PTCD3 mutations cause Leigh-like rather than Leigh syndrome.

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.

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.

Who cites it

2 citing papers in PubMed, 2 citations in OpenAlex.

1. Leigh syndrome is the main clinical characteristic of PTCD3 deficiency.Brain pathology (Zurich, Switzerland) · 2023
   Article
2. AmicroPublication biology · 2023
   Article

Corrections and comments

• Commented on by
  Reply to the "Letter to the Editor" from Dr. J Finsterer and colleagues.2019
• Comment on
  Mitochondrial ribosomal protein PTCD3 mutations cause oxidative phosphorylation defects with Leigh syndrome.2019

Authors and funding

3 authors at 2 institutions in 2 countries.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

Indexed as