Evidence map›Paper›PMID 20379378›Full record

ReviewJournal of biomedicine & biotechnology2010

Evidence for maternal-fetal genotype incompatibility as a risk factor for schizophrenia.

Christina G S Palmer

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of biomedicine & biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Fetal programming of schizophrenia: select mechanisms.Neuroscience and biobehavioral reviews · 2015
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Gene-gene interaction in maternal and perinatal research.Journal of biomedicine & biotechnology · 2010
    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

1 author.

Christina G S PalmerDepartment of Psychiatry, UCLA Semel Institute, 760 Westwood Plaza, Room 47-422, Los Angeles, CA 90095, USA. cpalmer@mednet.ucla.edu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prenatal/obstetric complications are implicated in schizophrenia susceptibility. Some complications may arise from maternal-fetal genotype incompatibility, a term used to describe maternal-fetal genotype combinations that produce an adverse prenatal environment. A review of maternal-fetal genotype incompatibility studies suggests that schizophrenia susceptibility is increased by maternal-fetal genotype combinations at the RHD and HLA-B loci. Maternal-fetal genotype combinations at these loci are hypothesized to have an effect on the maternal immune system during pregnancy which can affect fetal neurodevelopment and increase schizophrenia susceptibility. This article reviews maternal-fetal genotype incompatibility studies and schizophrenia and discusses the hypothesized biological role of these ''incompatibility genes". It concludes that research is needed to further elucidate the role of RHD and HLA-B maternal-fetal genotype incompatibility in schizophrenia and to identify other genes that produce an adverse prenatal environment through a maternal-fetal genotype incompatibility mechanism. Efforts to develop more sophisticated study designs and data analysis techniques for modeling maternal-fetal genotype incompatibility effects are warranted.

Indexed as

Genetic Predisposition to DiseaseFemaleGenetic LociHLA-B AntigensHumansMaternal-Fetal ExchangePregnancySchizophreniaHLA-B Antigens

Identifiers

PMID20379378
PMCPMC2850511
OpenAlexW2067355845

What OpenQuestion holds

Textmetadata
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.