Evidence map›Paper›PMID 14747332›Full record

ArticleBiophysical journal2004

Calcium buffering and excitation-contraction coupling in developing avian myocardium.

Tony L Creazzo, Jarrett Burch, Robert E Godt

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Avian cardiomyocyte architecture and what it reveals about the evolution of the vertebrate heart.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Review
  3. Review
  4. Article
  5. Article
  6. Article
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  8. Article
  9. Article
  10. Article
  11. Utilizing comparative models in biomedical research.Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology
    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

3 authors at 2 institutions in 1 country.

Tony L CreazzoNeonatal/Perinatal Research Institute, Department of Pediatrics/Neonatology Division, Duke University Medical Center, Durham, North Carolina 27710, USA. tcreazzo@duke.edu
Jarrett Burch
Robert E Godt
Duke University Hospital · USAugusta University · US

Funding

REGULATION AND FUNCTION OF THE OUTFLOW SEPTATION COMPLEXP01HL036059 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI KIRBY, MARGARET LOEWY · 1986 to 2004
$8.1M
Mechanisms of Auto-Rhythmicity in Heart DevelopmentR01HL071015 · NHLBI · DUKE UNIVERSITY · PI KIRBY, MARGARET LOEWY · 2002 to 2005
$1.5M
DEVELOPMENT OF CARDIAC EXCITATION/CONTRACTION COUPLINGR01HL058861 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI CREAZZO, TONY L · 1999 to 2002
$852k
NHLBI NIH HHS HL36059NHLBI NIH HHS HL58861NHLBI NIH HHS HL71015NHLBI NIH HHS P01 HL036059NHLBI NIH HHS R01 HL071015
6 · The paper itself

Abstract

This report provides a detailed analysis of developmental changes in cytoplasmic free calcium (Ca(2+)) buffering and excitation-contraction coupling in embryonic chick ventricular myocytes. The peak magnitude of field-stimulated Ca(2+) transients declined by 41% between embryonic day (ED) 5 and 15, with most of the decline occurring between ED5 and 11. This was due primarily to a decrease in Ca(2+) currents. Sarcoplasmic reticulum (SR) Ca(2+) content increased 14-fold from ED5 to 15. Ca(2+) transients in voltage-clamped myocytes after blockade of SR function permitted computation of the fast Ca buffer power of the cytosol as expressed as generalized values of B(max) and K(D). B(max) rose with development whereas K(D) did not change significantly. The computed SR Ca(2+) contribution to the Ca(2+) transient and gain factor for Ca(2+)-induced Ca(2+) release increased markedly between ED5 and 11 and slightly thereafter. These results paralleled the maturation of SR and peripheral couplings reported by others and demonstrated a strong relationship between structure and function in development of excitation-contraction coupling. Modeling of buffer power from estimates of the major cytosolic Ca binding moieties yielded a B(max) and K(D) in reasonable agreement with experiment. From ED5 to 15, troponin C was the major Ca(2+) binding moiety, followed by SR and calmodulin.

Indexed as

Ventricular FunctionAgingAnimalsBuffersCalciumCalcium SignalingCells, CulturedChick EmbryoChickensElectric StimulationHeart VentriclesMembrane PotentialsMyocardial ContractionMyocytes, CardiacSarcoplasmic ReticulumBuffersCalcium

Identifiers

PMID14747332
PMCPMC1303944
OpenAlexW2055521852

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.