No abstract

The average prevalence of reported foodborne illness from 1981 to 1995 was 2.44 per 100,000 population in Korea, and 28.01 in Japan. The mean case fatality rate in Korea was 0.74% and in Japan, 0.03%. When both prevalence and case fatality rates in Korea and Japan were compared during the same period, the prevalence in Japan was much higher than that in Korea. However, the case fatality rate of patients in Korea was much higher than that in Japan. The distribution of monthly and seasonal patterns of foodborne illness outbreaks strongly indicate the outbreaks may be associated with climatic conditions, frequencies of national holidays, and vacation seasons. Comparison study indicates that the foodborne illness outbreaks in Korea most frequently involved homemade foods (47% of the total cases); in Japan, restaurants accounted for 31.3%. Foodborne illness cases of bacterial origin in Korea were 59.3% of the total and included Salmonella spp. (20.7%). Vibrio (17.4%), Staphylococcus (9.7%), pathogenic Escherichia coli (2.4%), and other species (9.1%); in Japan, 72.8% of the total cases and the majority of the bacterial foodborne illness was caused by Vibrio (32.3%), Staphylococcus (15.9%), Salmonella (14.2%), pathogenic E. coli (3.0%), and other species (7.2%). In conclusion, the outbreaks of foodborne illness in Korea and Japan may be mainly caused by improper food handling, and their occurrences may be differentiated according to food sources.

Though the G(1) checkpoint in mammalian cells has been known for decades, the molecular targets that prevent S-phase entry remain unknown. Mimosine is a rare plant amino acid that arrests the cell cycle in the G(1) phase before entry into S phase. Here, we show that mimosine interrupts the binding of Ctf4 to chromatin, which is essential for the initiation of DNA replication in HeLa cells, and this effect is mediated by the Hif-1α-dependent increase in the level of p27. Depletion of Hif-1α results in an increased binding of Ctf4 to chromatin and the entry of cells into S phase even in the presence of mimosine. These results suggest that the binding of Ctf4 to chromatin is the target of the Hif-1α-dependent checkpoint pathway for cell cycle arrest in G(1) phase. Although we observed Hif-1α-dependent arrest in mimosine-treated cells, it is possible that Ctf4 may act as a common target for G(1) arrest in various other checkpoint pathways.

Though RecQL4 was shown to be essential for the initiation of DNA replication in mammalian cells, its role in initiation is poorly understood. Here, we show that RecQL4 is required for the origin binding of Mcm10 and Ctf4, and their physical interactions and association with replication origins are controlled by the concerted action of both CDK and DDK activities. Although RecQL4-dependent binding of Mcm10 and Ctf4 to chromatin can occur in the absence of pre-replicative complex, their association with replication origins requires the presence of the pre-replicative complex and CDK and DDK activities. Their association with replication origins and physical interactions are also targets of the DNA damage checkpoint pathways which prevent initiation of DNA replication at replication origins. Taken together, the RecQL4-dependent association of Mcm10 and Ctf4 with replication origins appears to be the first important step controlled by S phase promoting kinases and checkpoint pathways for the initiation of DNA replication in human cells.