Evidence map›Paper›PMID 18679166›Full record

ArticlePediatric research2008

Sulfonylurea receptor 1 in the germinal matrix of premature infants.

J Marc Simard, Rudolph J Castellani, Svetlana Ivanova, Michael T Koltz, Volodymyr Gerzanich

Open access · bronzeAbstract read
In one paragraph

Article in Pediatric research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Sulfonylurea Receptor 1 in Central Nervous System Injury: An Updated Review.International journal of molecular sciences · 2021
    Review
  3. Review
  4. Article
  5. Glibenclamide for the treatment of acute CNS injury.Pharmaceuticals (Basel, Switzerland) · 2013
    Article
  6. Sulfonylurea receptor 1 expression in human cerebral infarcts.Journal of neuropathology and experimental neurology · 2013
    Article
  7. Article
  8. Sulfonylurea receptor 1 in central nervous system injury: a focused review.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012
    Review
  9. Article
  10. 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

5 authors at 1 institution in 1 country.

J Marc SimardDepartment of Neurosurgery, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. msimard@smail.umaryland.edu
Rudolph J Castellani
Svetlana Ivanova
Michael T Koltz
Volodymyr Gerzanich
University of Maryland, Baltimore · US

Funding

Sulfonylurea receptor 1 (SUR1)- A novel therapeutic target in ischemic strokeR01HL082517 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2006 to 2021
$5.6M
Reactive astrocytes from gliotic capsuleR01NS048260 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SIMARD, J. MARC · 2004 to 2007
$1.1M
NHLBI NIH HHS HL082517NHLBI NIH HHS R01 HL082517NINDS NIH HHS NS048260NINDS NIH HHS R01 NS048260
6 · The paper itself

Abstract

Germinal matrix (GM) hemorrhage (GMH) is a major cause of mortality and of life-long morbidity from cerebral palsy. GMH is typically preceded by hypoxic/ischemic events and is believed to arise from rupture of weakened veins in the GM. In the CNS, hypoxia/ischemia up-regulate sulfonylurea receptor 1 (SUR1)-regulated NCCa-ATP channels in microvascular endothelium, with channel activation by depletion of ATP being responsible for progressive secondary hemorrhage. We hypothesized that this channel might be up-regulated in the GM of preterm infants at risk for GMH. Here, we studied expression of the regulatory subunit of the channel, SUR1, and its transcriptional antecedent, hypoxia inducible factor 1 (HIF1), in postmortem tissues of premature infants who either were at risk for or who sustained GMH. We found regionally specific up-regulation of HIF1 and of SUR1 protein and mRNA in GM tissues, compared with remote cortical tissues. Up-regulation was prominent in most progenitor cells, whereas in veins, SUR1 was found predominantly in infants who had sustained GMH compared with those without hemorrhage. Our data suggest that the SUR1-regulated NCCa-ATP channel may be associated with GMH, and that pharmacological block of these channels could potentially reduce the incidence of this devastating complication of prematurity.

Indexed as

Infant, PrematureAnimalsATP-Binding Cassette TransportersBrainCerebral HemorrhageCerebral PalsyHumansHypoxia-Inducible Factor 1Infant, NewbornPotassium Channels, Inwardly RectifyingPremature BirthReceptors, DrugSulfonylurea ReceptorsABCC8 protein, humanATP-Binding Cassette TransportersHypoxia-Inducible Factor 1Potassium Channels, Inwardly RectifyingReceptors, DrugSulfonylurea Receptors

Identifiers

PMID18679166
PMCPMC2647511
OpenAlexW2043178444

What OpenQuestion holds

Textmetadata
LicenceTDM
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.