Evidence map›Paper›PMID 26191130›Full record

ArticleInternational journal of clinical and experimental pathology2015

Calcium signaling is implicated in the diffuse axonal injury of brain stem.

Jiao Mu, Yucheng Song, Ji Zhang, Wei Lin, Hongmei Dong

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Multiscale Mechanobiology in Brain Physiology and Diseases.Frontiers in cell and developmental biology · 2022
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Myelin Damage in Diffuse Axonal Injury.Frontiers in neuroscience · 2019
    Article
  12. Diffuse Axonal Injury and Oxidative Stress: A Comprehensive Review.International journal of molecular sciences · 2017
    Review
  13. Article
  14. Article
  15. 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

5 authors at 2 institutions in 1 country.

Jiao MuDepartment of Forensic Medicine, Huazhong University of Science and Technology, Tongji Medical College No. 13 Hangkong Lu, Hankou, Wuhan 430030, Hubei, PR China ; Department of Pathology, Hebei North University No. 11 Zuanshinan Lu, Zhangjiakou 075000, Hebei, PR China.
Yucheng SongCriminal Investigation Brigade of Taicang No. 128 Loujiangbei Lu, Taicang, Suzhou 215400, Jiangsu, PR China.
Ji ZhangDepartment of Forensic Medicine, Huazhong University of Science and Technology, Tongji Medical College No. 13 Hangkong Lu, Hankou, Wuhan 430030, Hubei, PR China.
Wei LinDepartment of Forensic Medicine, Huazhong University of Science and Technology, Tongji Medical College No. 13 Hangkong Lu, Hankou, Wuhan 430030, Hubei, PR China.
Hongmei DongDepartment of Forensic Medicine, Huazhong University of Science and Technology, Tongji Medical College No. 13 Hangkong Lu, Hankou, Wuhan 430030, Hubei, PR China.
Huazhong University of Science and Technology · CNTaizhou Fourth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evaluating diffuse axonal injury (DAI) remains challenging in clinical sciences since the physiopathologic mechanism of DAI is still unclear. The calcium overload in the axoplasm is considered to be crucial for secondary axonal injury. The present study use calcium channel blocker, nimodipine, to explore the influence of Ca2+ in the pathogenesis of rat DAI. In the DAI group, the expressions of β-APP and NF-L in axons were increased from 12 to 72 h. The ultrastructural observation indicated the axon and vessel injury appeared at 12 h post-injury and severely aggravated from 24 to 72 h. The expression of vWF and brain water content was increased at 12 h after injury and further increased at 24 h. Nimodipine decreased the expression of β-APP, NF-L and vWF, and also attenuated the ultrastructural damage of vascular wall and axons. Furthermore, Ca-dependent enzyme, the calcineurin activity were increased in DAI and nimodipine suppressed the activity of calcineurins (CaN). However, the amount of CaN expression was not changed. Our results showed that disturbances of axonal calcium homeostasis play an important role in the secondary damage of the axon, neuron and capillary vessel which may be related with activating CaN during the acute phase of DAI. Nimodipine can alleviate the secondary damage by suppressing the calcineurin activity.

Indexed as

AnimalsAxonsBlotting, WesternBrain StemCalcium SignalingDiffuse Axonal InjuryDisease Models, AnimalImmunohistochemistryMicroscopy, Electron, TransmissionRatsRats, Sprague-Dawleyanimal studycalcium signalDiffuse axonal injurynimodipine

Identifiers

PMID26191130
PMCPMC4503002
OpenAlexW2418096847

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.