BACKGROUND: Hepatocellular carcinoma is the second most common cause of death among cancers in Korea. Epidemiological studies have revealed the carrier state of the hepatitis B virus and the dietary intake of aflatoxin B1 as possible causative agents of this neoplasm, but the precise molecular bases are still unknown. METHODS: We examined 24 cases of human hepatocellular carcinomas in Koreans for the presence of p53 aberrations in exons 4 to 9 of the gene by using single-strand conformation polymorphism (SSCP) analysis of the polymerase chain reaction (PCR) products. RESULTS: Four (17%) of the tumors demonstrated a SSCP band shift, 1 in exon 6 and 3 in exon 7. All of the abnormal DNA fragments were further characterized by direct DNA sequencing. All the mutations were missense mutations. One was an A to G transition at the second nucleotide of codon 214; 2 were G to T transversions at the second nucleotide of codon 245; and one was a G to T transversion at the third nucleotide of codon 249, a mutational 'hot spot' at which mutations have been frequently found, especially when aflatoxin B1 plays an important role in the hepatocarcinogenesis. CONCLUSIONS: These results indicate that the possibility of aflatoxin B1 being a causative agent of hepatocarcinogenesis in Korea can not be excluded.
Aflatoxin B1 ; Carcinoma, Hepatocellular* ; Carrier State ; Cause of Death ; Codon ; DNA ; Epidemiologic Studies ; Exons ; Genes, Tumor Suppressor* ; Hepatitis B virus ; Humans ; Korea ; Mutation, Missense ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Sequence Analysis, DNA

BACKGROUND: The objective of this study was to investigate the relationship between smoking and metabolic syndrome in men. METHODS: This cross-sectional study included 1,852 men over age 40 who underwent health screening from April 2009 to December 2010. We classified them into three smoking levels as non-, intermediate-, and heavy-smoker, considering their smoking status (non, ex, current) and amount (0, 1-29, > or =30 pack year [PYR]). The relationship between smoking level and metabolic syndrome was analyzed by logistic regression analysis, after covariates (age, body mass index, education, house income, alcohol intake, and physical activity) were controlled. RESULTS: The proportions of non-, intermediate-, and heavy-smokers were 31.8%, 56.2%, and 12.0%, respectively. Odds ratios (ORs) and 95% confidence intervals (95% CIs) for metabolic syndrome were 1.0, 1.58 (1.09-2.23), 1.92 (1.29-2.81) in non-, intermediate-, and heavy-smokers, respectively. For heavy-smokers compared with non-smokers, ORs and 95% CIs of a lower high density lipoprotein cholesterol, higher triglyceride, and higher fasting glucose were 2.47 (1.63-3.74), 1.71 (1.17-2.52), and 1.43 (1.02-2.00), respectively. In current-smokers, we divided into three subgroups according to PYR, and compared with 1-19 PYR, ORs and 95% CIs of 20-29 PYR and > or =30 PYR for metabolic syndrome were 2.07 (1.14-3.74) and 3.06 (1.66-5.62), respectively. CONCLUSION: This study showed a positive dose-response relationship between smoking level and metabolic syndrome in men.
Body Mass Index ; Cholesterol, HDL ; Cross-Sectional Studies ; Education ; Fasting ; Glucose ; Humans ; Logistic Models ; Male ; Mass Screening ; Metabolic Syndrome X ; Odds Ratio ; Smoke* ; Smoking* ; Triglycerides

Congenital cystic adenomatoid malformation of the Lung(CCAM) is characterized by anomalous fetal development of terminal respiratory structures, resulting in an adenomatoid proliferation of bronchiolar elements and cystic formation. CCAM was first described and differentiated from other cystic lung disease in the English literature by Ch'in and Tang in 1949. CCAM is a rare, potentially lethal form of congenital pulmonary cystic disease and the salient features of lesion are an irregular network of terminal respiratory bronchiole-like structures and macrocysts variably lined by pseudostratified ciliated columnar epithelium and simple cuboidal epithelium. Adult presentation of CCAM of the lung is so tare that only 9 cases have been reported in the literature of date. The pathogenesis of CCAM remains disputed and reseachers have variously proposed that the lesion represents a developmental anomaly, hamartoma, or a form of pulmonary dysplasia. Van Dijk and Wagenvoort divided CCAM into three subtypes: cystic, intermediated, and solid. These correspond to types I, II, and III of Stocker. In adults, the evaluation of cystic or multicystic lung disease requires consideration of a differential diagnosis including the acquired lesions of lung abscess, cavitary neoplasm or inflammatory mass, bullous disease, bronchiectasis, and postinflammatory pneumatocele. Congenital lesions such as sequestration, bronchopulmonary-foregut anomalies, and bronchogenic cyst are also encounted. The definitive treatment for CCAM is complete removal of the involved lobe. Partial lobectomy leads to multiple complications, including severe post-operative infection. We report a case of CCAM in a 14-year-old female presentated with a pneumothorax and large bullae, who was treated by surgical remove of the involved lobe.
Adolescent ; Adult ; Bronchiectasis ; Bronchogenic Cyst ; Cystic Adenomatoid Malformation of Lung, Congenital* ; Diagnosis, Differential ; Epithelium ; Female ; Fetal Development ; Hamartoma ; Humans ; Lung Abscess ; Lung Diseases ; Lung* ; Pneumothorax