Browsing by Author "Ali, Abdulrahman"

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    COVID‐19 under 19: A meta‐analysis
    (2021) Toba, Nagham; Gupta, Shreya; Ali, Abdulrahman; ElSaban, Mariam; Hassan Khamis, Amar; Ho, Samuel B; Popatia, Rizwana
    Background: The coronavirus disease 2019 (COVID‐19) pandemic continues to cause global havoc posing uncertainty to educational institutions worldwide. Understanding the clinical characteristics of COVID‐19 in children is important because of the potential impact on clinical management and public health decisions. Methods: A meta‐analysis was conducted for pediatric COVID‐19 studies using PubMed and Scopus. It reviewed demographics, co‐morbidities, clinical manifestations, laboratory investigations, radiological investigations, treatment, and outcomes. The 95% confidence interval (CI) was utilized. Results: Out of 3927 articles, 31 articles comprising of 1816 patients were selected from December 2019 to early October 2020 and were defined by 77 variables. Of these studies 58% originated from China and the remainder from North America, Europe and the Middle East. This meta‐analysis revealed that 19.2% (CI 13.6%–26.4%) of patients were asymptomatic. Fever (57%, CI 49.7%–64%) and cough (44.1%, CI 38.3%–50.2%) were the most common symptoms. The most frequently encountered white blood count abnormalities were lymphopenia 13.5% (CI 8.2%–21.4%) and leukopenia 12.6% (CI 8.5%–18.3%). Ground glass opacities were the most common radiological finding of children with COVID‐19 (35.5%, CI 28.9%–42.7%). Hospitalization rate was 96.3% (CI 92.4%–98.2%) of which 10.8% (CI 4.2%–25.3%) were ICU admissions, and 2.4% (CI 1.7%–3.4%) died. Conclusion: The majority of pediatric patients with COVID‐19 were asymptomatic or had mild manifestations. Among hospitalized patients there remains a significant number that require intensive care unit care. Overall across the literature, a considerable level of understanding of COVID‐19 in children was reached, yet emerging data related to multisystemic inflammatory syndrome in children should be explored.
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    Single-cell transcriptome identifes molecular subtype of autism spectrum disorder impacted by de novo loss-of-function variants regulating glial cells
    (2021) Nassir, Nasna; Bankapur, Asma; Ali, Abdulrahman; Ahmed, Awab; Inuwa, Ibrahim M.; Shabestari, Seyed Ali Safzadeh; Albanna, Ammar; Berdiev, Bakhrom; Uddin, Mohammed
    Background: In recent years, several hundred autism spectrum disorder (ASD) implicated genes have been discov ered impacting a wide range of molecular pathways. However, the molecular underpinning of ASD, particularly from the point of view of ‘brain to behaviour’ pathogenic mechanisms, remains largely unknown. Methods: We undertook a study to investigate patterns of spatiotemporal and cell type expression of ASD-impli cated genes by integrating large-scale brain single-cell transcriptomes (>million cells) and de novo loss-of-function (LOF) ASD variants (impacting 852 genes from 40,122 cases). Results: We identifed multiple single-cell clusters from three distinct developmental human brain regions (ante rior cingulate cortex, middle temporal gyrus and primary visual cortex) that evidenced high evolutionary constraint through enrichment for brain critical exons and high pLI genes. These clusters also showed signifcant enrichment with ASD loss-of-function variant genes (p<5.23 × 10–11) that are transcriptionally highly active in prenatal brain regions (visual cortex and dorsolateral prefrontal cortex). Mapping ASD de novo LOF variant genes into large-scale human and mouse brain single-cell transcriptome analysis demonstrate enrichment of such genes into neuronal sub types and are also enriched for subtype of non-neuronal glial cell types (astrocyte, p<6.40× 10–11, oligodendrocyte, p<1.31× 10–09). Conclusion: Among the ASD genes enriched with pathogenic de novo LOF variants (i.e. KANK1, PLXNB1), a subgroup has restricted transcriptional regulation in non-neuronal cell types that are evolutionarily conserved. This association strongly suggests the involvement of subtype of non-neuronal glial cells in the pathogenesis of ASD and the need to explore other biological pathways for this disorder.