Article in Human mutation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
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 registry
The 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.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
13 authors.
Julie A ChristensenAuditory and Vestibular Clinical Research Section, Neurotology Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0000-0002-9396-5973
Anne TranAuditory and Vestibular Clinical Research Section, Neurotology Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0009-0009-4773-4419
Hui ChengData Science Core, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0000-0001-5380-2830
Sara TalvacchioOffice of the Clinical Director, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0009-0006-6969-4735
Carmen C BrewerAuditory and Vestibular Clinical Research Section, Neurotology Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0000-0003-1462-049X
Christopher ZalewskiAuditory and Vestibular Clinical Research Section, Neurotology Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0000-0002-9196-0589
Jennifer ChisholmAuditory and Vestibular Clinical Research Section, Neurotology Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0009-0005-5626-8318
Talah T WafaAuditory and Vestibular Clinical Research Section, Neurotology Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0000-0001-6943-2205
L Noelle AllemangAuditory and Vestibular Clinical Research Section, Neurotology Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0009-0005-3456-6496
Elena F EvansSection on Heritable Disorders of Bone and Extracellular Matrix, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0009-0007-5459-8254
Alberta DerkyiOffice of the Clinical Director, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0009-0005-1596-7278
Joan C MariniSection on Heritable Disorders of Bone and Extracellular Matrix, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0000-0002-3685-0950
Gayla L PolingAuditory and Vestibular Clinical Research Section, Neurotology Branch, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, nih.gov.ORCID https://orcid.org/0000-0002-4132-4461
Funding
Clinical Analysis Of Disorders Of Hearing And BalanceZIADC000064 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI HERTZANO, RONNA · 2009 to 2025
$25.2M
Heritable Disorders of Connective TisueZIAHD008830 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MARINI, JOAN C · 2009 to 2023
Purpose: This study interrogates longitudinal natural history data to determine whether hearing loss (HL) incidence, onset, degree, and type in osteogenesis imperfecta (OI) caused by heterozygous collagen missense variants are associated with a specific gene or combinations of causal gene and OI type. Methods: Audiological evaluation was conducted in 73 children with Type III or IV OI carrying Results: A total of 71% of Type III OI participants experienced HL, compared with 39% of those with Type IV OI. Conductive HL persisted (33%) or transitioned to mixed conductive/sensorineural (67%) with progression. While HL was predominantly mild in most participants, six Type III participants (25%) but only one Type IV OI participant (7%) progressed to more severe loss. Most Type III and IV OI participants had HL onset in the first decade of life, with 46% and 33% of onsets, respectively, occurring before school age. More than half of participants with Conclusions: Our data reveal significant HL onset in the first decade, and an interaction of Type III OI and COL1A1 variants among those with HL progression. These findings will guide clinical management, facilitating early monitoring tailored to genotype and phenotype.
Indexed as
Collagen Type IHearing LossOsteogenesis ImperfectaAdolescentAdultChildChild, PreschoolCollagen Type I, alpha 1 ChainDisease ProgressionFemaleGenetic Association StudiesHumansIncidenceInfantMaleMutation, MissenseCOL1A2 protein, humanCollagen Type ICollagen Type I, alpha 1 Chain
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Type III Osteogenesis Imperfecta and · full record | OpenQuestion