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Analysis of expression of FLI1 and MMP1 in American cutaneous leishmaniasis caused by Leishmania braziliensis infectionMMP1 is regulated by factors other than FLI1, and that the influence of IL-6 on MMP1 was independent of its effect on FLI1 in Leishmania braziliensis
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Determinants for progression from asymptomatic infection to symptomatic visceral leishmaniasis: A cohort studyWe confirmed the strong association between high DAT and/or rK39 titers and progression to disease among asymptomatic subjects
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Genetic and functional evidence for a role for SLC11A1 in susceptibility to otitis media in early childhood in a Western Australian populationOtitis media (OM) is a common disease in early childhood characterised by inflammation of the middle ear.
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Association of a NOD2 gene polymorphism and T-helper 17 cells with presumed ocular toxoplasmosisWe assessed 30 sibships and 89 parent/case trios of presumed ocular toxoplasmosis (POT) to evaluate associations with polymorphisms in the NOD2 gene.
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Cytokine responses to novel antigens in a peri-urban population in Brazil exposed to Leishmania infantum chagasiVisceral leishmaniasis (VL) is fatal if untreated, and there are no vaccines for this disease
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Genome-Wide Association Study to Identify the Genetic Determinants of Otitis Media Susceptibility in ChildhoodWe identified several novel candidate genes which warrant further analysis in cohorts matched more precisely for clinical phenotypes.
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A genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1To identify new susceptibility loci for psoriasis, we undertook a genome-wide association study of 594,224 SNPs in 2,622 individuals with psoriasis...
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Zika: Is there an underlying genetic/epigenetic basis to microcephaly and eye damage due to congenital Zika virus infection?Our hypothesis is that congenital Zika virus infection dysregulates these genes early in the developing fetus.
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Confirmation of childhood acute lymphoblastic leukemia Variants, ARID5B and IKZF1, and interaction with parental environmental exposuresThe polygenic nature of childhood ALL predisposition together with the timing of environmental triggers may hold vital clues for disease etiology.