PURPOSE: Multidrug resistance mediated by several drug resistant genes impedes the successful outcome of anti-cancer chemotherapy. In this study, we investigated the expressions of drug resistant genes encoding multidrug resistance (MDR1), multidrug resistance-associated protein (MRP), topoisomerase I (Topo I), topoisomerase II g (Topo II a) in narmal volunteers (n=12) in and patients with myeloid leukemia (n=34). Material and Method: We compared the levels of their transcripts in bone matrow mononuclear cells by semiquantitative RT-PCR. The amount of specific transcripts was represented as the optical density ratio of PCR product of target gene to that of B2- microglobulin (MG). Twenty patients of acute myelogenous leukemia (eight in remission state, twelve in refractory) and fourteen patients of chronic myelogenous leukemia (nine in chronic phase and five in blastic crisis) were examined. Twelve normal healthy persons were compared with leukemic patients. RESULTS: The expression levels of all resistant genes in normal volunteers were relatively high as those of AML patients. Regardless of the disease status including remission status of AML (complete remission versus refractory) and the phase of CML (chronic phase versus blastic phase), the expression levels of all resistant genes in patients with CML were significantly lower than in the patients with AML (p < 0.05). Of interest, the patients with refractary AML did not show any statistical difference in comparison with normal controls and even the patients with AML in complete remission. Among the four drug resistant genes, the optical density ratio of MDRl was significantly lower than that of any other genes (p<0.05). Using HL-60 cell line, we compared the changes of various resistant gene expressions before and after differentiation induced by dimethylsulfoxide. The expressions of resistant genes declined in paralle1 with granulocytic differentiation, suggesting that the induction of cell differentiation might make leukemic cells susceptible to chemotherapeutic agents. CONCLUSION: It is impossibble to explain the mechanism of drug resistance by comparing the level of drug resistant gene expression between nonnal subjects and patients with myeloid leukemias. Therefore, we suppose that longitudinal study of drug resistant gene expression is necessary to demonstrate the development of drug resistant during chemotherapy.
Bone Marrow* ; Cell Differentiation ; Dimethyl Sulfoxide ; DNA Topoisomerases, Type I ; DNA Topoisomerases, Type II ; Drug Resistance ; Drug Resistance, Multiple ; Drug Therapy ; Gene Expression ; Healthy Volunteers ; HL-60 Cells ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Leukemia, Myeloid* ; Leukemia, Myeloid, Acute ; Multidrug Resistance-Associated Proteins ; Polymerase Chain Reaction ; Volunteers

BACKGROUND AND OBJECTIVES: Cardiovascuar MR using contrast enhancement has recently been reported to be useful for diagnosing myocarditis. It is also well known that irreversible myocardial injury by epicardial coronary artery flow obstruction spreads from the endocardium to the epicardium in a wave-front pattern with a time-dependent manner. We investigated characteristics of the patterns of contrast-enhanced MR imaging according to the underlying myocardial injury mechanism. SUBJECTS AND METHODS: Of all 275 patients who underwent coronary angiogram at our hospital due to cheat pain and elevated cardiac enzymes between October, 2002 and August, 2003, 48 patients who underwent cardiac MR were enrolled in this study. We retrospectively analyzed the pattern of delayed hyperenhancement according to presence or absence of a documented infarct related artery. Endomyocardial biopsies were done in selected patients. RESULTS: Contrast MR images of all patients showed delayed hyperenhancement. The study group was divided into 2 groups according to whether the areas of hyper-enhancement were involved in the sub-endocardial portion (endocardial sparing pattern, ESP) or not. In 8 patients (Group A, 17%) who showed the endocardial sparing pattern on contrast MR, the findings of coronary angiogram were all normal. In 40 patients (Group B, 83%), who did not show the endocardial sparing pattern on contrast MR, 39 patients (97.5 %) had an infarct related artery on coronary angiogram (p=0.001). Endomyocardial biopsies were performed in 3 patients of group A. The findings of the 3 biopsies were 2 cases of definite myocarditis and 1 case of myocardial degeneration. CONCLUSION: The endocardial sparing pattern of myocardial injury demonstrated by delayed enhancement MR imaging was very useful to predict the presence of an infarct related artery in patients with myocardial necrosis that has been determined by elevated cardiac enzymes. This result can be a useful clue to determine the nature of the underlying injury mechanism such as ischemic or non-ischemic.
Arteries ; Biopsy ; Coronary Vessels ; Endocardium ; Humans ; Magnetic Resonance Imaging* ; Myocardial Infarction ; Myocarditis ; Necrosis ; Pericardium ; Retrospective Studies

Purpose: We evaluated the risk factors for progression to chronic complicated bronchopleural fistula (BPF) after pulmonary resection using follow-up CT. Materials and Methods: We retrospectively reviewed 45 cases with BPF that had undergone pulmonary resection during 2010-2018. We compared the clinical and radiological characteristics of those with complicated BPF (n = 24) and those without complicated (sterilized) BPF (n = 21). The clinical and radiological risk factors for progression to chronic complicated BPF were examined by logistic regression analysis. Results: The thickness of the pleural cavity wall (p = 0.022), the size of the pleural cavity (p = 0.029), and the size increase of BPF on follow-up (p = 0.012) were significantly different between the two groups. The risk factors for progression to chronic complicated BPF were age > 70 years (odds ratio, 6.43; 95% confidence interval, 1.2–33.7), the thickness of the cavity wall > 5 mm (odds ratio, 52.5; 95% confidence interval, 5.1–545.4), and an increase in the size of the pleural cavity on follow-up CT (odds ratio, 12.5; 95% confidence interval, 2.1–73.5), only in the univariate analysis. Conclusion The risk factors for progression to chronic complicated BPF can be evaluated using follow-up CT.