Background and purpose: Diazoxide, a well-known opener of the mitochondrial ATP-sensitive potassium (mitoK ATP ) channel, has been demonstrated to exert cardioprotective effect against ischemic injury through the mitoK ATP channel and protein kinase C (PKC). We aimed to clarify the role of PKC isoforms and the relationship between the PKC isoforms and the mitoK ATP channel in diazoxide-induced cardioprotection. Experimental approach: In H9c2 cells and neonatal rat cardiomyocytes, PKC-e activation was examined by Western blotting and kinase assay. Flavoprotein fluorescence, mitochondrial Ca 2 þ and mitochondrial membrane potential were measured by confocal microscopy. Cell death was determined by TUNEL assay. Key results: Diazoxide (100 mM) induced translocation of PKC-e from the cytosolic to the mitochondrial fraction. Specific blockade of PKC-e by either eV1-2 or dominant negative mutant PKC-e (PKC-e KR) abolished the anti-apoptotic effect of diazoxide. Diazoxide-induced flavoprotein oxidation was inhibited by either eV1-2 or PKC-e KR transfection. Treatment with 5-hydroxydecanoate (5-HD) did not affect translocation and activation of PKC-e induced by diazoxide. Transfection with wild type PKC-e mimicked the flavoprotein-oxidizing effect of diazoxide, and this effect was completely blocked by eV1-2 or 5-HD. Diazoxide prevented the increase in mitochondrial Ca 2 þ , mitochondrial depolarization and cytochrome c release induced by hypoxia and all these effects of diazoxide were blocked by eV1-2 or 5-HD. Conclusions and Implications: Diazoxide induced isoform-specific translocation of PKC-e as an upstream signaling molecule for the mitoK ATP channel, rendering cardiomyocytes resistant to hypoxic injury through inhibition of the mitochondrial death pathway.

PurposeTo investigate whether hospitalization influences serum prostate-specific antigen (PSA) values.Materials and MethodsTransrectal ultrasound-guided prostate biopsies were performed for detecting prostate cancer in 2,017 patients between February 2001 and April 2011 at Ajou University Hospital. Of those patients, 416 patients who were hospitalized for prostate biopsies, whose serum PSA values were measured at the outpatient department within 1 month of admission and also just after admission, and who had negative prostate biopsy results were included in the present study. We retrospectively reviewed the data of the 416 patients and compared the serum PSA values measured in the outpatient department with those measured during hospitalization.ResultsAmong all 416 patients, the interval between the two PSA measurements was 22.2 days (range, 3 to 30 days) and the prostate size measured by transrectal ultrasonography was 53.63 mL (range, 12.8 to 197.9 mL). Among all patients, mean serum PSA levels measured during hospitalization were significantly lower than those measured in the outpatient department (6.69 ng/mL vs. 8.01 ng/mL, p<0.001). When stratified according to age, the presence or absence of chronic prostatitis in the biopsy pathology, serum PSA levels, and prostate size, the serum PSA levels measured during hospitalization were significantly lower than those measured in the outpatient department in all subgroups, except in cases aged 20 to 39 years and those with PSA <4 ng/mL, in whom no significant differences were shown.ConclusionsHospitalization decreases serum PSA values compared with those measured on an outpatient basis in patients with benign prostatic diseases. Therefore, serum PSA values should be checked on an outpatient basis for serial monitoring.