Recent increase of genetic diversity in Plasmodium vivax population in the Republic of Korea

<p>Abstract</p> <p>Background</p> <p>The reemergence of <it>Plasmodium vivax </it>in South Korea since 1993 represents a serious public health concern. Despite the importance in understanding genetic diversity for control strategies, however, studies remain inconclusive with the general premise that due to low rate of malaria transmission, there is generally low genetic diversity with very few strains involved. In this study, the genetic diversity and population structure of <it>P. vivax </it>in South Korea were explored by analysing microsatellite polymorphism.</p> <p>Methods</p> <p>Sequences for 13 microsatellite loci distributed across the twelve chromosomes of <it>P. vivax </it>were obtained from 58 South Korean isolates collected during two sampling periods, namely 1997-2000 and 2007. The sequences were used for the analysis of expected heterozygosity and multilocus genotype diversity. Population structure was evaluated using STRUCTURE version 2.3.2. Linkage disequilibrium was also analysed to investigate the extent of outbreeding in the <it>P. vivax </it>population.</p> <p>Results</p> <p>Mean expected heterozygosity significantly increased from 0.382 in 1997-2000 to 0.545 in 2007 (<it>P </it>< 0.05). The number of multilocus genotypes was 7 and 27; and genotype diversity was statistically significant (<it>P </it>< 0.01) at 0.661 and 0.995 in 1997-2000 and 2007, respectively. Analysis by STRUCTURE showed a more complex population structure in 2007 than in 1997-2000. Linkage disequilibrium between 13 microsatellites, although significant in both time points, was notably lower in 2007.</p> <p>Conclusions</p> <p>The present microsatellite analysis clearly showed recent increase of genetic diversity and recent relaxation of the strong population structure observed in 1997-2000. These results suggest that multiple genotypes not present previously recently migrated into South Korea, accompanied by substantial outbreeding between different genotypes.</p

The Development of the Neural Substrates of Cognitive Control in Adolescents with Autism Spectrum Disorders

BACKGROUND: Autism spectrum disorders (ASD) involve impairments in cognitive control. In typical development (TYP), neural systems underlying cognitive control undergo substantial maturation during adolescence. Development is delayed in adolescents with ASD. Little is known about the neural substrates of this delay. METHOD: We used event-related functional magnetic resonance imaging (fMRI) and a cognitive control task involving overcoming a prepotent response tendency to examine the development of cognitive control in young (ages 12–15; n = 13 with ASD and n = 13 with TYP) and older (ages 16–18; n= 14 with ASD and n = 14 with TYP) adolescents with whole-brain voxel-wise univariate and task-related functional connectivity analyses. RESULTS: Older ASD and TYP showed reduced activation in sensory and premotor areas relative to younger ones. The older ASD group showed reduced left parietal activation relative to TYP. Functional connectivity analyses showed a significant age by group interaction with the older ASD group exhibiting increased functional connectivity strength between the ventrolateral prefrontal cortex (VLPFC) and the anterior cingulate cortex (ACC), bilaterally. This functional connectivity strength was related to task performance in ASD, whereas that between DLPFC and parietal cortex (BA 9 and BA 40) was related to task performance in TYP. CONCLUSIONS: Adolescents with ASD rely more on “reactive” cognitive control, involving last minute conflict detection and control implementation by the ACC and VLPFC, versus “proactive” cognitive control requiring processing by DLPFC and parietal cortex. Findings await replication in larger longitudinal studies that examine their functional consequences and amenability to intervention