Evidence map›Paper›PMID 33611823›Full record

ArticleJournal of cellular and molecular medicine2021

Identification of rare variants causing urea cycle disorders: A clinical, genetic, and biophysical study.

Fang Liu, Li-Sha Bao, Ru-Jia Liang, Xiao-Ying Zhao, Zhi Li, Zhi-Fang Du, Shao-Guang Lv

Open access · goldAbstract readCase Reports
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
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

7 authors at 1 institution in 1 country.

Fang LiuDepartment of Pediatrics, NICU, Bethune International Peace Hospital (the 980th Hospital of the People's Liberation Army Joint Service Support Force), Shijiazhuang, China.
Li-Sha BaoDepartment of Pediatrics, NICU, Bethune International Peace Hospital (the 980th Hospital of the People's Liberation Army Joint Service Support Force), Shijiazhuang, China.ORCID 0000-0002-2320-4650
Ru-Jia LiangDepartment of Pediatrics, NICU, Bethune International Peace Hospital (the 980th Hospital of the People's Liberation Army Joint Service Support Force), Shijiazhuang, China.
Xiao-Ying ZhaoDepartment of Pediatrics, NICU, Bethune International Peace Hospital (the 980th Hospital of the People's Liberation Army Joint Service Support Force), Shijiazhuang, China.
Zhi LiDepartment of Pediatrics, NICU, Bethune International Peace Hospital (the 980th Hospital of the People's Liberation Army Joint Service Support Force), Shijiazhuang, China.
Zhi-Fang DuDepartment of Pediatrics, NICU, Bethune International Peace Hospital (the 980th Hospital of the People's Liberation Army Joint Service Support Force), Shijiazhuang, China.
Shao-Guang LvDepartment of Pediatrics, NICU, Bethune International Peace Hospital (the 980th Hospital of the People's Liberation Army Joint Service Support Force), Shijiazhuang, China.
Bethune International Peace Hospital · CN

Funding

the Key R&D Program Project of Hebei Province-Special Project on Health and Biomedicine 182777128D
6 · The paper itself

Abstract

Urea cycle disorders (UCDs) are a group of rare metabolic conditions characterized by hyperammonemia and a broad spectrum of phenotypic severity. They are caused by the congenital deficiency in the eight biomolecules involved in urea cycle. In the present study, five cases of UCD were recruited and submitted to a series of clinical, biochemical, and genetic analysis with a combination of high throughput techniques. Moreover, in silico analysis was conducted on the identified missense genetic variants. Various clinical and biochemical indications (including profiles of amino acids and urinary orotic acids) of UCD were manifested by the five probands. Sequence analysis revealed nine diagnostic variants, including three novel ones, which caused Argininosuccinic aciduria (ASA) in one case, Carbamoyl phosphate synthetase 1deficiency (CPS1D) in two cases, Ornithine transcarbamylase deficiency (OTCD) in one case, and Citrin deficiency in 1case. Results of in silico biophysical analysis strongly suggested the pathogenicity of each the five missense variants and provided insight into their intramolecular impacts. In conclusion, this study expanded the genetic variation spectrum of UCD, gave solid evidence for counselling to the affected families, and should facilitate the functional study on the proteins in urea cycle.

Indexed as

Computer SimulationMutation, MissenseDNA Mutational AnalysisFemaleHumansInfantInfant, NewbornMaleOrnithine CarbamoyltransferasePedigreePrognosisUrea Cycle Disorders, InbornOrnithine CarbamoyltransferaseOTC protein, humanargininosuccinic aciduriacarbamoyl phosphate synthetase 1deficiencycitrin deficiencyornithine transcarbamylase deficiencyurea cycle disorderwhole-exome sequencing

Identifiers

PMID33611823
PMCPMC8051738
OpenAlexW3132755116

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.