, when free kappa light chains were noticeably reduced in the serum. After discontinuation of bortezomib, liver enzymes recovered gradually to baseline. Then, the patient was started on a thalidomide-containing regimen, which he was able to tolerate well. The patient achieved complete remission prior to autologous stem cell transplantation (ASCT). The patient underwent ASCT without occurrence of further liver toxicity.
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