Evidence map›Paper›PMID 25266949›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2014

Correlation of PCSK9 gene polymorphism with cerebral ischemic stroke in Xinjiang Han and Uygur populations.

Dengfeng Han, Jianhua Ma, Xiaoning Zhang, Jian Cai, Jinlan Li, Tuerhong Tuerxun, Chenguang Hao, Lei Du, Jing Lei

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 4 pooled it
3.8field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 4 syntheses or guidelines pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  12. Impact of Tag Single Nucleotide Polymorphisms (SNPs) in CCL11 Gene on Risk of Subtypes of Ischemic Stroke in Xinjiang Han Populations.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  13. Article
  14. Review
  15. Article
  16. Angiotensinogen polymorphism and ischemic stroke risk.International journal of clinical and experimental medicine · 2015
    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

9 authors at 1 institution in 1 country.

Dengfeng HanDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
Jianhua MaDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
Xiaoning ZhangDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
Jian CaiDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
Jinlan LiDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
Tuerhong TuerxunDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
Chenguang HaoDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
Lei DuDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
Jing LeiDepartment of Neurology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China (mainland).
First Affiliated Hospital of Xinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebral ischemic stroke (CIS) is a major cause of morbidity and mortality. Its main pathological basis is atherosclerosis (AS); in turn, the main risk factor in AS is dyslipidemia. Human proprotein convertase subtilisin/kexin9 (PCSK9) plays a key role in regulating plasma low-density lipoprotein (LDL) cholesterol levels. We sought to assess the association between PCSK9 and CIS in Chinese Han and Uygur populations. MATERIAL AND

methodsWe selected 408 CIS patients and 348 control subjects and used a single-base terminal extension (SNaPshot) method to detect the genotypes of the 20 single-nucleotide polymorphisms (SNPs) in PCSK9.

resultsDistribution of SNP8 (rs529787) genotypes showed a significant difference between CIS and control participants (P=0.049). However, when analyzing Han and Uygur populations separately, we found that only Han subjects showed distribution of SNP1 (rs1711503), SNP2 (rs2479408), and SNP8 (rs529787) alleles that was significantly different between CIS and control participants (P=0.028, P=0.013, P=0.006, respectively), and distribution of SNP2 (rs2479408) in the dominant model (CC vs. CG + GG) was significantly different between CIS and control participants (P=0.013), even after adjustment for covariates (OR: 75.262, 95% confidence interval [CI]: 7.232-783.278, P<0.001). Distribution of the 2 haplotypes (A-C and G-C) (rs1711503 and rs2479408) was significantly different between CIS and control participants (both, P=0.011).

conclusionsBoth rs1711503 and rs2479408 of PCSK9 genes were associated with CIS in the Han population of China. A-C haplotype may be a genetic marker of CIS risk in this population.

Indexed as

Genetic Predisposition to DiseaseAllelesBrain IschemiaCase-Control StudiesEthnicityFemaleGene FrequencyHaplotypesHumansLinkage DisequilibriumLogistic ModelsMaleMiddle AgedPolymorphism, Single NucleotideProprotein Convertase 9Proprotein ConvertasesPCSK9 protein, humanProprotein Convertase 9Proprotein ConvertasesSerine Endopeptidases

Identifiers

PMID25266949
PMCPMC4189717
OpenAlexW2153820013

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.