• The Korean Journal of Nuclear Medicine
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• v.37 no.4
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• pp.219-228
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• 2003

Purpose: The amount of salvaged myocardium is an important prognostic factor in patients with acute myocardial infarction (MI). We investigated if early Tl-201 SPECT imaging could be used to predict the salvaged myocardium and functional recovery in acute MI after primary PTCA. Materials and Methods: In 36 patients with first acute MI treated with primary PTCA, serial echocardiography and Tl-201 SPECT imaging ($5.8{\pm}2.1$ days after PTDA) were performed. Regional wall motion and perfusion were quantified with on 16-segment myocardial model with 5-point and 4-point scaling system, respectively. Results: Wall motion was improved in 78 of the 212 dyssynergic segments on 1 month follow-up echocardiography and 97 on 7 months follow-up echocardiography, which were proved to be salvaged myocardium. The areas under receiver operating characteristic curves of Tl-201 perfusion score for detecting salvaged myocardial segments were 0.79 for 1 month follow-up and 0.83 for 7 months follow-up. The sensitivity and specificity of Tl-201 redistribution images with optimum cutoff of 40% of peak thallium activity for detecting salvaged myocardium were 84.6% and 55.2% for 1 month follow-up, and 87.6% and 64.3% for 7 months follow-up, respectively. There was a linear relationship between the percentage of peak thallium activity on early redistribution imaging and the likelihood of segmental functional improvement 7 months after reperfusion. Conclusion: Tl-201 myocardial perfusion SPECT imaging performed early within 10 days after reperfusion can be used to predict the salvaged myocardium and functional recovery with high sensitivity during the 7 months following primary PTCA in patients with acute MI.

• Journal of Preventive Medicine and Public Health
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• v.28 no.2 s.50
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• pp.511-525
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• 1995

To elucidate some DNA adducts as a biological marker for workers of chromate pigment, the effects of chromium exposure on the formation of 8-hydroxydeoxyguanosine(8-OH-dG) and sister chromatid exchanges(SCEs) frequency in 38 workers of a pigment plant in Bucheon which utilized lead chromates, were examined. The chromium contents of venous blood and urine were measured as working environmental exposure level. The concentrations of 8-OH-dG in DNA isolated from lymphocytes were determined with high performance liquid chromatography and electrochemical detector and denoted as a molar ratio of 8-OH-dG to deoxyguanosine(dG). The SCEs frequency were analyzed in DNA isolated from lymphocytes. A significant correlation was found between creatinine adjusted urine chromium concentration and the molar ratio of 8-OH-dG to dG(r=0.47, p<0.01). After adjusting the current smoking habit, the correlation coefficient was increased(r=0.62, p<0.05). However, there was no significant correlation between the SCE frequency and chromium exposure. This significant results between molar ratio of 8-OH-dG to dG and chromium exposure are in good agreement with in vitro studies that support the importance of DNA adduct formation for the carcinogenic effect of chromium.

• Journal of Life Science
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• v.23 no.10
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• pp.1230-1238
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• 2013

The regulatory effect of the tumor-suppressor protein p53 on the apoptogenic activity of $17{\alpha}$-estradiol ($17{\alpha}-E_2$) was compared between HCT116 ($p53^{+/+}$) and HCT116 ($p53^{-/-}$) cells. When the HCT116 ($p53^{+/+}$) and HCT116 ($p53^{-/-}$) cells were treated with $2.5{\sim}10{\mu}M$ $17{\alpha}-E_2$ for 48 h or with $10{\mu}M$for various time periods, cytotoxicity and an apoptotic sub-$G_1$ peak were induced in the HCT116 ($p53^{+/+}$) cells in a dose- and time-dependent manner. However, the HCT116 ($p53^{-/-}$) cells were much less sensitive to the apoptotic effect of $17{\alpha}-E_2$. Although $17{\alpha}-E_2$ induced aberrant mitotic spindle organization and incomplete chromosome congregation at the equatorial plate, $G_2/M$ arrest was induced to a similar extent in both cell types. In addition, $17{\alpha}-E_2$-induced activation of Bak and Bax, ${\Delta}{\Psi}m$ loss, and PARP degradation were more dominant in the HCT116 ($p53^{+/+}$) than in the HCT116 ($p53^{-/-}$) cells. In accordance with enhancement of p53 phosphorylation (Ser-15) and p53 levels, p21 and Bax levels were elevated in the HCT116 ($p53^{+/+}$) cells treated with $17{\alpha}-E_2$. The HCT116 ($p53^{-/-}$) cells exhibited barely or undetectable levels of p21 and Bax, regardless of $17{\alpha}-E_2$ treatment. On the other hand, although the level of Bcl-2 was slightly lower in the HCT116 ($p53^{+/+}$) than in the HCT116 ($p53^{-/-}$) cells, it remained relatively constant after the $17{\alpha}-E_2$ treatment. Together, these results show that among the components of the $17{\alpha}-E_2$-induced apoptotic-signaling pathway, which proceeds through mitotic spindle defects causing mitotic arrest, subsequent activation of Bak and Bax and the mitochondria-dependent caspase cascade, leading to PARP degradation, $17{\alpha}-E_2$-induced activation of Bak and Bax is the upstream target of proapoptotic action of p53.