ABSTRACT
Survival of CHD has significantly improved, but children with CHD remain susceptible to neurodevelopmental and psychosocial impairments. Our goal was to investigate the association between socio-demographic factors and psychosocial adaptation for future intervention. A retrospective cross-sectional study of an independent children's hospital's records was conducted. Psychosocial adaptation was measured by the Pediatric Cardiac Quality of Life Inventory Psychosocial Impact score (range 0-50, higher score indicates greater psychosocial adaptation). Bivariate and regression analyses were performed to estimate relationships between Psychosocial Impact score and socio-demographic variables including Child Opportunity Index, family support, financial support, academic support, and extracurricular activities. A total of 159 patients were included. Compared to patients in high opportunity neighbourhoods, patients in low opportunity neighbourhoods had a 9.27 (95% confidence interval [-17.15, -1.40], p = 0.021) point lower Psychosocial Impact score, whereas patients in moderate opportunity neighbourhoods had a 15.30 (95% confidence interval [-25.38, -5.22], p = 0.003) point lower Psychosocial Impact score. Compared to patients with adequate family support, those with limited support had a 6.23 point (95% confidence interval [-11.82, -0.643], p = 0.029) lower Psychosocial Impact score. Patients in moderate opportunity neighbourhoods had a higher Psychosocial Impact score by 11.80 (95% confidence interval [1.68, 21.91], p = 0.022) when they also had adequate family support compared to those with limited family support. Our findings indicate that among children with CHD, psychosocial adaptation is significantly impacted by neighbourhood resources and family support structures. These findings identify possible modifiable and protective factors to improve psychosocial adaptation in this vulnerable population.
ABSTRACT
Background and Aim: Animal trypanosomiasis is a major contributor to agricultural and economic losses, especially in sub-Saharan Africa. We have shown that some animal species expressed genes that are significant players in immune response to bovine trypanosomosis, impeding signs and symptoms of the disease. We hypothesize that such animals are contributors to disease transmission dynamics and severe outcomes. Therefore, this study aims to ascertain trypanosome species diversity in cattle and their potential role as reservoirs for the transmission of human disease. Materials and Methods: We performed a molecular genotyping of trypanosome internal transcribed spacer 1 (ITS-1) and 18S ribosomal RNA genes on genomic DNA extracts from randomly sampled N'Dama cattle from slaughterhouses in Nigeria. We identified trypanosome species circulating among the animals through polymerase chain reaction and genomic sequencing. We performed multiple sequence alignments as well as conducted a phylogenetic relationship between identified species. Results: In all, 9 of 127 (7.1%) samples were positively amplified (band sizes ranging from 250 bp to 710 bp), including an isolate with two distinct bands (700 and 710 bp), indicating two trypanosome types. Sequence similarity and homology analysis identified four species, namely: Trypanosoma vivax, Trypanosoma congolense forest type, T. congolense savannah type, and Trypanosoma brucei. Interestingly, one of the bands, additionally verified by nucleotide sequencing, was identified as a human trypanosome (Trypanosoma brucei gambiense), confirming our hypothesis that cattle are potential reservoir hosts for human trypanosomes. Conclusion: Overall, we observed different trypanosome species in our study area, with animals on the same farm infected with multiple species, which could complicate treatment and disease control strategies. Finding human trypanosome species strengthens the argument that disease transmission dynamics are modulated by other vertebrates, further complicating control programs.
ABSTRACT
Malaria remains a significant disease, causing epic health problems and challenges all over the world, especially in sub-Saharan Africa. CD209 and CD28 genes act as co-stimulators and regulators of the immune system, while the STAT6 gene has been reported to mediate cytokine-induced responses. Single nucleotide polymorphisms of these genes might lead to differential disease susceptibility among populations at risk for malaria, due to alterations in the immune response. We aim to identify key drivers of the immune response to malaria infection among the three SNPs: CD209 (rs4804803), CD28 (rs35593994) and STAT6 (rs3024974). After approval and informed consent, we genotyped blood samples from a total of 531 children recruited from Nigeria using the Taqman SNP genotyping assay and performed comparative analysis of clinical covariates among malaria-infected children. Our results reveal the CD209 (rs4804803) polymorphism as a susceptibility factor for malaria infection, significantly increasing the risk of disease among children, but not CD28 (rs35593994) or STAT6 (rs3024974) polymorphisms. Specifically, individuals with the homozygous mutant allele (rs4804803G/G) for the CD209 gene have a significantly greater susceptibility to malaria, and presented with higher mean parasitemia. This observation may be due to a defective antigen presentation and priming, leading to an ineffective downstream adaptive immune response needed to combat infection, as well as the resultant higher parasitemia and disease manifestation. We conclude that the CD209 gene is a critical driver of the immune response during malaria infection, and can serve as a predictor of disease susceptibility or a biomarker for disease diagnosis.
