Evidence map›Paper›PMID 35328066›Full record

ArticleGenes2022

Association Study of

Bolesław Banach, Andrzej Modrzejewski, Zygmunt Juzyszyn, Mateusz Kurzawski, Tomasz Sroczynski, Andrzej Pawlik

Open access · goldAbstract read
In one paragraph

Article in Genes, 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
0.6field-weighted citation impact, top 31% 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, 7 citations in OpenAlex.

  1. Article
  2. Association ofPharmaceuticals (Basel, Switzerland) · 2025
    Article
  3. Article
  4. Article
  5. 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

6 authors at 1 institution in 1 country.

Bolesław BanachDepartment of Physiology, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland.
Andrzej ModrzejewskiClinical Department of General Surgery, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland.
Zygmunt JuzyszynDepartment of Physiology, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland.
Mateusz KurzawskiDepartment of Experimental and Clinical Pharmacology, Pomeranian Medical University, 70-111 Szczecin, Poland.
Tomasz SroczynskiDepartment of Physiology, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland.
Andrzej PawlikDepartment of Physiology, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland.ORCID 0000-0001-6557-1208
Pomeranian Medical University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is growing evidence that gallstone formation may be genetically determined. Recent studies have shown that polymorphism of genes encoding proteins involved in bile acid transport may be associated with the risk of gallstone disease. The aim of this study was to investigate the association between SLCO1B3 (rs4149117:G>T, rs7311358:A>G) and ABCC3 (rs4793665:T>C, rs11568591:G>A) genetic variants and susceptibility to cholesterol gallstone disease, as well as gallstone composition. The study included 317 patients suffering from cholelithiasis who underwent cholecystostomy and 249 controls with no evidence of stones, confirmed by ultrasound examination. There were no statistically significant differences in the distribution of studied gene polymorphisms between patients with gallstone disease and healthy controls. No significant associations were observed between studied genotypes and the content of analyzed gallstone components: total cholesterol, bilirubin, CaCO3, nor the total bile acids. There was also no association between bile acid content in gallstones and the polymorphisms studied. The results of this study suggest that polymorphisms of SLCO1B3 and ABCC3 genes are not a valuable marker of gallstone disease susceptibility and do not influence gallstone composition.

Indexed as

ATP-Binding Cassette, Sub-Family C ProteinsGallstonesSolute Carrier Organic Anion Transporter Family Member 1B3Bile Acids and SaltsCholesterolGenotypeHumansPolymorphism, GeneticATP-Binding Cassette, Sub-Family C ProteinsBile Acids and SaltsCholesterolmultidrug resistance-associated protein 3SLCO1B3 protein, humanSolute Carrier Organic Anion Transporter Family Member 1B3ABCC3bile acidsgallbladder diseasegenetic polymorphismSLCO1B3

Identifiers

PMID35328066
PMCPMC8951115
OpenAlexW4220810096

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.