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dc.contributor.authorOguz, O
dc.contributor.authorUslu, I
dc.contributor.authorNisli, C
dc.contributor.authorOnsel, C
dc.contributor.authorCivi, G
dc.contributor.authorKabasakal, L
dc.contributor.authorHalac, M
dc.date.accessioned2021-03-05T20:40:48Z
dc.date.available2021-03-05T20:40:48Z
dc.date.issued2000
dc.identifier.citationKabasakal L., Halac M., Nisli C., Oguz O., Onsel C., Civi G., Uslu I., "The effect of P-glycoprotein function inhibition with cyclosporine A on the biodistribution of Tc-99m sestamibi", CLINICAL NUCLEAR MEDICINE, cilt.25, ss.20-23, 2000
dc.identifier.issn0363-9762
dc.identifier.othervv_1032021
dc.identifier.otherav_d5570ffe-4414-449b-942b-9e1764485160
dc.identifier.urihttp://hdl.handle.net/20.500.12627/140776
dc.identifier.urihttps://doi.org/10.1097/00003072-200001000-00005
dc.description.abstractPurpose: The failure to cure persons with cancer is caused primarily by the development of drug resistance by overexpression of p-glycoprotein. Diverse groups of drugs have been identified, including cyclosporine A, which can reverse drug resistance by inhibiting P-glycoprotein transport. Tc-99m sestamibi is a substrate for P-glycoprotein. P-glycoprotein is normally expressed in biliary canalicular surfaces of hepatocytes and is responsible for the excretion of cationic metabolites from the liver. The aim of the current study was to evaluate the effect of cyclosporine A on the biological distribution of Tc-99m sestamibi in vivo.
dc.language.isoeng
dc.subjectNükleer Tıp
dc.subjectDahili Tıp Bilimleri
dc.subjectSağlık Bilimleri
dc.subjectTıp
dc.subjectKlinik Tıp (MED)
dc.subjectKlinik Tıp
dc.subjectRADYOLOJİ, NÜKLEER TIP ve MEDİKAL GÖRÜNTÜLEME
dc.titleThe effect of P-glycoprotein function inhibition with cyclosporine A on the biodistribution of Tc-99m sestamibi
dc.typeMakale
dc.relation.journalCLINICAL NUCLEAR MEDICINE
dc.contributor.department, ,
dc.identifier.volume25
dc.identifier.issue1
dc.identifier.startpage20
dc.identifier.endpage23
dc.contributor.firstauthorID124772


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