Evidence map›Paper›PMID 36339418›Full record

ArticleFrontiers in endocrinology2022

Integration of genomic analysis and transcript expression of ABCC8 and KCNJ11 in focal form of congenital hyperinsulinism.

Ilse Wieland, Ina Schanze, Ina Marianti Felgendreher, Winfried Barthlen, Silke Vogelgesang, Klaus Mohnike, Martin Zenker

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. A case of congenital hyperinsulinism withClinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Congenital Hyperinsulinism Caused by Mutations inInternational journal of molecular sciences · 2024
    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 2 institutions in 1 country.

Ilse WielandInstitute of Human Genetics, University Hospital Otto-von-Guericke- University Magdeburg, Magdeburg, Germany.
Ina SchanzeInstitute of Human Genetics, University Hospital Otto-von-Guericke- University Magdeburg, Magdeburg, Germany.
Ina Marianti FelgendreherInstitute of Human Genetics, University Hospital Otto-von-Guericke- University Magdeburg, Magdeburg, Germany.
Winfried BarthlenDepartment of Pediatric Surgery, Protestant Hospital of Bethel Foundation, University Hospital OWL, University of Bielefeld, Bielefeld, Germany.
Silke VogelgesangUniversity Medicine, Institute of Pathology, University of Greifswald, Greifswald, Germany.
Klaus MohnikeDept of Pediatrics, University Hospital Otto-von-Guericke-University Magdeburg, Magdeburg, Germany.
Martin ZenkerInstitute of Human Genetics, University Hospital Otto-von-Guericke- University Magdeburg, Magdeburg, Germany.
Otto-von-Guericke University Magdeburg · DEUniversität Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The focal form of CHI is caused by an autosomal recessive pathogenic variant affecting the paternal homologue of genes Research Design and Methods: Patients receiving therapeutic surgery and with proven Results: Both genes, Conclusions: Paternal UPD on the short arm of chromosome 11 appears to be the major second genetic event specifically within focal lesions of CHI but no common breakpoint for UDP can be delineated. We show for the first time upregulation of growth promoting

Indexed as

Congenital HyperinsulinismPotassium Channels, Inwardly RectifyingBasic Helix-Loop-Helix ProteinsGenomicsHumansLoss of HeterozygositySulfonylurea ReceptorsUniparental DisomyABCC8 protein, humanASCL2 protein, humanBasic Helix-Loop-Helix ProteinsPotassium Channels, Inwardly RectifyingSulfonylurea ReceptorsABCC8Achaete-scute complex homolog 2CHIKCNJ11UPD 11p

Identifiers

PMID36339418
PMCPMC9634566
OpenAlexW4307165594

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.