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The Republic of Korea experienced a re-emergence of Plasmodium vivax malaria in 1993. The incidence of this disease increased rapidly through 2000 with its geographic distribution expanding from the vicinity near the Demilitarized Zone to the adjacent outlying areas. However, the number of cases of P. vivax malaria since that time period has decreased. A total of 2,538 cases occurred in 2001, and this decreased to 1,761 cases and 1,164 cases in the two subsequent years. A total of 5,463 cases of P. vivax malaria were reported from 2001 through 2003; 25.26% (1,380) were reported among Republic of Korea military personnel, 27.48% (1,501) were among veterans who had been discharged from the military within two years, and 47.26% (2,582) were among the civilian population. Mosquito control activities by the North Korean and South Korean governments, chemoprophylaxis of Republic of Korea Army personnel, and the low level of Anopheles mosquitoes in 2001 may have been factors responsible for the decreasing number of malaria cases. However, local transmission might have taken place in urban regions of the malaria-risk areas that are within 30 km south of the Demilitarized Zone. Extensive intervention and continued surveillance are warranted to prevent the epidemic from re-expanding and to eliminate this disease in the Republic of Korea.

Apigenin (5,7,4′-trihydroxyflavone) is a principal ingredient of Cirsium japonicum. These experiments were performed to determine whether apigenin has neuroprotective effects against kainic acid (KA)-induced excitotoxicity in vitro and in vivo. Intraperitoneal (i.p.) administration of apigenin (25, 50 mg/kg) decreased the seizure scores induced by KA injection (40 mg/kg, i.p.) in mice. In addition, the convulsion onset time was significantly delayed by apigenin administration. Moreover, we found that apigenin blocked KA-induced seizure-form electroencephalogram (EEG) discharge activity in the brain cortex. In hippocampal cells, apigenin inhibited KA-induced excitotoxicity in a dose-dependent manner as measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. To study the possible mechanisms underlying the in vitro neuroprotective effects of apigenin against KA-induced cytotoxicity, we also examined the effect of apigenin on intracellular reactive oxygen species (ROS) elevations in cultured hippocampal neurons and found that apigenin treatment dose-dependently inhibited intracellular ROS elevation. The remarkable reduction of glutathione (GSH) levels induced by KA in hippocampal tissues was reversed by apigenin in a dose-dependent manner. In addition, similar results were obtained after pretreatment with free radical scavengers such as trolox and dimethylthiourea (DMTU). Finally, after confirming the protective effect of apigenin in hippocampal CA3 region, we found apigenin is an active compound in KA-induced neuroprotection. These results collectively indicate that apigenin alleviates KA-induced excitotoxicity by quenching ROS as well as inhibiting GSH depletion in hippocampal neurons.

Vivax malaria re-emerged in the Republic of Korea (ROK) in 1993. The annual incidence of this disease, which had increased rapidly through 2000 with geographic expansion, started to decrease in 2001, reaching 864 cases in 2004; however, the trends changed in 2005 when 1,304 cases were reported. Among 2,168 cases of vivax malaria reported from 2004 through 2005, 389 cases (17.9%) were ROK military personnel, 565 cases (26.1%) were veterans who had been discharged from the military within 2 years of report of infection, and 1,214 cases (56.0%) were civilians. Local transmission might have taken place during this period in the southern side of the Demilitarized Zone. Regional increase of vivax malaria in North Korea, increased local transmissions in ROK, and active transmission by vector mosquitoes during the transmission season might be important factors responsible for the re-increase of vivax malaria in ROK during 2005.

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