Evidence map›Paper›PMID 8455588›Full record

ReviewMolecular and cellular biochemistry1993

Cardiac contractile proteins and autoimmune myocarditis.

T Izumi, H Hanawa, M Saeki, M Kodama

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular and cellular biochemistry, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Myosin-induced autoimmune myocarditis in BALB/C mice.Journal of Tongji Medical University = Tong ji yi ke da xue xue bao · 1999
    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

4 authors at 1 institution in 1 country.

T IzumiFirst Department of Internal Medicine, Niigata University School of Medicine, Japan.
H Hanawa
M Saeki
M Kodama
Niigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Concerning cardiac contractile proteins, antigenicity and myocardiotogenicity were discussed. In normal states, these proteins are immunologically tolerant, and can not provoke any heart-specific disease. Why the proteins can provoke such lethal autoimmune myocarditis has not been completely elucidated. Shortly after cardiac infection or myocardial ischemia, these proteins may work as the antigen for the autoimmune myocarditis. First of all, the role of cardiac myosin has been strongly emphasized. But, the antigen determinants: epitope proteins remain unclear. Either cross-activity to the streptococcal M protein and/or the alpha-helical coiled-coil protein may be an important factor to determine antigenicity. In this autoimmune myocarditis, the roles of T-lymphocyte and cardiac dendritic cell are noticeable. Through further study on the relation between antigen epitope and the infectious agents in the heart; on cardio-cytotoxicity of the T-lymphocyte and on the precise contribution of cardiac dendritic cells, this autoimmune myocarditis will be more clarified.

Indexed as

Antigens, BacterialBacterial Outer Membrane ProteinsCarrier ProteinsActinsAnimalsAutoimmune DiseasesBacterial ProteinsCross ReactionsDendritic CellsHumansMyocardial IschemiaMyocarditisMyosinsT-LymphocytesActinsAntigens, BacterialBacterial Outer Membrane ProteinsBacterial ProteinsCarrier ProteinsMyosinsstreptococcal M protein

Identifiers

PMID8455588
OpenAlexW1980188752

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.