BACKGROUND: The brain is a common site of a metastasis in lung cancer patients. If left untreated, the patients succumb to progressive neurological deterioration with a lower survival rate than with other metastases sites. Contrast-enhanced MR imaging in the absence of symptoms or clinical signs is not recommended for identifying a cerebral metastasis in lung cancer patients because of management effectiveness. This pilot study was performed to estimate whether or not limited brain MR imaging, which has a lower cost, could be used to replace conventional brain MR imaging. METHOD: Between April 1999 and March 2001, 43 patients with a primary lung cancer and the others (breast cancer, stomach cancer, colon cancer, malignant melanoma etc), who had neurological symptoms and signs, were examined using conventional brain MR imaging to examine brain metastases. The control group involved four patients who had no evidence of brain metastases the sensitivity, specificity and correlation of limited brain MR imaging were compared with conventional brain MR imaging. RESULTS: All the 43 patients who were examined with conventional brain MR imaging showed evidence of brain metastases, whereas limited brain MR imaging indicated that 42 patients had brain metastases(sensitivity=97.67%). One patient in whom limited brain MR imaging showed no brain metastasis had a metastasis in the cerebellum, as shown by the contrast-enhanced T1 weighted axial view using conventional brain MR imaging. The conventional brain MR imaging and the limited brain MI imaging of the 4 control patients both indicated no brain metastases (specificity=100 %). The Pearson Correlation of the two groups was 0.884(Confidence Interval : 99%) observed. CONCLUSION: Limited brain MR imaging can detect a brain metastasis with the same accuracy. In addition, it is cost-effective (229,000 won, 180$) compared to conventional brain MR imaging(529,000 won, 480$) when patients had neurological symptoms and signs or staging.
Brain* ; Cerebellum ; Colonic Neoplasms ; Humans ; Lung Neoplasms ; Magnetic Resonance Imaging* ; Melanoma ; Neoplasm Metastasis* ; Pilot Projects ; Stomach Neoplasms ; Survival Rate

BACKGROUND: Activation of the transcription factor NF-kappaB has been shown to protect cells from tumor necrosis factor-alpha, chemotherapy, and radiation-induced apoptosis. NF-kappaB-dependent cIAP expression is a major antiapoptotic mechanism for that. NF-kappaB activation and cIAP expression in A549 lung cancer cells which is relatively resistant to radiation-induced cell death were investigated for the mechanism of radioresistance. MATERIALS AND METHODS: We used A549 lung cancer cells and Clinac 1800C linear accelerator for radiation. Cell viability test was done by MTT assay. NF-kappaB activation was tested by luciferase reporter gene assay, Western blot for IkappaBalpha degradation, and electromobility shift assay. For blocking NF-kappaB, MG132 and transfection of IkappaBalpha-superrepressor plasmid construct were used. cIAP expression was analyzed by RT-PCR and cIAP2 promoter activity was performed using luciferase assay system. RESULTS: MTT assay showed that cytotoxicity even 48 hr after radiation in A549 cells were less than 20%. Luciferas assay demonstrated weak NF-kappaB activation of 1.6+/-0.2 fold compared to PMA-induced 3.4+/-0.9 fold. Radiation-induced IkappaBalpha degradation was observed in Western blot and NF-kappaB DNA binding was confirmed by EMSA. However, blocking NF-kappaB using MG132 and IkappaBalpha-superrepressor transfection did not show any sensitizing effect for radiation-induced cell death. The result of RT-PCR for cIAP1 & 2 expression was negative induction while TNF-alpha showed strong expression for cIAP1 & 2. The cIAP2 promoter activity also did not show any change compared to positive control with TNF-alpha. CONCLUSIONS: We conclude that activation of NF-kappaB does not determine the intrinsic radiosensitivity of cancer cells, at least for the cell lines tested in this study.
Apoptosis ; Blotting, Western ; Cell Death* ; Cell Line ; Cell Survival ; DNA ; Drug Therapy ; Genes, Reporter ; Luciferases ; Lung Neoplasms* ; Lung* ; NF-kappa B* ; Particle Accelerators ; Plasmids ; Radiation Tolerance ; Transcription Factors ; Transfection ; Tumor Necrosis Factor-alpha

BACKGROUND: There have been several studies showing that the angiotensin II and angiotensin converting enzyme(ACE) contributes to the apoptosis of alveolar epithelial cells in idiopathic interstitial pneumonia and the activation of fibroblasts during the process of pulmonary fibrosis. These results suggest that the pulmonary fibrosis can be inhibited by the angiotensin II receptor antagonist(AGIIRA). This study was performed to identify the therapeutic effect of AGIIRA in idiopathic pulmonary fibrosis(IPF). METHOD: Thirteen patients with IPF, who were diagnosed with an open lung biopsy(6 patients) and furfilling the ATS criteria(7 patients) between March 1999 and October 2001 at the Gachon medical center, were enrolled in this study. Of these patients, eight patients were treated with a regimen including AGIIRA(AT group), and five were treated without AGIIRA(NT group). The pulmonary function tests and dyspnea(ATS scale) were measured at diagnosis and 1 year after treatment. All the data was collected to analyze the therapeutic effect of AGIIRA on the patients with IPF. RESULTS: The AT group contained 8 patients(M:F=4:4) and the NT group contained 5 patients (M:F=3:2). There was no significant difference in the serum angiotensin II level between the two groups(202.5+/-58.5 vs 163.7+/-47.3pg/ml, p>0.05). The AT group showed an upward trend in TLC(+3%), FVC(+4%), FEV1(+3%) and DLco(+2%) compared to the NT group(TLC(-14%), FVC(-3%), FEV1(-4%) except for DLco(+5%)). The dyspnea score in the AT group improved significantly but not in the NT group. CONCLUSION: These results suggest that the angiotensin II receptor antagonist may have an effect on stabilizing IPF.
Angiotensin II* ; Angiotensins* ; Apoptosis ; Diagnosis ; Dyspnea ; Epithelial Cells ; Fibroblasts ; Humans ; Idiopathic Interstitial Pneumonias ; Idiopathic Pulmonary Fibrosis* ; Lung ; Pulmonary Fibrosis ; Receptors, Angiotensin* ; Respiratory Function Tests

BACKGROUND: Pleural effusions are generally divided into transudates and exudates. If it is exudative, more diagnostic tests are required in order to determine the cause of the local disease. A malignancy is a common and important cause of exudative pleural effusions. Because the pleural fluid cytology and pleural biopsy specimens do not provide a diagnosis in a high percentage of malignant effusions, several tumor markers have been examined. In order to overcome this limitation, this study hypothesized that C-reactive protein(CRP) and vascular endothelial growth factor(VEGF) measurements would be useful for differentiating trasudates from exudates and determining the differences between a benign and malignant effusion. METHODS: Eighty consecutive patients with a pleural effusion (tuberculous 20, parapneumonic 20, malignant 20, transudative 20) were examined prospectively: 60 of them were classified according to Light's criteria as having an exudative fluid and 20 had a transudative fluid. The standard parameters of a pleural effusion were examined and the serum and pleural effusion VEGF levels were measured using enzyme linked immunosorbent assay(ELISA). CRP in the serum and pleural fluid was determined by a turbidimetric immunoassay. RESULTS: The pleural CRP levels in the exudates were significantly higher than those in the transudates, 4.19+/-4.22 mg/dl and 1.29+/-1.45 mg/dl, respectively. The VEGF levels in the pleural effusions were significantly elevated in the exudates compared to the transudate, 1,011+/-1,055 pg/ml and 389+/-325 pg/ml, respectively. The VEGF ratio in the exudative effusion is significantly higher than a transudative effusions, 3.9+/-4.7 and 1.6+/-0.9, respectively. The pleural CRP levels in the patients with a benign effusion(4.15+/-4.20 mg/dl) were significantly higher than those in the malignant effusion(1.43+/-1.91 mg/dl). The VEGF ratio is significantly higher in malignant effusions(4.9+/-5.5) than in benign effusions(2.8+/-3.6). CONCLUSION: In conclusion, the CRP and VEGF levels in the serum and pleural effusion can distinguish between transudates and exudates. Moreover it can differentiate between benign and malignant pleural effusions.
Biopsy ; C-Reactive Protein ; Diagnosis ; Diagnostic Tests, Routine ; Exudates and Transudates ; Humans ; Immunoassay ; Pleural Effusion* ; Pleural Effusion, Malignant ; Prospective Studies ; Biomarkers, Tumor ; Vascular Endothelial Growth Factor A*

BACKGROUND: Asthma and eosinophilic bronchitis(EB) are eosinophilic inflammatory diseases of the airway. However, EB differs from asthma in that there is no variable airway obstruction or airway hyper-responsiveness. Pathologically, asthma is characterized by the accumulation of eosinophils and CD4+ T lymphocytes in the submucosa. A recent study showed that there was no significant difference between asthma and EB in terms of the submucosal eosinophil and T lymphocyte count. However, it is not known whether or not an infiltration of CD4+ and CD8+ T lymphocytes occurs in the airways of EB patients. The aim of this study was to identify the difference between the two conditions by measuring the submucosal CD4+ and CD8+ T lymphocyte count. METHODS: Immunohistochemical analysis of bronchial-biopsy specimens was performed in 17 subjects with asthma and 24 subjects with EB. RESULTS: The CD4+ T lymphocytes count in the asthma subjects and the EB subjects was similar (median, 58.6 vs 50.0 cells/mm2, respectively; P=0.341). In contrast, the number of CD8+ T lymphocytes in the EB subjects was higher than that in the asthma subjects (median, 46.7 vs 11.8 cells/mm2, respectively; P=0.003). CONCLUSION: The infiltration of submucosal CD8+ T lymphocytes may be associated with the pathophysiology of EB.
Airway Obstruction ; Asthma* ; Bronchitis* ; Eosinophils* ; Humans ; Lymphocyte Count ; Lymphocytes* ; T-Lymphocytes

BACKGROUND: The poor prognostic factors of far-advanced pulmonary tuberculosis(FAPTB) are lymphocytopenia in the peripheral blood(PB)(<1,000/mm3) and T4-cell count < or =500/mm3. However, the cause of PB lymphocytopenia in FAPTB is unclear. The aim of this study was to analyze the lymphocyte proportion and cytokines of the bone marrow(BM) in FAPTB patients with peripheral lymphocytopenia in order to clarify whether the limiting step of the lymphocytopenia occurs in production, differentiation, or circulation. METHODS: This study included patients with FAPTB between August 1999 and August 2002 who visited Gachon Medical School Gil Medical Center. The exclusion criteria were old age(> or =65years), cachexia or a low body weight, shock, hematologic diseases, or BM involvement of tuberculosis. The distributions of cells in PB and BM were analyzed and compared to the control group. The interleukin(IL)-2, IL-7, IL-10, TNF-alpha, Interferon-gamma, and TGF-beta levels in the BM were measured by ELISA. RESULTS: Thirteen patients(male : female=9:4) were included and the mean age was 42+/-12years. The proportion and count of the lymphocytes in the PB were significantly lower in the FAPTB group (7.4+/- 3.0%, 694+/-255/mm3 vs. 17.5+/-5.8%, 1,377+/-436/mm3, each p=0.0001 and 0.002). The proportion of immature lymphocyte in the BM showed a decreasing trend in the FAPTB group(9+/-4% vs. 12+/-3%, p=0.138). The IL-2(26.0+/-29.1 vs. 112.2+/-42.4pg/mL, p=0.001) and IL-10(3.4+/-4.7 vs. 12.0+/-8.0pg/mL, p=0.031) levels in the BM were significantly lower in the FAPTB group than those in control. The levels of the other cytokines in FAPTB group and control were similar. CONCLUSION: These results suggest that the cause of lymphocytopenia in PB is associated with a abnormality IL-2 and IL-10 production in the BM. More study will be needed to define the mechanism of a decreased reservoir in BM.
Body Weight ; Bone Marrow* ; Cachexia ; Cytokines* ; Enzyme-Linked Immunosorbent Assay ; Hematologic Diseases ; Humans ; Interferon-gamma ; Interleukin-10 ; Interleukin-2 ; Interleukin-7 ; Lymphocytes* ; Lymphopenia* ; Schools, Medical ; Shock ; Transforming Growth Factor beta ; Tuberculosis ; Tuberculosis, Pulmonary* ; Tumor Necrosis Factor-alpha

BACKGROUND: Development of rapid drug susceptibility testing provides the opportunity for rapid identification of individuals with drug resistant tubercle bacilli, allowing selection of appropriate therapeutic regimens. METHODS: A total of 502 drug resistant isolates were subjected to reverse blot hybridization assay to detect mutations within genes (rpoB, katG, inhA, and ahpC) associated with rifampicin (RMP) and isoniazid (INH) resistance. RESULTS: Among the 264 RMP resistant strains (RMPR) tested, the most prevalent mutation was the Ser531Leu seen in 121 strains (46%). The second common mutation occurred in 84 strains (32%) at codon 526. And 27 strains (10%) showed the mutation at codon 516. Among all 469 INH resistant strains (INHR), the katG mutation was responsible for INH. The inhA mutation was present in 88 strains (19%). In 11 isolates (2%), coexisting of the katG and inhA mutations were identified. Reverse hybridization assay successfully detected over 80% of INHR and over 92% of RMPR among Korean isolates. CONCLUSION: Reverse hybridization was useful for rapid detection of INHR and RMPR.
Codon ; Genotype ; Isoniazid* ; Korea ; Mycobacterium tuberculosis ; Rifampin*

No abstract available.
Magnetic Resonance Imaging ; Pulmonary Artery ; Pulmonary Embolism* ; Radionuclide Imaging

No abstract available.
Real-Time Polymerase Chain Reaction*

Raoultella species are gram-negative, non-motile, aerobic bacilli that are primarily considered as environmental bacteria. Raoultella planticola is reportedly a rare cause of human infections. Also, the definite pathological mechanism of Raoultella planticola is currently unknown. We report a case of pneumonia caused by Raoultella planticola.
Bacteria ; Humans ; Pneumonia*