ArticleFrontiers in neurology2022
Association of
Article in Frontiers in neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD): a scoping review.Pediatric research · 2026Article
- Immunological mechanisms and prevention strategies for febrile seizures in children.Frontiers in immunology · 2026Review
- Identification of Genetic Variants in Status Epilepticus Associated With Fever.Brain and behavior · 2025Observational
- Genetic and environmental risk factors of acute infection-triggered encephalopathy.Frontiers in neuroscience · 2023Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is a severe neurologic complication of febrile infectious diseases in children. At the onset, AESD is clinically manifested as febrile status epilepticus. Subsequent damage to the cerebral cortex is ascribed to neurotoxicity. The incidence of AESD is remarkably high in Japan, suggesting the involvement of genetic factors. The expression of interleukin 1 beta (IL-1β), a member of the cytokine family involved in the inflammatory response, is reportedly associated with rs16944, a polymorphism in the upstream region of the Methods: We genotyped rs16944 by Sanger sequencing on 283 patients with AESD. As controls, we used genotyping data of 104 Japanese individuals obtained from the 1,000 Genomes Project. Then, we performed a case-control association study using the chi-square test. Results: The ratio of individuals with TT vs. those with CC+CT genotype was significantly lower in AESD than in the controls [ Conclusion: The AESD has a genetic background distinct from FS and is not a severe type of FS.
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Registered trials
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