Evidence map›Paper›PMID 26622506›Full record

ArticleExperimental and therapeutic medicine2015

Subclavian steal syndrome decreases neurogenesis in the cerebellar cortex and affects cognitive function in rabbits.

Xiao-Yang Fu, Zhi-Dong Zhang, Kai Liang, Shuai-Tao Shi, Guo-Quan Wang, Ke-Wei Zhang, Kun Li, Wei-Xiao Li, Tian-Xiao Li, Shui-Ting Zhai

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 38% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 2 citations in OpenAlex.

  1. Pooled it
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

10 authors at 1 institution in 1 country.

Xiao-Yang FuDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Zhi-Dong ZhangDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Kai LiangDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Shuai-Tao ShiDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Guo-Quan WangDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Ke-Wei ZhangDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Kun LiDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Wei-Xiao LiDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Tian-Xiao LiDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Shui-Ting ZhaiDepartment of Vascular and Endovascular Surgery, Henan Provincial Hospital, Zhengzhou, Henan 450003, P.R. China ; Department of Vascular and Endovascular Surgery, The Affiliated People's Hospital, Zhengzhou University Medical School, Zhengzhou, Henan 450003, P.R. China.
Henan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subclavian steal syndrome (SSS) is a condition characterized by a steno-occlusive impairment of the proximal subclavian artery. The majority of patients with SSS are asymptomatic, while symptomatic patients present with neurological symptoms. SSS is a risk factor for cerebral ischemia, which reacts badly upon cognitive function; however, it remains unknown whether SSS is able to cause progressive cognitive impairment. In the present study, the potential effects of SSS on cognitive function were investigated using atherosclerotic rabbits as a model of SSS. A total of 48 male New Zealand rabbits were divided into the control, sham and SSS groups. The results of eyeblink experiments indicated no significant differences among the three groups; however, SSS did appear to exert a negative impact on neurogenesis in the cerebellar cortex. In order to further clarify the mechanisms underlying this SSS-mediated reduction in cell proliferation, the energy metabolism, immune function and oxidative stress statuses were evaluated by determining the levels of adenosine triphosphate (ATP), adenosine, interleukin (IL)-1β, IL-6, malondialdehyde, 8-hydroxy-2'-deoxyguanosine, CuZn-superoxide dismutase and catalase. The results showed that the levels of extracellular ATP in the cerebellar cortex had decreased, while levels of adenosine had also decreased. These findings suggest that SSS is able to inhibit neurogenesis in the cerebellar cortex by decreasing the extracellular ATP levels. Furthermore, these changes may result in an impairment of the cognition of the rabbits. The early diagnosis and treatment of SSS may, therefore, prevent or mitigate cognitive impairment in the future.

Indexed as

adenosine triphosphatecerebellar cortexcognitionneurogenesissubclavian steal syndrome

Identifiers

PMID26622506
PMCPMC4578009
OpenAlexW2143434545

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.