Evidence map›Paper›PMID 24519436›Full record

SynthesisMolecular biology reports2014

CD14 -159C/T polymorphism contributes to the susceptibility to tuberculosis: evidence from pooled 1,700 cases and 1,816 controls.

Ruifen Miao, Haibo Ge, Lin Xu, Fei Xu

Abstract readMeta-Analysis
PubMed Publisher
In one paragraph

Synthesis in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Association betweenInternational journal of clinical and experimental pathology · 2017
    Article
  4. Review
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

4 authors at 2 institutions in 1 country.

Ruifen MiaoDepartment of Chronic Communicable Disease, Nanjing Municipal Center for Disease Control and Prevention, 2 Zi-Zhu-Lin, Nanjing, 210003, China, ruifenmiao@gmail.com.
Haibo Ge
Lin Xu
Fei Xu
Nanjing Chest Hospital · CNNanjing Municipal Center for Disease Control And Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD14 is a receptor for lipopolysaccharide and plays an important role in innate immune against infections induced by microorganisms. A functional polymorphism in promoter region of CD14 gene, -159C/T, was extensively investigated with tuberculosis (TB) risk, but the association results were inconclusive. We performed a meta-analysis to synthesize association results of CD14 -159C/T polymorphism with TB risk from 8 studies including 1,700 TB cases and 1,816 controls. Based on the heterogeneity between studies evaluated by χ2-based Q test, a fixed- or random-effect model was applied to estimate the pooled odds ratio (OR) and 95% confidence interval (CI). Potential publication bias was evaluated with the funnel plot as well as the linear regression asymmetry test proposed by Egger et al. We found that the -159T allele was significantly associated with an increased risk of TB (OR 1.27, 95% CI 1.01-1.61) as compared with -159C allele. Individuals with -159TT genotype showed a significantly increased risk of TB than those with -159CT/CC genotype (OR 1.52, 95% CI 1.11-2.08). These associations were not attributed to potential publication bias (P>0.05 for Egger's test). The results from this meta-analysis indicate that CD14 -159C/T polymorphism is associated with TB predisposition and may serve as a candidate of susceptibility biomarker for TB.

Indexed as

AllelesGenetic Predisposition to DiseasePolymorphism, Single NucleotideCase-Control StudiesGenotypeHumansLipopolysaccharide ReceptorsOdds RatioPublication BiasTuberculosisLipopolysaccharide Receptors

Identifiers

PMID24519436
OpenAlexW2038773375

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.