Background and objective: Because the mortality and social burden associated with COPD is increasing, repeated surveys of the prevalence of COPD have been used to assess risk factors, detect potential patients, and establish early diagnoses and management protocols. We report the prevalence of spirometrically detected COPD in Korea in 2008, using data from the fourth Korean National Health and Nutrition Survey. Methods: Using nationwide stratified random sampling, based on the Korean Statistical Office census, 6840 subjects aged Ն19 years underwent spirometry, which was performed by four trained technicians, during 2008. The place of residence, levels of education and income and smoking status, as well as other results from a COPD survey questionnaire were also assessed.

Recent cytogenetic studies indicated that loss of the long arm of chromosome 10 is a frequent event in small cell lung cancer (SCLC) and that a common region of the deletion is at 10q24-qter, which suggests the presence of a tumor-suppressor gene there. To map precise tumorsuppressor loci on the chromosome arm for further positional cloning e orts, we tested 46 primary SCLCs using microsatellite analysis. By analysing 11 highly polymorphic microsatellite markers located in 10q23-q26, we found that at least 78% (36/46) of the tumors exhibited loss of heterozygosity (LOH) at 10q with at least two distinct minimally deleted regions. LOH at one region (10q24) was found in at least 74% (32/43) of informative cases with a minimally deleted region between D10S198 and D10S192 (about 2 cM); LOH at another region (10q24-q25) was observed in at least 66% (29/44) of informative tumors with a minimally deleted region between D10S221 and D10S587 (about 11 cM). LOH at both regions or across both regions was observed in at least 52% (24/46) of the tumors tested. However, no mutations or homozygous deletions were found in the coding region of MXI1, a candidate tumor suppressor gene at 10q24-q25, in a panel of SCLC cell lines. Our data demonstrate that at least two tumorsuppressor loci exist on 10q and that they may play an important role in SCLC tumorigenesis.

Loss of heterozygosity (LOH) at chromosome 10q23-q25 is frequent in small cell lung cancer (SCLC), indicating the presence of putative tumor suppressor genes. PTEN/ MMAC1, a newly cloned candidate tumor suppressor gene at 10q23, was mutated in multiple human cancers. We investigated whether mutations of PTEN/MMAC1 play an important role in SCLC tumorigenesis. We examined 16 SCLC cell lines for PTEN/MMAC1 mRNA expression by reverse-transcriptase polymerase chain reaction (RT ± PCR) and potential mutations by sequencing analysis of the PTEN/MMAC1 coding region. No mutation was observed in PTEN/MMAC1 cDNAs in 15 cell lines expressing PTEN/MMAC1. One SCLC cell line, DMS79, did not have detectable PTEN/ MMAC1 expression. Importantly, we identi®ed a novel homologue of PTEN/MMAC1, termed PTH2, localized to chromosome 9p21-q13 and containing only ten amino acid substitutions compared with the PTEN/MMAC1 coding region. However, because the putative initiation codon for PTEN/MMAC1 gene was changed to arginine in PTH2, the translational initiation site of PTH2 is very likely to di er from that of the PTEN/MMAC1. PTH2 was expressed in two normal lung tissues and two normal colon tissues, but in only four of 16 SCLC cell lines. A missense mutation in PTH2 was identi®ed in a SCLC cell line that did not express PTEN/MMAC1 mRNA. Our data suggest that inactivation of PTEN/ MMAC1 is a rare event in SCLC tumorigenesis. However, the PTEN/MMAC1 homologue PTH2 may play a role in SCLC tumorigenesis.

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The SMS is a more rapid, simple prognostic score for predicting 28-day mortality and stratifying risk than the APACHE II or SOFA scores. However, external validation using a larger sample is needed.