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Record W2792455947 · doi:10.1038/hgv.2018.1

Identification of a rare BMP pathway mutation in a non-syndromic human brain arteriovenous malformation via exome sequencing

2018· article· en· W2792455947 on OpenAlexaff
Brian P. Walcott, Ethan A. Winkler, Sirui Zhou, Harjus Birk, Diana E. Guo, Matthew J. Koch, Christopher J. Stapleton, Dan Spiegelman, Alexandre Dionne‐Laporte, Patrick A. Dion, Kristopher T. Kahle, Guy A. Rouleau, Michael T. Lawton

Bibliographic record

VenueHuman Genome Variation · 2018
Typearticle
Languageen
FieldMedicine
TopicVascular Malformations Diagnosis and Treatment
Canadian institutionsMcGill UniversityMontreal Neurological Institute and Hospital
FundersNational Institute of Neurological Disorders and StrokeNational Institutes of HealthCongress of Neurological Surgeons
KeywordsExome sequencingArteriovenous malformationPathologyMedicineZebrafishMutationBiologyGeneticsGeneRadiology

Abstract

fetched live from OpenAlex

Brain arteriovenous malformations (AVMs) are abnormal connections between arteries and veins that can result in hemorrhagic stroke. A genetic basis for AVMs is suspected, and we investigated potential mutations in a 14-year-old girl who developed a recurrent brain AVM. Whole-exome sequencing (WES) of AVM lesion tissue and blood was performed accompanied by in silico modeling, protein expression observation in lesion tissue and zebrafish modeling. A stop-gain mutation (c.C739T:p.R247X) in the gene SMAD family member 9 (SMAD9) was discovered. In the human brain tissue, immunofluorescent staining demonstrated a vascular predominance of SMAD9 at the protein level. Vascular SMAD9 was markedly reduced in AVM peri-nidal blood vessels, which was accompanied by a decrease in phosphorylated SMAD4, a downstream effector protein of the bone morphogenic protein signaling pathway. Zebrafish modeling (Tg kdrl:eGFP) of the morpholino splice site and translation-blocking knockdown of SMAD9 resulted in abnormal cerebral artery-to-vein connections with morphologic similarities to human AVMs. Orthogonal trajectories of evidence established a relationship between the candidate mutation discovered in SMAD9 via WES and the clinical phenotype. Replication in similar rare cases of recurrent AVM, or even more broadly sporadic AVM, may be informative in building a more comprehensive understanding of AVM pathogenesis. Disordered growth of abnormal blood vessels in the brain, leading to hemorrhagic stroke, can be caused by a rare genetic mutation. Brain arteriovenous malformations (AVMs), in which blood vessels in the brain form tangles that are prone to rupture, are a significant cause of stroke in both adults and children. The causes of AVMs remain poorly understood. Brian Walcott at the University of Southern California and co-workers searched for a potential genetic cause underlying a recurring AVM in a 14-year old girl. Genetic analysis identified a mutation in the SMAD9 gene, which resulted in decreased production of its protein. When the researchers modeled the same mutation in microscopic zebrafish, their blood vessels showed vascular development patterns with striking similarities to human AVMs. This research may help improve our understanding of how AVMs develop.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.001
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.006

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.001
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0000.001
Bibliometrics0.0010.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0010.000
Insufficient payload (model declined to judge)0.0020.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.018
GPT teacher head0.261
Teacher spread0.242 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations21
Published2018
Admission routes1
Has abstractyes

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