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Record W4412379229 · doi:10.1097/tp.0000000000005453

Chronic Rejection Series: Heart Cardiac Allograft Vasculopathy

2025· article· en· W4412379229 on OpenAlexaff
Michael Rheaume, Natasha Aleksova, Joren C. Madsen, Gilles Bénichou

Bibliographic record

VenueTransplantation · 2025
Typearticle
Languageen
FieldMedicine
TopicTransplantation: Methods and Outcomes
Canadian institutionsWomen's College HospitalToronto General Hospital
Fundersnot available
KeywordsAllorecognitionImmunologyImmune systemMedicineTransplantationMajor histocompatibility complexAcquired immune systemAntigenHeart transplantationT cellInflammationAutoantibodyBiologyAntibodyInternal medicine

Abstract

fetched live from OpenAlex

Cardiac allograft vasculopathy (CAV) is a leading contributor to late allograft failure, mortality, and morbidity after heart transplantation. The prevalence of moderate to severe CAV over time has not changed significantly, and CAV remains an important contemporary consideration in post-heart transplantation management. The diagnosis and surveillance of CAV include both established and emerging invasive and noninvasive modalities, with a growing interest in understanding microvascular function and coronary physiology. The management of CAV is primarily focused on the prevention of CAV progression and optimizing traditional cardiovascular risk factors. Although mammalian target of rapamycin inhibitors and statins are central to the prevention of CAV progression, there is a lack of novel therapeutics for CAV. The development of new therapies for CAV will require a better understanding of the immune mechanisms underlying the initiation and perpetuation of this condition. CAV is mediated through a complex process involving cells and soluble factors of both innate and adaptive immune systems. Animal studies demonstrated that T cells play a central role in CAV. Both alloreactive T cells, which recognize donor major histocompatibility complex peptides (indirect allorecognition), and autoreactive T cells directed against heart tissue-specific antigens such as cardiac myosin have been shown to trigger CAV in mice. These processes involve the production of donor-specific antibodies and autoantibodies, respectively. Other studies suggest that CAV could be mediated by bystander T cells in a T cell receptor-independent manner and that CAV requires cooperation between T cells and natural killer cells. In addition, the essential role of interferon-γ in CAV has been documented. Whether any of these mechanisms pertain to CAV observed in transplanted patients has not been thoroughly investigated. Gaining insights into this question will be instrumental to the design of immune-based therapies for CAV.

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)0.001
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 score0.016
Threshold uncertainty score0.052

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0010.001
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0010.001
Science and technology studies0.0010.000
Scholarly communication0.0010.001
Open science0.0010.001
Research integrity0.0010.002
Insufficient payload (model declined to judge)0.0160.005

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 head0.011
GPT teacher head0.304
Teacher spread0.294 · 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

Citations3
Published2025
Admission routes1
Has abstractyes

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