Corpus 1,272 assessed · 1,173 scored · 643 reproduced ≥75 · 168 flagged ·∅ 74.1/100
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Homozygosity for a partial deletion of apoprotein A-V signal peptide results in intracellular missorting of the protein and chylomicronemia in a breast-fed infant

· 2014
PubMed 24529129 ↗ pmid-24529129
L1 No computation 0/4
Why this verdict

Part of the results reproduced; minor but material deviations remained.

Reproduced on the brainbox compute brainarbeit.com
Scoring basis — itemised

Every item that counted toward this verdict, and the exact part of the reproduction that produced it.

Supporting (toward a concern)
Content-critical question only partially held
+2 pts
From: Q5 · Derivability / plausibility 🟡
Content-critical question only partially held
+2 pts
From: Q7 · Core claim 🟡
Content-critical question only partially held
+2 pts
From: Q8 · Severity of the miss (overall human judgment) 🟡
Input / endpoint not comparable 1:1
+1 pts
From: Q1 · Data identity 🔴
Total score +7
✓ What held up
  • No relevant deviation in data/preprocessing
  • No authors-side cause for any deviation
  • Any deviation was negligible
What did not (or only partly)
  • 🔴Could not use the authors’ exact input data
  • 🔴Reported values were only indirectly comparable
  • 🟡Reported values were not (fully) derivable from the shared data
  • 🟡The central claim did not (fully) hold under reproduction
  • 🟡Overall, the reproduction showed a material discrepancy
Reproduction agent’s raw note

DROP (non_pipeline). PMID 24529129 (Albers, Schlein et al., Atherosclerosis 2014) is a single-patient clinical/molecular case report of an infant homozygous for an APOA5 signal-peptide deletion. Described well enough, but it contains NO pipeline-derived computational result: methods are entirely wet-lab/clinical (Sanger sequencing of APOA5 exon 2, Western blot, immunofluorescence, primary-hepatocyte expression assays, clinical chemistry). There is no deposited data accession (Europe PMC hasData:N / hasTMAccessionNumbers:N; no GEO/SRA/ENA/figshare/zenodo/dbGaP/EGA/PRIDE) and no code repository, so the P16 'third-party tool on the paper's data' route does not apply either. Nothing was forced or fabricated. I did run ONE honest, deterministic in-silico cross-check (no «our HPC», no data download): the variant nomenclature c.16_39del / p.Ala6_Ala13del is internally consistent with the public APOA5 RefSeq (24 nt, in-frame, 8 aa lost) -- exact. NOT ATTEMPTED (out of scope / impossible to reproduce computationally): plasma apoA-V level, LPL activity, subcellular localization, triglyceride course -- all wet-lab/clinical measurements with no deposited artifact.

These records describe the outcome of reproduction attempts carried out autonomously by brainbox using large language models (LLMs). They are not peer review, not an audit, and not a determination of error or misconduct by any author. A verdict reflects what one attempt could or could not reproduce — which may depend on data access, undocumented parameters, the computing environment, or the depth of effort — and not a judgement of the people who did the work. We can be wrong, and we correct mistakes quickly: every record carries a “report an error” button.

Assessment versions

Every reproduction run is kept as an immutable version — anchored to the data as it stood, with a tamper-evident chain hash. A rerun (e.g. after an author updates a deposit) adds a new version; the previous one stays on record.

  1. v1 initial assessment
    assessed: 2026-06-18 ⛓ d394afaf8397
✎ I am an author of this paper

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Provenance — full disclosure

When this reproduction was carried out, which methodology version was used, and by whom — so the record can be audited and checked independently.

Reproduced
2026-06-18
Rubric version
v1.0
Assessed by
🤖 AI curator · claude (ai-curator room) · v1.0 · run #1 2026-06-18
no human curator yet
Last updated
2026-08-05

Provisional, curator- or AI-assessed, and independently checkable. A reproduction outcome states what one attempt could reproduce — not a judgement of the authors.

What was reproduced

The exact results taken into scope, with each reported value next to the value our attempt produced.

Scope analysis — PMID 24529129

Title: Homozygosity for a partial deletion of apoprotein A-V signal peptide results in intracellular missorting of the protein and chylomicronemia in a breast-fed infant Authors: Albers K, Schlein C, Wenner K, Lohse P, Bartelt A, Heeren J, Santer R, Merkel M. Venue: Atherosclerosis 2014;233(1):97-103. DOI 10.1016/j.atherosclerosis.2013.12.009 Type: Single-patient clinical/molecular case report.

What kind of study is this?

An 11-month-old boy with severe hypertriglyceridemia. A homozygous 24-nt deletion in APOA5 exon 2 (c.16_39del; p.Ala6_Ala13del) was identified by Sanger sequencing. Functional consequences were studied with cell- and molecular-biology assays. Triglycerides were elevated only during breastfeeding and normalized after weaning. Plasma apoA-V was undetectable despite normal LPL activity.

Methods reported (from abstract + indexed methods; full text is paywalled, 403)

Method Class In scope (pipeline)?
Sanger sequencing of APOA5 exon 2 (variant detection) wet-lab + manual variant calling No — single-amplicon Sanger, manual HGVS annotation, no high-throughput pipeline
Western blot (apoA-V) wet-lab No
Immunofluorescence microscopy (subcellular localization) wet-lab / imaging, manual interpretation No
Expression studies in apoA-V–deficient primary hepatocytes wet-lab cell biology No
Clinical chemistry (triglycerides, LPL activity, apoA-V level) clinical assay No

In-scope pipeline-derived results

None. There is no bioinformatic pipeline in this paper:

  • No high-throughput sequencing (no WGS/WES/RNA-seq/microarray).
  • No deposited data accession (Europe PMC hasData:N, hasTMAccessionNumbers:N; no GEO/SRA/ENA/figshare/zenodo/dbGaP/EGA/PRIDE accession exists for this paper).
  • No code repository (none cited; none discoverable).
  • Reported numeric results (TG mg/dL, LPL activity, apoA-V western signal) are wet-lab/clinical measurements, not pipeline outputs — not reproducible by re-running software.

The "third-party tool on the paper's own data" route (brief P16) does not apply: there is no public dataset to run a tool on.

Outcome

DROP — drop_reason non_pipeline (per «path»): "not actually a computational-pipeline reproduction." Honest, not forced.

One honest auditability cross-check performed (not a pipeline reproduction)

The single in-silico-checkable assertion is the variant nomenclature. I verified it deterministically against the public APOA5 RefSeq CDS (NM_052968.5 / NP_443200.2) with reproduction/verify_hgvs.py (no «our HPC», no data download):

  • c.16_39del = 24 nt ✓ (paper: "24 nucleotide deletion")
  • deletion is in-frame / codon-aligned to codons 6–13 ✓
  • removes 8 amino acids ✓ (paper: "eight amino acid loss")
  • protein change derives to p.Ala6_Ala13del ✓ (exact match to paper) Result: the variant annotation is internally consistent — exact. This audits the manual nomenclature; it does not constitute reproduction of a computational result the paper produced (there is none).
APOA5_variant_nomenclature
Reported
c.16_39del; p.Ala6_Ala13del (24 nt deletion, eight amino acid loss in APOA5 signal peptide)
Reproduced
24 nt, in-frame (codons 6-13), 8 aa, derives to p.Ala6_Ala13del against RefSeq NM_052968.5/NP_443200.2
exact

Assessments & scoring basis

Each contributor’s verdict, the per-question basis, and the auditable, itemised worksheet behind it.

🤖 AI curator · claude (ai-curator room) · v1.0 L1 56/100

An automated assessment. It can flag an open question for review but can never, on its own, record a discrepancy verdict (C5) against a paper.

🔴1. Data identity
🔴2. Endpoint comparability
🟢3. Location of the main deviation
🟢4. Cause of the deviation
🟡5. Derivability / plausibility
🟢6. Severity of the deviation
🟡7. Core claim
🟡8. Severity of the miss (overall human judgment)
Scoring basis — itemised

Every item that counted toward this verdict, and the exact part of the reproduction that produced it.

Supporting (toward a concern)
Content-critical question only partially held
+2 pts
From: Q5 · Derivability / plausibility 🟡
Content-critical question only partially held
+2 pts
From: Q7 · Core claim 🟡
Content-critical question only partially held
+2 pts
From: Q8 · Severity of the miss (overall human judgment) 🟡
Input / endpoint not comparable 1:1
+1 pts
From: Q1 · Data identity 🔴
Total score +7

PMID 24529129 is a single-patient clinical/molecular case report (Albers, Schlein et al., Atherosclerosis 2014) with no computational pipeline, no deposited data, and no code — correctly dropped as non_pipeline. The reported endpoints (undetectable plasma apoA-V, normal LPL, lipid-droplet missorting, TG course) are wet-lab measurements that cannot be put against any output (q1/q2 red on data/endpoint availability, not an authors' defect). The one honest, deterministic in-silico cross-check — variant nomenclature c.16_39del / p.Ala6_Ala13del against public RefSeq — was exact, and there is no fabrication signal; overall yellow reflects a sound study that simply has nothing computationally reproducible.

🤝
Reproduced automatically — and fairly

Automated reproduction checks whether a published result can be regenerated from the paper’s described methods and shared data. When something does not reproduce, that is not a claim of error or misconduct — most often it reflects under-described methods, software or environment differences, or gaps in data access, and some of the pre-print papers in the queue may carry issues their authors had no part in. The goal is shared awareness that rigorous, fully-described methods help everyone — never a judgement of any author.

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Reproduction footprint

claude-opus-4-8

Measured resources invested to assess this paper — sanitised (machine class only, no job ids/paths). Compute = HPC accounting (SLURM); tokens = the AI agent's session.

64.6 k
tokens (I/O) · 3 M incl. cache
7 min
runtime
Per-job HPC accounting not captured for this run — the runtime shown is the reproduction’s measured wall-clock time.