Evidence map›Paper›PMID 31635789›Full record

ArticleBiophysical journal2019

Multiscale Modeling of Dyadic Structure-Function Relation in Ventricular Cardiac Myocytes.

Filippo G Cosi, Wolfgang Giese, Wilhelm Neubert, Stefan Luther, Nagaiah Chamakuri, Ulrich Parlitz, Martin Falcke

Open access · hybridAbstract read
In one paragraph

Article in Biophysical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Three-Dimensional Model of Sub-Plasmalemmal CaFrontiers in immunology · 2021
    Article
  6. Article
  7. The Heart by Numbers.Biophysical journal · 2019
    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

7 authors at 3 institutions in 1 country.

Filippo G CosiMax Planck Institute for Dynamics and Self-Organization, Göttingen, Germany; Georg-August-Universität Göttingen, Institute for the Dynamics of Complex Systems, Göttingen, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Göttingen, Göttingen, Germany.
Wolfgang GieseMax Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Wilhelm NeubertMax Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Stefan LutherMax Planck Institute for Dynamics and Self-Organization, Göttingen, Germany; Georg-August-Universität Göttingen, Institute for the Dynamics of Complex Systems, Göttingen, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Göttingen, Göttingen, Germany.
Nagaiah ChamakuriInstitute of Applied Mathematics, University of Hohenheim, Stuttgart, Germany.
Ulrich ParlitzMax Planck Institute for Dynamics and Self-Organization, Göttingen, Germany; Georg-August-Universität Göttingen, Institute for the Dynamics of Complex Systems, Göttingen, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Göttingen, Göttingen, Germany.
Martin FalckeMax Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Berlin, Berlin, Germany; Department of Physics, Humboldt University Berlin, Germany. Electronic address: martin.falcke@mdc-berlin.de.
Max Delbrück Center · DEMax Planck Institute for Dynamics and Self-Organization · DEUniversity of Hohenheim · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease is often related to defects of subcellular components in cardiac myocytes, specifically in the dyadic cleft, which include changes in cleft geometry and channel placement. Modeling of these pathological changes requires both spatially resolved cleft as well as whole cell level descriptions. We use a multiscale model to create dyadic structure-function relationships to explore the impact of molecular changes on whole cell electrophysiology and calcium cycling. This multiscale model incorporates stochastic simulation of individual L-type calcium channels and ryanodine receptor channels, spatially detailed concentration dynamics in dyadic clefts, rabbit membrane potential dynamics, and a system of partial differential equations for myoplasmic and lumenal free Ca

Indexed as

Models, CardiovascularAction PotentialsHeart VentriclesMyocytes, CardiacRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumRyanodine Receptor Calcium Release Channel

Identifiers

PMID31635789
PMCPMC6990380
OpenAlexW2976642807

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.