No abstract available.
Pleural Effusion*

BACKGROUND: It is well known that the prevalence of lung cancer is higher in idiopathic pulmonary fibrosis(IPF) patients than in the general population. This high prevalence is explained by the concept of 'scar carcinoma'. There have been several reports on the prevalence of histologic type of lung cancer in IPF with conflicting results. Despite of the high smoker rate in almost all previous reports, none considered the smoking history of patients. Therefore we performed a separate studies on fibrosis associated lung cancer and smoking associated lung cancer. The purpose of this study is to investigate the proportion of lung cancer in IPF that is fibrosis assiciated and to determine the most common histologic type in fibrosis associated lung cancer in IPF. METHODS: A retrospective review of medical records and radilolgic studies was performed for cases of lung cancer with IPF. We investigated smoking history, sequence of diagnosis of lung cancer and IPF, histologic type of lung cancer and the cancer location, especially whether the location is associated with fibrosis. To evaluate the proportion of fibrous associated lung cancer, the lung cancer in IPF were categorized according to the presence of fibrosis at cancer location. RESULTS: Fifty seven patients were subjects for this analysis. Six(11%) cases were diagnosed as lung cancer during follow-up for IPF, and both diseases were diagnosed simultaneously in the others. Ninety four percent of patients were smokers and the average smoking amount was 47.1±21.9 pack-year. Among the patients with IPF and lung cancer, 42(80.8%) cases were considered as 'fibrosis associated'. The remainder was 'not fibrosis associated' and probably was due to smoking etc. Although the most frequent histologic type was squamous cell carcinoma as a whole, adenocarcinoma was the prominent histologic type in 'fibrosis associated lung cancer.' CONCLUSION: Considering the proportion of 'fibrosis not associated lung cancer' in the patients with IPF and lung cancer, significant proportion of lung cancer in IPF may not be fibrosis induced. This may influence the distribution of histologic type of lung cancer in IPF.
Adenocarcinoma ; Carcinoma, Squamous Cell ; Diagnosis ; Fibrosis* ; Follow-Up Studies ; Humans ; Idiopathic Pulmonary Fibrosis* ; Lung Neoplasms* ; Lung* ; Medical Records ; Prevalence ; Retrospective Studies ; Smoke ; Smoking

BACKGROUND: Current non-invasive methods for evaluating the mediastinum by computed tomographic(CT) scan have limited sensitivity and specificity. The recently introduced PET was reported to be a more sensitive and specific method for the mediastinal staging of NSCLC(sensitivity:76-100%, specificity:81-100%) than CT or MRI. We assessed the usefulness of PET in the mediastinal staging of NSCLC. METHODS: We reviewed the medical records of NSCLC patients that had undertaken staging work-up by both CT and PET before thoracotomy between January 1997 and December 1998. A total of 23 patients were enrolled in the study(14 males and 7 females) with a mean age of 61±9 years. By comparing the clinical(CT and PET) and pathologic stagings, we evaluated the sensitivity, specificity, positive predictive value, negative predictive value and accuracy of PET in thoracic nodal staging. RESULTS: Sensitivity, specificity, positive predicted value and negative predicted value were 38%, 40%, 25% and 50% respectively for computed tomography, and 50%, 60%, 30% and 69% for PET. The accuracy of FDG-PET in our study was lower than that reported by previous other studies. CONCLUSION: Tne addition of FDG-PET to CT scanning has limited benefit for the thoracic nodal staging of NSCLC, but its value in our study was lower than that observed by others.
Carcinoma, Non-Small-Cell Lung* ; Humans ; Magnetic Resonance Imaging ; Male ; Mediastinum ; Medical Records ; Sensitivity and Specificity ; Thoracotomy ; Tomography, X-Ray Computed

BACKGROUND: It is well known that when macrophages are stimulated with endotoxin, they produce a wide variety of cytokine mediators, including TNF-α and IL-1β. However, there is an alterationnin the macrophages responsiveness when they are challenged with repeated bouts of endotoxin, termed 'endotoxin tolerance' which is regarded as a self-protective phenomenon from continuous stimulation. In this study, endotoxin tolerance in the peripheral blood monocytes of sepsis patients was evaluated. METHODS: Fourteen patients with organism-documented sepsis were included. The severity of illness was evaluated by APACHE IIscore. Peripheral blood monocytes were isolated from the patients and diluted to 1×105/well. After stimulation with endotoxin(LPS of E. coli O114:B4, 100 ng/ml), they were incubated at 37℃ in 5% CO2 incubator for 24 hours. Supernatant was collected for the measurement of TNF-αand IL-1β with ELISA method. Peripheral blood monocytes of seven healthy volunteers were used as control. RESULTS: The APACHE IIscore(mean±SD) of the patients at the time of blood sampling was 12.2±5.7. The primary infection foci were urinary tract infection, pneumonia, subacute bacterial endocarditis, and catheter related infection, etc. The causative organisms were gram negative rods(10 cases), gram positive cocci(6 cases) with two cases of mixed infection. Serum TNF-α could be measured in 4 cases with 29.9±27.7 pg/ml. Serum IL-1β was measureable in only one patient. The TNF-α level of supernatant of cultured peripheral blood monocytes was 2,703±2,066 pg/ml in patients and 2,102±1,914 pg/ml in controls. The IL-1β level of supernatant was 884±1,050 pg/ml in patients and 575±558 pg/ml in controls. There was no difference of TNF-α and IL-1β level between patients and controls. CONCLUSION: We cannot prove the phenomenon of endotoxin tolerance in this study. Future study needs to be focused on the more severe sepsis patients who were taken for sampling earlier. Addition of serum to the culture medium could be an another valuable option for the success of this study.
APACHE ; Catheters ; Coinfection ; Endocarditis, Subacute Bacterial ; Enzyme-Linked Immunosorbent Assay ; Healthy Volunteers ; Humans ; Incubators ; Macrophages ; Monocytes ; Pneumonia ; Sepsis* ; Tumor Necrosis Factor-alpha* ; Urinary Tract Infections

BACKGROUND: Tissue inhibitor of metalloproteinase is a natural inhibitor that counteracts proteolytic enzymes essential to the invasion of cancer cell. Whether or not TIMP-2 gene transfer via adenovirus could inhibit the invasion of lung cancer cell in vitro was evaluated for the future purpose of gene therapy against lung cancer. METHODS: Recombinant adenvirus-TIMP-2(Ad-TIMP-2) was generated by homologeous recombination after pACCMV-TIMP-2 and pJM17 were cotransfected into 293 cell by standard calcium phosphate coprecipitate mathod. Calu-6, one of the most invasive lung cancer cells, was transduced with Ad-TIMP-2 or Ad-β-gal. An-chorage-independent growth and invasiveness were assessed by soft agar clonogenicity assay and invasion assay using two-chamber, well divided by matrigel. RESULTS: Ad-TIMP-2 transduced calu-6 cells produced bilolgically active TIMP-2 more than 50 times more than parental calu-6. TIMP-2 gene transfer did not suppress the in vitro tumorgenicity. However, two chamber well assay revealed that Ad-TIMP-2 transduction reduced the invasiveness of calu-6 efficiently (12% compared with parental cell) even at low 10moi. CONCLUSION: Even though TIMP-2 gene transfer did not inhibit in vitr tumorigenicity, it did inhibit invasion of lung cancer cell in vitro. The inhibition of invasion by Ad-TIMP-2 may be a useful strategy for the treatment of lung cancer.
Adenoviridae* ; Agar ; Calcium ; Genetic Therapy ; Humans ; Lung Neoplasms* ; Lung* ; Parents ; Peptide Hydrolases ; Recombination, Genetic ; Tissue Inhibitor of Metalloproteinase-2*

BACKGROUND: NF-kappaB is a characteristic transcriptional factor whose functional activity is determined by post- translational modification of protein and subsequent change of subcellular localization. The involvement of the NF- kappaB family of the transcription factors in the control of such vital cellular functions as immune response, acute phase reaction, replication of certain viruses and development and differentiation of cells has been clearly documented in many previous studies. Several recent observations have suggested that the NF-kappaB might also be involved in the carcinogenesis of some hematological and solid tumors. Investigating the possibility that members of the NF- kappaB family participate in the molecular control of malignant cell transformation could provide invaluable information on both molecular pathogenesis and cancer-related gene therapy. METHOD: To determine the expression patterns and functional roles of NF-kappaB family transcription factors in human lung cancer cell lines NCI -H792, NCI-H709, NCI-H226 and NCI-H157 were analys ed by western blot, using their respective antibodies. The nuclear and the cytoplasmic fraction of protein extract of these cell lines were subsequently obtained and NF- kappaB expression in each fraction was again determined by western blot analysis. The type of NF-kappaB complex present in the cells was determined by immunoprecipitation. To detect the binding ability of cell- line nuclear extracts to the kappaB consensus oligonucleotide, electrophoretic mobility shift assay(EMSA) was performed. RESULTS: In the cultured human lung cancer cell lines tested, transcription factors of the NF- kappaB family, namely the p50 and p65 subunit were expressed and localized in the nuclear fraction of the cellular extract by western blot analysis and immunocytochemistry. Immunoprecipitation assay showed that in the cell, the p50 and p65 subunits made NF- kappaB complex. Finally it was shown by Electrophoretic Mobility Shift Assay(EMSA) that nuclear extracts of lung cancer cell lines are able to bind to NF-kappaB consensus DNA sequences. CONCLUSION: These data suggest that in human lung cancer cell lines the NF-kappaB p50/p65 complex might be activated, and strengthen the hypothesis that NF-kappaB family transcription factors might be involved in the carcinogenesis of human lung cancer.
Acute-Phase Reaction ; Antibodies ; Base Sequence ; Blotting, Western ; Carcinogenesis ; Cell Line* ; Consensus ; Cytoplasm ; Genetic Therapy ; Humans* ; Immunohistochemistry ; Immunoprecipitation ; Lung Neoplasms* ; Lung* ; NF-kappa B* ; Transcription Factors

BACKGROUND: The purpose decortication is to eliminate the infection focus and to improve the decreased lung function due to chronic empyema. However, lung function is not improved in all cases. It would be clinically useful it we could predict preoperatively whether lung function would improve after decortication. The purpose of this study is to find useful indices for predicting the possible improvement of lung function after decortication. METHOD: The medical records of 37 tuberculous empyema patients who underwent pleural decortication were analyzed retrospectively from 1990 to 1996. The measurements of preoperative and postoperative forced vital capacity(FVC) were used for evaluating the effects of decortication. RESULTS: The sex ratio was 29 : 8 (male to female), and the median age was 34 years. The time interval between the formation of empyema and operation was 1 month to 30 years. Postoperative pulmonary function test was performed 5.4±2.6 months later. FVC(forced vital capacity) was significantly increased from 2.77±0.67(L) to 2.95± 0.81(L). Interestingly, postoperative pulmonary function was significantly improved in patients who were less than 40 years old, within 4 months after diagnosis of tuberculous empyema, in the group with FVC of less than 60% of the predicted value and in the absence of calcification. CONCLUSION: The improvement of lung function after decortication was expected in patients younger than 40 years old, within 4 months after diagnosis of tuberculous empyema, in the group having less than 60% of the predicted FVC, without calcification.
Diagnosis ; Empyema ; Empyema, Tuberculous* ; Humans ; Lung ; Medical Records ; Respiratory Function Tests ; Retrospective Studies ; Sex Ratio

BACKGROUND: Because of the common etiologic factor, such as smoking, lung cancer and chronic obstructive Pulmonary disease are often present in the same patient. The preoperative prediction of remaining pulmonary function after the resectional surgery is very important to prevent serious complication and postoperative respiratory failure. 99mTc-MAA perfusion scan has been used for the prediction of postoperative pulmonary function, but it may be inaccurate in case of large V/Q mismatching. We compared 99mTc-DTPA radioaerosol inhalation scan with 99mTc-MAA perfusion scan in predicting postoperative lung function. METHOD: Preoperative inhalation scan and/or perfusion scan were performed and pulmonary function test were performed preoperatively and 2 month after operation. We predicted the postoperative pulmonary functions using the following equations. Postpneumonectomy FEV1=Preop FEV1x% of total function of lung to remain RESULTS: 1) The inhalation scan showed good correlations between measured and predicted FEV1, FVC and FEF25-75%. (correlation coefficiency; 0.94, 0.91, 0.87 respectively). 2) The perfusion scan also showed good correlations between measured and predicted FEV1, FVC and FEF25-75%. (correlation coefficiency; 0.86, 0.72, 0.97 respectively). 3) Among three parameters, FEV1 showed the best correlations in the prediction by lung scans. 4) Comparison between inhalation scan and perfusion scan in predicting pulmonary function did not show any significant differneces except FVC. CONCLUSION: The inhalation scan and perfusion scan are very useful in the prediction of postoperative lung function and don't make a difference in the prediction of pulmonary function although the former showed a better correlation in FVC.
Humans ; Inhalation* ; Lung ; Lung Neoplasms ; Perfusion* ; Pulmonary Disease, Chronic Obstructive ; Respiratory Function Tests ; Respiratory Insufficiency ; Smoke ; Smoking

BACKGROUND: Pulmonary Langerhans cell histiocytosis forms part of a spectrum of diseases that are characterized by a monoclonal proliferation and infiltration of organs by Langerhans cells. Several organ systems may be involved in Langerhans cell histiocytosis, including the lungs, bone, skin, pituitary gland, liver, lymph nodes and thyroid. Pulmonary histiocytosis X represents 2.8% of interstitial lung disease. Here we present the clinical, radiological, therapeutic aspects of pulmonary histiocytosis X. METHOD: Fourteen cases of biopsy-proven pulmonary histiocytosis X patients who were diagnosed in Seoul National University Hospital during the period from January 1990 to December 1998 were analyzed retrospectively. RESULT: There were 12 men and 2 women in this study. The initial presenting symptoms were dyspnea, cough, chest pain, which was associated with the pneumothorax, and chest radiography abnormalities. Only 8 patients (57%) were smokers. There were 5 patients with extra-pulmonary histiocytosis (pituitary, bone, skin). Eight patients had received the chemotherapy. There were no mortalities and only one patient experienced an aggravation of symptom during the follow-up period. CONCLUSION: In contrast to previous reports from other countries, the patients with pulmonary histiocytosis X in this study presented with several different clinical characteristics, such as a male predominance, relatively low smoker's rate, and a better prognosis.
Chest Pain ; Cough ; Drug Therapy ; Dyspnea ; Female ; Follow-Up Studies ; Histiocytosis ; Histiocytosis, Langerhans-Cell* ; Humans ; Langerhans Cells ; Liver ; Lung ; Lung Diseases, Interstitial ; Lymph Nodes ; Male ; Mortality ; Pituitary Gland ; Pneumothorax ; Prognosis ; Radiography ; Retrospective Studies ; Seoul ; Skin ; Thorax ; Thyroid Gland

BACKGROUND: The importance of pro-inflammatory cytokines, especially tumor necrosis factor α(TNF-α) and interleukin-1β(IL-1β), have been extensively documented in the generation of inflammatory lung disease. Lung epithelial cells are also actively involved in initiating and maintaining inflammation by producing pro-inflammatory mediators. Understanding the mechanism of pro-inflammatory cytokine expression in lung epithelial cells is crucial to the development of new therapeutic modalities for inflammatory lung disease. Transcription of most pro-inflammatory cytokines is dependent on the actiation of NF-κB. However, the relationship between pro-inflammatory cytokine expression and NF-κB/IκB pathway in lung epithelial cells is not clear. METHODS: BEAS-2B, A549, NCI-H719 cells were stimulated with IL-1β or TNF-α at various times, and then IL-8 and TNF-αmRNA expressions were assayed by Northern blot analysis. IL-1β or TNF-α-induced NF-κB activation was assessed by the nuclear translocation of p65 NF-κB subunit. The degradation of IκBα and IκBβ by IL-1βor TNF-α stimulation was assayed by Western blot analysis. The phosphorylation of IκBαwas evaluated by Western blot analysis after pre-treating cells with proteasome inhibitor followed by IL-1β or TNF-α stimulation. The basal level of IKKα expression was evaluated by Western blot analysis. RESULTS: IκBαand IκBβ was repidly degraded after 5 minutes of incubation with IL-1β or TNF-α in BEAS-2B, A549, and NCI-H157 cells. The activation of NF-κB and the induction of IL-8 and TNF-α mRNA expressions were observed by IL-1β or TNF-α stimulation in these cells. In contrast, neither the changes in NF-κB/IκB pathway nor IL-8 and TNF-α mRNA expression was induces by IL-1β or TNF-α stimulation in NCI-H719 cell. IL-1β and TNF-α-induced IκB phoshorylation was observed in BEAS-2B, A549, and NCI-H157 cells, but not in NCI-H719 cells. The basal level of IKKα expression was not different between cells. CONCLUSION: NF-κB/IκB pathway plays an important role in the ixpression of pro-inflammatory cytokine in most lung epithelial cells. The absence of the effect on NF-κB/IκB pathway in NCI-H719 cells seems to be due to the defect in the intracellular signal transduction pathway upstream to IKK.
Blotting, Northern ; Blotting, Western ; Cytokines ; Epithelial Cells* ; Inflammation ; Interleukin-8 ; Lung Diseases ; Lung* ; Phosphorylation ; Proteasome Inhibitors ; RNA, Messenger ; Signal Transduction ; Tumor Necrosis Factor-alpha