Evidence map›Paper›PMID 19884328›Full record

ArticleInfection and immunity2010

A novel functional variant in the stem cell growth factor promoter protects against severe malarial anemia.

Collins Ouma, Christopher C Keller, Gregory C Davenport, Tom Were, Stephen Konah, Michael F Otieno, James B Hittner, John M Vulule, Jeremy Martinson, John M Ong'echa and 2 more

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Loss of Parathyroid Hormone Receptor Signaling in Osteoprogenitors Is Associated With Accumulation of Multiple Hematopoietic Lineages in the Bone Marrow.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Severe malarial anemia: innate immunity and pathogenesis.International journal of biological sciences · 2011
    Review
  17. Article
  18. 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

12 authors at 6 institutions in 3 countries.

Collins OumaUniversity of New Mexico/KEMRI Laboratories of Parasitic and Viral Diseases, Centre for Global Health Research, Kenya Medical Research Institute, Kisumu, Kenya.
Christopher C Keller
Gregory C Davenport
Tom Were
Stephen Konah
Michael F Otieno
James B Hittner
John M Vulule
Jeremy Martinson
John M Ong'echa
Robert E Ferrell
Douglas J Perkins
Kenya Medical Research Institute · KEMaseno University · KEUniversity of New Mexico · USUniversity of Pittsburgh · USCollege of Charleston · USKenyatta University · KE

Funding

TRAINING AND RESEARCH ON SEVERE MALARIAL ANEMIAD43TW005884 · FIC · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Collins Ouma, Douglas Jay Perkins · 2002 to 2026
$5.2M
Biology of Infectious Diseases &InflammationT32AI007538 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Michelle A Ozbun · 1998 to 2026
$5.2M
GENETIC BASIS OF SEVERE MALARIAL ANEMIAR01AI051305 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI PERKINS, DOUGLAS JAY · 2002 to 2011
$4.7M
FIC NIH HHS D43 TW005884FIC NIH HHS TW05884-02NIAID NIH HHS AI51305-02NIAID NIH HHS R01 AI051305NIAID NIH HHS T32 AI007538
6 · The paper itself

Abstract

Plasmodium falciparum malaria is a leading global cause of infectious disease burden. In areas in which P. falciparum transmission is holoendemic, such as western Kenya, severe malarial anemia (SMA) results in high rates of pediatric morbidity and mortality. Although the pathophysiological basis of SMA is multifactorial, we recently discovered that suppression of unexplored hematopoietic growth factors that promote erythroid and myeloid colony development, such as stem cell growth factor (SCGF) (C-type lectin domain family member 11A [CLEC11A]), was associated with enhanced development of SMA and reduced erythropoietic responses. To extend these investigations, the relationships between a novel SCGF promoter variant (-539C/T, rs7246355), SMA (hemoglobin [Hb] < 6.0 g/dl), and reduced erythropoietic responses (reticulocyte production index [RPI], <2.0) were investigated with Kenyan children (n = 486) with falciparum malaria from western Kenya. Circulating SCGF was positively correlated with hemoglobin levels (r = 0.251; P = 0.022) and the reticulocyte production index (RPI) (r = 0.268; P = 0.025). Children with SMA also had lower SCGF levels than those in the non-SMA group (P = 0.005). Multivariate logistic regression analyses controlling for covariates demonstrated that individuals with the homologous T allele were protected against SMA (odds ratio, 0.57; 95% confidence interval [95% CI] 0.34 to 0.94; P = 0.027) relative to CC (wild-type) carriers. Carriers of the TT genotype also had higher SCGF levels in circulation (P = 0.018) and in peripheral blood mononuclear cell culture supernatants (P = 0.041), as well as an elevated RPI (P = 0.005) relative to individuals with the CC genotype. The results presented here demonstrate that homozygous T at -539 in the SCGF promoter is associated with elevated SCGF production, enhanced erythropoiesis, and protection against the development of SMA in children with falciparum malaria.

Indexed as

AnemiaChild, PreschoolFemaleGene Expression RegulationGenetic VariationGenotypeHematopoietic Cell Growth FactorsHumansInfantLectins, C-TypeMalaria, FalciparumMalePromoter Regions, GeneticCLEC11A protein, humanHematopoietic Cell Growth FactorsLectins, C-Type

Identifiers

PMID19884328
PMCPMC2798205
OpenAlexW2153694545

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.