Evidence map›Paper›PMID 19528216›Full record

ArticleInfection and immunity2009

Suppression of a novel hematopoietic mediator in children with severe malarial anemia.

Christopher C Keller, Collins Ouma, Yamo Ouma, Gordon A Awandare, Gregory C Davenport, Tom Were, James B Hittner, John M Vulule, John M Ong'echa, Douglas J Perkins

Abstract read
In one paragraph

Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. 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
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Severe malarial anemia: innate immunity and pathogenesis.International journal of biological sciences · 2011
    Review
  12. Article
  13. 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

10 authors at 5 institutions in 3 countries.

Christopher C KellerDepartment of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, USA.
Collins Ouma
Yamo Ouma
Gordon A Awandare
Gregory C Davenport
Tom Were
James B Hittner
John M Vulule
John M Ong'echa
Douglas J Perkins
Kenya Medical Research Institute · KEUniversity of Pittsburgh · USCollege of Charleston · USUniversity of Ghana · GHUniversity of New Mexico · US

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 TW05884-07NIAID NIH HHS AI51305-07NIAID NIH HHS R01 AI051305NIAID NIH HHS T32 AI007538
6 · The paper itself

Abstract

In areas of holoendemic Plasmodium falciparum transmission, severe malarial anemia (SMA) is a leading cause of pediatric morbidity and mortality. Although many soluble mediators regulate erythropoiesis, it is unclear how these factors contribute to development of SMA. Investigation of novel genes dysregulated in response to malarial pigment (hemozoin [PfHz]) revealed that stem cell growth factor (SCGF; also called C-type lectin domain family member 11A [CLEC11A]), a hematopoietic growth factor important for development of erythroid and myeloid progenitors, was one of the most differentially expressed genes. Additional experiments with cultured peripheral blood mononuclear cells (PBMCs) demonstrated that PfHz decreased SCGF/CLEC11A transcriptional expression in a time-dependent manner. Circulating SCGF levels were then determined for Kenyan children (n = 90; aged 3 to 36 months) presenting at a rural hospital with various severities of malarial anemia. SCGF levels in circulation (P = 0.001) and in cultured PBMCs (P = 0.004) were suppressed in children with SMA. Circulating SCGF also correlated positively with hemoglobin levels (r = 0.241; P = 0.022) and the reticulocyte production index (RPI) (r = 0.280; P = 0.029). In addition, SCGF was decreased in children with reduced erythropoiesis (RPI of <2) (P < 0.001) and in children with elevated levels of naturally acquired monocytic PfHz (P = 0.019). Thus, phagocytosis of PfHz promotes a decrease in SCGF gene products, which may contribute to reduced erythropoiesis in children with SMA.

Indexed as

AnemiaChild, PreschoolErythropoiesisFemaleGene Expression ProfilingGene Expression RegulationHematopoietic Cell Growth FactorsHemeproteinsHumansInfantLectins, C-TypeMalariaMalePhagocytosisReticulocytesCLEC11A protein, humanHematopoietic Cell Growth FactorsHemeproteinshemozoinLectins, C-Type

Identifiers

PMID19528216
PMCPMC2737985
OpenAlexW2146324035

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.