25 research outputs found

    Risk factors and mode of transmission of toxoplasmosis in Nigeria: a review

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    Toxoplasmosis is a cosmopolitan infection caused by an obligate intracellular protozoan, Toxoplasma gondii. The parasite was described as the most successful having full potentials to聽 be transmitted聽 through various routes from contamination of the environment and food substances to continuous spread as tissue cyst in meat, among its intermediate host, bypassing its sexual stage of life cycle in its definitive host. Relevant English databases were searched for the prevalence studies conducted in Nigeria. In this review, we identified the various ways through which the infection can be spread within human population as reported by various studies in Nigeria.Keywords: cosmopolitan, environment, intracellular, protozoan, toxoplasmosi

    Single-cell RNA sequencing reveals dysregulated cellular programs in the inflamed epithelium of Crohn's disease patients.

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    <p><strong>Crohn’s disease (CD) is a complex inflammatory disorder of incompletely understood molecular aetiology. We generated a large single-cell RNA sequencing dataset from the terminal ileal biopsies of two independent cohorts comprising a total of 50 CD patients and 71 healthy controls. We performed transcriptomic analyses to reveal genes, cell types and mechanisms perturbed in CD, leveraging the power of the two cohorts to confirm our findings and assess replicability. In addition to mapping widespread alterations in cytokine signalling, we provide evidence of pan-epithelial upregulation of MHC class I genes and pathways in CD. Using non-negative matrix factorization we revealed intra- and inter-cellular upregulation of expression programs such as G-protein coupled receptor signalling and interferon signalling, respectively, in CD. We observed an enrichment of CD heritability among marker genes for various activated T cell types and myeloid cells, supporting a causal role for these cell-types in CD aetiology. Comparisons between our discovery and replication cohort revealed significant variation in differential gene-expression replicability across cell types. B, T and myeloid cells showed particularly poor replicability, suggesting caution should be exercised when interpreting unreplicated differential gene-expression result in these cell types. Overall, our results provide a rich resource for identifying cell-type specific biomarkers of Crohn’s disease and identifying genes, cell types and pathways that are causally and replicably associated with disease.</strong></p&gt
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