Evidence map›Paper›PMID 36459202›Full record

ReviewPathologie (Heidelberg, Germany)2023

[Neuropathology I: muscular diseases].

Anne Schänzer, Carsten Dittmayer, Stefan Porubsky, Joachim Weis, Hans-Hilmar Goebel, Werner Stenzel

Abstract readEnglish AbstractReview
In one paragraph

Review in Pathologie (Heidelberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Anne SchänzerInstitut für Neuropathologie, Justus-Liebig-Universität Gießen, Arndstr. 16, 35392, Gießen, Deutschland. anne.schaenzer@patho.med.uni-giessen.de.
Carsten DittmayerInstitut für Neuropathologie, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin und Humboldt-Universität zu Berlin, 10117, Berlin, Deutschland.
Stefan PorubskyInstitut für Pathologie, JGU Universitätsmedizin Mainz, 55131, Mainz, Deutschland.
Joachim WeisInstitut für Neuropathologie, Universitätsklinikum der RWTH Aachen, 52074, Aachen, Deutschland.
Hans-Hilmar GoebelInstitut für Neuropathologie, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin und Humboldt-Universität zu Berlin, 10117, Berlin, Deutschland.
Werner StenzelInstitut für Neuropathologie, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin und Humboldt-Universität zu Berlin, 10117, Berlin, Deutschland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle diseases include hereditary and acquired diseases with clinical manifestation in both childhood and adulthood. The different muscle diseases may have ultrastructural alterations that help us further understand the pathology of the disease. Specific changes in sarcomere structure help to classify a congenital myopathy. The detection of cellular aggregates supports the classification of myositis. Pathologically altered mitochondria, on the other hand, can occur both in genetic mitochondriopathies but also secondarily in acquired muscle diseases like myositis. Ultrastructural analysis of the myocardium is also helpful in the diagnosis of hereditary cardiomyopathies in childhood. This review article highlights the ultrastructural features of different muscle diseases and pathognomonic findings in specific disease groups.

Indexed as

Muscular DiseasesMyositisHumansMyocardiumSarcomeresCardiomyopathyElectron microscopyMitochondriaMyositisVacuoles

Identifiers

PMID36459202
PMCPMC9984347

What OpenQuestion holds

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LicenceCC BY
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.