Swine influenza is a respiratory infectious disease in pigs caused by Orthomyxoviridae influenza virus A. As a multihost pathogen, the virus can infect humans, birds, and pigs and has pandemic potential due to rapid mutation rate. This study investigated the seroprevalence of influenza A antibodies in pigs in Chungbuk Province to overview its temporal and spatial distribution. From March to November 2021, blood samples collected for swine fever and foot-and-mouth disease antibody tests from swine farms located in Cheongju, Jincheon, Jeungpyeong, and Goesan within the jurisdiction of the Chungbuk Animal Health Laboratory were used. Blood samples from both sows and growing pigs were collected. Additionally, three farms participating in the Expendable Disease Guidance Support Project were chosen to investigate the seroprevalence status by parity of sows and age of piglets. A total of 468 sows and 1,519 growing-finishing pigs were employed in this study. The results showed that Jincheon had the highest seropositivity rate, suggesting that more effort should be made in biosecurity to prevent mechanical transmission, given the close proximity of farms. The analysis of antibody levels in farms targeted by the Expendable Disease Guidance Support Project could suggest that once the virus enters a farm, it spreads throughout the entire pig population regardless of age. Farms that were positive in the first half of the year remained positive in 86% of cases in the second half, suggesting continuous infection within the farm unless depopulation or all-in-all-out practices are implemented. Moreover, 67% of farms that were negative in the first half remained negative in the second half, and farms managed by the same person showed identical antibody change patterns, indicating that the swine influenza virus can be transmitted by humans or vehicles. The results highlight the need for further analysis of biosecurity systems and geographical risk factors.

Selenium (Se) is known as an antioxidant mineral and heme iron is a major source for iron intake which can promote carcinogenesis in the body. This study was to investigate the effect of Se on heme-aggravated colon carcinogenesis in mice. Three experimental groups included control [normal diet + AOM (10 mg/kg body weight in saline)/DSS (2% in the drinking water)], [AOM/DSS + hemin (534 mg/kg body weight in CMC)], and [AOM/DSS + hemin + Se (2.82 mg/kg diet in CMC)] groups. Colonic mucosa were stained with 0.3% methylene blue and the colonic polyps, aberrant crypt (AC) and aberrant crypt foci (ACF) were counted. Lipid peroxidation in liver was evaluated by the thiobarbituric acid-reactive substances (TBARS) assay. The number of polyps in the hemin + Se group was 31.6% lower than that in the control group, and 41.4% lower than that in the hemin group. The number of AC in the hemin + Se group was 42.8% lower than that in the control group, and 49.1% lower than that in the hemin group. The number of ACF in the hemin + Se group was 49.0% lower than that in the control group, 45.7% than that in the hemin group. Hepatic TBARS level in the hemin + Se group was significantly low compared with the control group or the hemin group (p<0.05). These findings suggest that Se treatment may be protective against colon carcinogenesis promoted by a high heme-containing diet.