Evidence map›Paper›PMID 33375250›Full record

ArticleInternational journal of molecular sciences2020

Postnatal Smoke Exposure Further Increases the Hepatic Nicotine Metabolism in Prenatally Smoke Exposed Male Offspring and Is Linked with Aberrant

Khosbayar Lkhagvadorj, Zhijun Zeng, Karolin F Meyer, Laura P Verweij, Wierd Kooistra, Marjan Reinders-Luinge, Henk W Dijkhuizen, Inge A M de Graaf, Torsten Plösch, Machteld N Hylkema

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

Article in International journal of molecular sciences, 2020. 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
0.6field-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

4 citing papers in PubMed, 8 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

10 authors at 2 institutions in 2 countries.

Khosbayar LkhagvadorjUniversity Medical Center Groningen, Department of Pathology and Medical Biology, University of Groningen, 9713 GZ Groningen, The Netherlands.ORCID 0000-0002-5718-4256
Zhijun ZengUniversity Medical Center Groningen, Department of Pathology and Medical Biology, University of Groningen, 9713 GZ Groningen, The Netherlands.ORCID 0000-0002-6133-7075
Karolin F MeyerUniversity Medical Center Groningen, Department of Pathology and Medical Biology, University of Groningen, 9713 GZ Groningen, The Netherlands.
Laura P VerweijUniversity Medical Center Groningen, Department of Pathology and Medical Biology, University of Groningen, 9713 GZ Groningen, The Netherlands.
Wierd KooistraUniversity Medical Center Groningen, Department of Pathology and Medical Biology, University of Groningen, 9713 GZ Groningen, The Netherlands.
Marjan Reinders-LuingeUniversity Medical Center Groningen, Department of Pathology and Medical Biology, University of Groningen, 9713 GZ Groningen, The Netherlands.
Henk W DijkhuizenFaculty of Science and Engineering, University of Groningen, 9713 GZ Groningen, The Netherlands.
Inge A M de GraafDepartment of Pharmacokinetics, Toxicology and Targeting, Groningen Research Institute of Pharmacy, University of Groningen, 9713 AV Groningen, The Netherlands.
Torsten PlöschUniversity Medical Center Groningen, Department of Obstetrics and Gynecology, University of Groningen, 9713 GZ Groningen, The Netherlands.
Machteld N HylkemaUniversity Medical Center Groningen, Department of Pathology and Medical Biology, University of Groningen, 9713 GZ Groningen, The Netherlands.ORCID 0000-0002-6732-8903
University Medical Center Groningen · NLUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prenatal smoke exposure (PreSE) is a risk factor for nicotine dependence, which is further enhanced by postnatal smoke exposure (PostSE). One susceptibility gene to nicotine dependence is Cytochrome P450 (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine in the liver. Higher CYP2A6 activity is associated with nicotine dependence and could be regulated through DNA methylation. In this study we investigated whether PostSE further impaired PreSE-induced effects on nicotine metabolism, along with

Indexed as

DNA MethylationInactivation, MetabolicAnimalsAnimals, NewbornAryl Hydrocarbon HydroxylasesCytochrome P450 Family 2FemaleGene Expression RegulationMaleMiceMice, Inbred C57BLNicotinePregnancyPrenatal Exposure Delayed EffectsPromoter Regions, GeneticSmokeAryl Hydrocarbon HydroxylasesCyp2a5 protein, mouseCytochrome P450 Family 2NicotineSmokeCYP2A5epigeneticsnicotine addictionpostnatal smoke exposuresex-difference

Identifiers

PMID33375250
PMCPMC7795156
OpenAlexW3113675492

What Socratic 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 Socratic graph.