Evidence map›Paper›PMID 32155129›Full record

ArticleAging2020

Transient ischemia-reperfusion induces cortical hyperactivity and AMPAR trafficking in the somatosensory cortex.

Yuanyuan Li, Ran Ding, Feifei Wang, Cuiping Guo, Aili Liu, Liangpeng Wei, Shiyang Yuan, Feng Chen, Shaowei Hou, Zengguang Ma and 4 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. GluA1 Degradation by Autophagy Contributes to Circadian Rhythm Effects on Cerebral Ischemia Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  2. Review
  3. 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

14 authors at 5 institutions in 2 countries.

Yuanyuan LiSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Ran DingChinese Institute for Brain Research, Beijing (CIBR), Beijing, China.
Feifei WangSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Cuiping GuoDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Aili LiuSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Liangpeng WeiSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Shiyang YuanSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Feng ChenSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Shaowei HouSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Zengguang MaSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Yan ZhangTianjin Key Laboratory of Retinal Function and Diseases, Tianjin Medical University Eye Hospital, Eye Institute and School of Optometry and Ophthalmology, Tianjin Medical University, Tianjin, China.
Robert H CudmoreDepartment of Physiology and Membrane Biology, University of California Davis School of Medicine, Sacramento, CA 95817, USA.
Xiaochuan WangDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hui ShenSchool of Biomedical Engineering, Tianjin Medical University, Tianjin, China.
Tianjin Medical University · CNChinese Institute for Brain Research · CNHuazhong University of Science and Technology · CNNantong University · CNUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain ischemia results from cardiac arrest, stroke or head trauma. The structural basis of rescuing the synaptic impairment and cortical dysfunctions induced in the stage of ischemic-reperfusion can occur if therapeutic interventions are applied in time, but the functional basis for this resilience remains elusive. Here, we explore the changes in cortical activity and a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) GluA1 subunit in spine (sGluA1) after transient ischemia-reperfusion

Indexed as

AnimalsCalcium SignalingDendritic SpinesMiceNeuronsProtein TransportReceptors, AMPAReperfusion InjurySomatosensory CortexReceptors, AMPAAMPA receptorCa transients 2+dendritic spinesomatosensory cortextransient ischemia-reperfusion

Identifiers

PMID32155129
PMCPMC7093173
OpenAlexW3011475350

What OpenQuestion holds

Textmetadata
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.