Evidence map›Paper›PMID 28706458›Full record

ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2017

Electrophysiological characteristics of R47W and A298T mutations in CLC-1 of myotonia congenita patients and evaluation of clinical features.

Hyung Jin Chin, Chan Hyeong Kim, Kotdaji Ha, Jin Hong Shin, Dae-Seong Kim, Insuk So

Abstract read
In one paragraph

Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

6 authors.

Hyung Jin ChinDepartment of Physiology, Seoul National University College of Medicine, Seoul 03080, Korea.
Chan Hyeong KimDepartment of Physiology, Seoul National University College of Medicine, Seoul 03080, Korea.
Kotdaji HaDepartment of Physiology, Seoul National University College of Medicine, Seoul 03080, Korea.
Jin Hong ShinDepartment of Neurology, Research Institute for Convergence of Biomedical Research and Technology, Pusan University Yangsan Hospital, Yangsan 50612, Korea.
Dae-Seong KimDepartment of Neurology, Research Institute for Convergence of Biomedical Research and Technology, Pusan University Yangsan Hospital, Yangsan 50612, Korea.
Insuk SoDepartment of Physiology, Seoul National University College of Medicine, Seoul 03080, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myotonia congenita (MC) is a genetic disease that displays impaired relaxation of skeletal muscle and muscle hypertrophy. This disease is mainly caused by mutations of

Indexed as

CLCN1Clinical featuresElectrophysiologyMutationMyotonia CongenitaVoltage gated chloride channel CLC-1

Identifiers

PMID28706458
PMCPMC5507783

What OpenQuestion holds

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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.