blood feeding behaviour are not due to synergistic interactions between PM and the two repellents DEET and KBR but to additive effect of the compounds. The model that best fit the data took into account the main effects treatment and time and their interaction with the season. Exophily and blood feeding explain a significant part of the deviance of the mortality data depending on the treatment. At the beginning of the dry season trial, PM was killing less than 50 of exposed mosquitoes. DEET and KBR were killing less than 30. In contrast at the same time, PM+DEET was killing 93 of mosquitoes that entered in the hut and PM+KBR about 99. In the rainy season, the mortality at the beginning of the trial was Acid Yellow 23 significantly lower than in the dry season for PM, DEET and KBR used alone. The mortality Eliglustat (hemitartrate) induced by PM+DEET did not decrease significantly in the rainy season, in contrast with PM+KBR. Moreover the maximal efficacy did not last as long as it did in dry season. T This region functions by regulating interactions between H19 and IGF2 promoters and their shared enhancers, which are located downstream of the H19 coding sequence and can, in the absence of a chromatin barrier, stimulate transcription of the IGF2 gene in cis. The methylation status of specific conserved sequences regulates the binding of the ubiquitously expressed factor CTCF to the ICR, which functions as an insulator and enhancer blocker. In most adult tissues, binding of CTCF to the unmethylated maternal allele prevents H19 enhancers from inducing IGF2 expression, leaving them available to induce H19. Methylation of the paternal H19 ICR abrogates CTCF binding resulting in enhancer stimulation of IGF2 expression and H19 silencing. Recent studies using chromosome conformation capture have shown that long range allele-specific interactions constitute part of the insulation mechanism but our understanding of these interactions is still incomplete. A complex three-dimensional, multiple-loop model organized by the CTCF-ICR complex on the maternal allele has been recently proposed and both intra and inter-chromosomal interactions have been shown to involve the H19 ICR. Loss of imprinting concurrent to hypomethylation at the H19/IGF2 intergenic region has been observed in a limited number of primary synovial sarcomas and SYT-SSX expression has been shown to induce IGF2 in immortalized MRC5 fibroblasts and HEK 293 cells. In the latter case, IGF2 induction could be attributed to epigenetic mechanism
