Evidence map›Paper›PMID 28955196›Full record

ArticleFrontiers in neuroscience2017

Minocycline-Suppression of Early Peripheral Inflammation Reduces Hypoxia-Induced Neonatal Brain Injury.

Yingjun Min, Hongchun Li, Kaiyu Xu, Yilong Huang, Jie Xiao, Weizhou Wang, Longjun Li, Ting Yang, Lixuan Huang, Ling Yang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

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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

16 authors at 2 institutions in 1 country.

Yingjun MinDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Hongchun LiDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Kaiyu XuDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Yilong HuangDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Jie XiaoDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Weizhou WangDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Longjun LiDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Ting YangDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Lixuan HuangDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Ling YangDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Hong JiangDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Qian WangDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Min ZhaoDepartment of Human Anatomy and Histoembryology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
HaiRong HuaDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Rong MeiDepartment of Neurology, Yunnan First People's HospitalKunming, China.
Fan LiDepartment of Pathology and Pathophysiology, School of Basic Medical Science, Kunming Medical UniversityKunming, China.
Kunming Medical University · CNFirst People's Hospital of Yunnan Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While extensive studies report that neonatal hypoxia-ischemia (HI) induces long-term cognitive impairment via inflammatory responses in the brain, little is known about the role of early peripheral inflammation response in HI injury. Here we used a neonatal hypoxia rodent model by subjecting postnatal day 0 (P0d) rat pups to systemic hypoxia (3.5 h), a condition that is commonly seen in clinic neonates, Then, an initial dose of minocycline (45 mg/kg) was injected intraperitoneally (i.p.) 2 h after the hypoxia exposure ended, followed by half dosage (22.5 mg/kg) minocycline treatment for next 6 consecutive days daily. Saline was injected as vehicle control. To examine how early peripheral inflammation responded to hypoxia and whether this peripheral inflammation response was associated to cognitive deficits. We found that neonatal hypoxia significantly increased leukocytes not only in blood, but also increased the monocytes in central nervous system (CNS), indicated by presence of C-C chemokine receptor type 2 (CCR2

Indexed as

hypomyelinationinflammationleukocyteminocyclineneonatal hypoxia

Identifiers

PMID28955196
PMCPMC5600962
OpenAlexW2755138422

What OpenQuestion holds

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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.