Background:The regulatory mechanism of BLT2 is largely unknown. Results: RanBPM interacts with BLT2 and inhibits BLT2-induced ROS generation and chemotaxis. Conclusion: Our findings suggest that RanBPM acts as a negative regulator of BLT2. Significance: Identification of regulators would provide better understanding of BLT2 signaling and potentially various BLT2-associated inflammatory pathogenesis.

ObjectivesTo estimate the resistance rate and to correlate the clinical characteristics of resistant tuberculosis with the patients of pulmonary tuberculosis who were referred to the university hospital.MethodsWe prospectively performed sensitivity tests for all patients who were diagnosed as active tuberculosis by sputum smear or sputum culture from January, 1995 to June, 1996. Patients profile, previous treatment history, patterns of drug resistance, initial chest films and other clinical findings were analysed.ResultsOverall, 24(26.0%) of the 92 patients had resistance to at least one drug and 8(8.6%) had resistance to isoniazid (INH) and rifampin (RFP). Among the 66 patients without previous tuberculosis therapy, 11 (16.6%) were drug-resistant and 2 (3.0%) were multi-drug resistant. Among the 26 patients with previous therapy, 13 (50.0%) were drug-resistant and 6 (23.0%) were multi-drug resistant. For all 92, resistance to INH was most common (19.5%), followed by RFP (9.7%) and ethambutol (9.7%). Drug resistance was significantly high in previously treated patients and in cavity-positive patients. Treatment failure was also high in previously treated patients with resistant tuberculosis. In patients with primary resistance, treatment failure was not observed.ConclusionSensitivity tests are strongly recommended in all culture positive patients with previous therapy but, in patients with primary resistance, sensitivity tests are not required. Proper combination chemotherapy should be given under careful surveillance.

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ObjectivesSince conventional cytogenetic analysis for bronchogenic carcinogenesis is limited by the difficulty to get enough number of high quality metaphase spreads, the development of new method to overcome above problems is strongly needed. Therefore, the introduction of non-radioactive in situ hybridization (ISH) with pericentromeric chromosome probes gave us the way to investigate the genetic events during carcinogenic process. We applied this method on lung cancer tissue to validate the possibility of this method for general usage and to analyze numerical chromosome aberration status and their clinical correlations.MethodsA set of satellite DNA probes specific for chromosome 3, 7, 9, 11, and 17 was hybridized directly to paraffin-embedded tissue section of 30 non-small cell lung cancers. Mean chromosome index of each chromosome and frequency of polysomy for each chromosome were calculated.ResultsMean chromosome indices for chromosome 3, 7, 9, 11, and 17 were 1.10, 1.13, 1.17, 1.12, and 1.17. respectively. Polysomy for a set of chromosomes was detected in all 30 cases except 4 cases which showed hypoploidy only for chromosome 3 or 7 in 2 cases and diploidy only for chromosome 3 or 11 in 2 cases. Among the set of chromosomes, mean chromosome index and polysomy frequency for chromosome 9 & 17 were significantly higher than that for others. Mean chromosome index or polysomy pattern for each chromosome was not much different among cell types or clinical stages.ConclusionsOur results show that chromosome ISH can be used to screen for numerical chromosome aberrations on paraffin tissue sections and further studies for ISH analysis with different probes on same tumor area or double-target ISH in large scale are needed to confirm above results and to elucidate the specific meanings.