In one paragraphArticle in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registryThe trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
6 authors.
Janaina Sena de SouzaDepartment of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, CA 90037, USA.ORCID 0000-0003-3904-7458 Sandra Sanchez-SanchezDepartment of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, CA 90037, USA.
Nicolas Amelinez-RoblesDepartment of Bioengineering, University of California, San Diego, La Jolla, CA 90037, USA.ORCID 0000-0003-1203-6345 B S GuerraDepartment of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, CA 90037, USA.ORCID 0000-0002-7843-8745 Gisele GiannoccoLaboratory of Molecular and Translational Endocrinology, Division of Endocrinology, Department of Medicine, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo 04039-032, SP, Brazil.
Alysson R MuotriDepartment of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, CA 90037, USA.ORCID 0000-0003-0867-2875 Funding
Novel SETD5-based Molecular Mechanisms and Therapeutic Tools to Understand and Revert Neuronal Dysfunction Associated with Intellectual disability and AutismR01MH127077 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Alon Goren, Alysson R. Muotri · 2022 to 2026
$3.9MBrain pathology and function in a chronic mouse model of ZIKV transmissionR01NS105969 · NINDS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI MUOTRI, ALYSSON R., OLSON, STEVEN H · 2019 to 2023
$3.3MInvestigating neurodevelopmental toxicity of perfluoroalkyl acids and their derivatives in human brain organoids modelsR01ES033636 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LILIA M IAKOUCHEVA, Alysson R. Muotri · 2022 to 2026
$3.0MThe Impact of hiPSC-Derived Microglia in Human Brain Development in Health and DiseaseR01NS123642 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MUOTRI, ALYSSON R. · 2021 to 2025
$2.2MInvestigation of Pitt-Hopkins Syndrome pathophysiology using a human modelR01MH123828 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MUOTRI, ALYSSON R. · 2021 to 2025
$1.9MCortical organoid models to study autism-associated 16p.11.2.CNVR56MH128365 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI IAKOUCHEVA, LILIA M, MUOTRI, ALYSSON R. · 2022 to 2022
$706kDepartment of Defense W81XWH2110306NIEHS NIH HHS R01 ES033636NIH HHS 1R01ES033636-22NIH HHS 1R01MH123828-21NIH HHS 1R01MH127077-22NIH HHS 1R01MH128365-24NIH HHS 1R01NS105969-19NIH HHS 1R01NS123642-21NIMH NIH HHS R01 MH123828NIMH NIH HHS R01 MH127077NIMH NIH HHS R56 MH128365NINDS NIH HHS R01 NS105969NINDS NIH HHS R01 NS123642
6 · The paper itselfAbstract
Thyroid hormones (THs) are essential for brain development, and their dysregulation is associated with cognitive deficits and neurodevelopmental disorders. Down syndrome (DS), caused by trisomy 21, is frequently associated with thyroid dysfunction and impaired neurogenesis. Here, we investigated THs signaling dynamics during neural differentiation using human induced pluripotent stem cells (hiPSCs) derived from individuals with DS and controls. We analyzed the gene expression of key THs regulators-deiodinases, transporters, and receptors-and downstream target genes in hiPSCs, hiPSC-derived neural progenitor cells (NPCs), hiPSC-derived astrocytes, and hiPSC-derived neurons. DS-derived hiPSCs, hiPSC-derived NPCs, and hiPSC-derived neurons exhibited 2- to 7-fold increases in the gene expression of
Indexed as
Cell DifferentiationDown SyndromeInduced Pluripotent Stem CellsNeuronsSignal TransductionThyroid HormonesAstrocytesHumansIodide PeroxidaseNeural Stem CellsNeurogenesisIodide PeroxidaseThyroid Hormonesastrocytesdeiodinasedown syndromegene expressioniPSCneuronsreceptorsthyroid hormonestransporters
Identifiers
PMID41002374
PMCPMC12468339
What Socratic holds
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