Evidence map›Paper›PMID 25206614›Full record

ArticleNeural regeneration research2013

Acute high-altitude hypoxic brain injury: Identification of ten differential proteins.

Jianyu Li, Yuting Qi, Hui Liu, Ying Cui, Li Zhang, Haiying Gong, Yaxiao Li, Lingzhi Li, Yongliang Zhang

Open access · greenAbstract read
In one paragraph

Article in Neural regeneration research, 2013. 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
0.5field-weighted citation impact, top 30% 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, 24 citations in OpenAlex.

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  11. Protective Effect ofOxidative medicine and cellular longevity · 2022
    Article
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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

9 authors at 3 institutions in 1 country.

Jianyu LiDepartment of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China.
Yuting QiDepartment of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China.
Hui LiuDepartment of Hepatobiliary, Tianjin Third Central Hospital, Tianjin 300170, China.
Ying CuiDepartment of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China ; Tianjin Key Laboratory of Occupational and Environmental Hazards Biomarkers, Tianjin 300162, China.
Li ZhangTianjin Key Laboratory of Occupational and Environmental Hazards Biomarkers, Tianjin 300162, China.
Haiying GongDepartment of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China.
Yaxiao LiDepartment of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China.
Lingzhi LiDepartment of Pharmaceutical Chemistry, Logistics College of Chinese People's Armed Police Forces, Tianjin 300162, China ; Tianjin Key Laboratory of Occupational and Environmental Hazards Biomarkers, Tianjin 300162, China.
Yongliang ZhangTianjin Key Laboratory of Occupational and Environmental Hazards Biomarkers, Tianjin 300162, China.
Logistics University of People's Armed Police Force · CNTianjin University · CNTianjin Third Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypobaric hypoxia can cause severe brain damage and mitochondrial dysfunction, and is involved in hypoxic brain injury. However, little is currently known about the mechanisms responsible for mitochondrial dysfunction in hypobaric hypoxic brain damage. In this study, a rat model of hypobaric hypoxic brain injury was established to investigate the molecular mechanisms associated with mitochondrial dysfunction. As revealed by two-dimensional electrophoresis analysis, 16, 21, and 36 differential protein spots in cerebral mitochondria were observed at 6, 12, and 24 hours post-hypobaric hypoxia, respectively. Furthermore, ten protein spots selected from each hypobaric hypoxia subgroup were similarly regulated and were identified by mass spectrometry. These detected proteins included dihydropyrimidinase-related protein 2, creatine kinase B-type, isovaleryl-CoA dehydrogenase, elongation factor Ts, ATP synthase beta-subunit, 3-mercaptopyruvate sulfurtransferase, electron transfer flavoprotein alpha-subunit, Chain A of 2-enoyl-CoA hydratase, NADH dehydrogenase iron-sulfur protein 8 and tropomyosin beta chain. These ten proteins are all involved in the electron transport chain and the function of ATP synthase. Our findings indicate that hypobaric hypoxia can induce the differential expression of several cerebral mitochondrial proteins, which are involved in the regulation of mitochondrial energy production.

Indexed as

brain injurycerebral edemacognitive functiondifferential expressionelectron transport chainenergy metabolismgrants-supported paperhypobaric hypoxiamitochondrianeural regenerationneuroregenerationproteomics

Identifiers

PMID25206614
PMCPMC4146176
OpenAlexW1520332021

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.