Evidence map›Paper›PMID 38312695›Full record

ArticleHeliyon2024

Characterization of heterozygous ATTR Tyr114Cys amyloidosis-specific induced pluripotent stem cells.

Kenta Ouchi, Kaori Isono, Yuki Ohya, Nobuaki Shiraki, Masayoshi Tasaki, Yukihiro Inomata, Mitsuharu Ueda, Takumi Era, Shoen Kume, Yukio Ando and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
4 · The record

Corrections and comments

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

11 authors at 5 institutions in 1 country.

Kenta OuchiDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 2-2-1 Honjo, Chuo Ward, Kumamoto City, Kumamoto Prefecture, 860-8556, Japan.
Kaori IsonoDepartment of Transplantation and Paediatric Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Chuo Ward, Kumamoto City, Kumamoto Prefecture, 860-8556, Japan.
Yuki OhyaDepartment of Transplantation and Paediatric Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Chuo Ward, Kumamoto City, Kumamoto Prefecture, 860-8556, Japan.
Nobuaki ShirakiSchool of Life Science and Technology, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori Ward, Yokohama City, Kanagawa Prefecture, 226-8501, Japan.
Masayoshi TasakiDepartment of Biomedical Laboratory Sciences, Graduate School of Health Sciences, Kumamoto University, Kumamoto, 1-1-1 Honjo, Chuo Ward, Kumamoto City, Kumamoto Prefecture, 860-8556, Japan.
Yukihiro InomataDepartment of Pediatric Surgery, Kumamoto Rosai Hospital, 1670 Takehara-cho, Yatsushiro City, Kumamoto Prefecture, 866-0826, Japan.
Mitsuharu UedaDepartment of Neurology, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Chuo Ward, Kumamoto City, Kumamoto Prefecture, 860-8556, Japan.
Takumi EraDepartment of Cell Modulation, Institute of Molecular Embryology and Genetics, Kumamoto University, 2-2-1 Honjo, Chuo Ward, Kumamoto City, Kumamoto Prefecture, 860-8556, Japan.
Shoen KumeSchool of Life Science and Technology, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori Ward, Yokohama City, Kanagawa Prefecture, 226-8501, Japan.
Yukio AndoDepartment of Amyloidosis Research, Nagasaki International University, 2825-7 Huis Ten Bosch Cho, Sasebo City, Nagasaki Prefecture, 859-3298, Japan.
Hirofumi JonoDepartment of Clinical Pharmaceutical Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 2-2-1 Honjo, Chuo Ward, Kumamoto City, Kumamoto Prefecture, 860-8556, Japan.
Kumamoto University · JPTokyo Institute of Technology · JPKumamoto Health Science University · JPKumamoto University Hospital · JPNagasaki International University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary transthyretin (TTR) amyloidosis (ATTRv amyloidosis) is autosomal dominant and caused by mutation of

Indexed as

Hereditary transthyretin amyloidosisiPS cellsTransthyretinTyr114Cys

Identifiers

PMID38312695
PMCPMC10835262
OpenAlexW4391062480

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.