Evidence map›Paper›PMID 24682730›Full record

ArticleMolecular and cellular biochemistry2014

Does toll-like receptor-3 (TLR-3) have any role in Indian AMD phenotype?

Neel Kamal Sharma, Kaushal Sharma, Amod Gupta, Sudesh Prabhakar, Ramandeep Singh, Pawan Kumar Gupta, Akshay Anand

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 35% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Genotyping of Clinical Parameters in Age-Related Macular Degeneration.Clinical ophthalmology (Auckland, N.Z.) · 2022
    Article
  7. Review
  8. Article
  9. AMD Genetics in India: The Missing Links.Frontiers in aging neuroscience · 2016
    Review
  10. 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

7 authors at 1 institution in 1 country.

Neel Kamal SharmaNeuroscience Research Lab, Department of Neurology, Post Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Kaushal Sharma
Amod Gupta
Sudesh Prabhakar
Ramandeep Singh
Pawan Kumar Gupta
Akshay Anand
Post Graduate Institute of Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is a devastating disease that results in irreversible central vision loss. TLRs signaling pathway has been found to play an important role in AMD pathogenesis as evidenced by several studies. The objective of the study was to determine the single nucleotide polymorphism (SNP) changes in TLR3 in North Indian AMD patients. We recruited 176 patients comprising 115 AMD patients and 61 controls. Real time PCR was used to evaluate the SNP changes at rs3775291 locus. Pearson's χ(2) test was used evaluate association between various groups. No significant association in genotype and allele frequency was found in AMD patients as compared to control. The results suggest that AMD pathology in North Indian AMD patients is not affected by TLR3 signaling but it could be influenced by other genetic or environmental factors unique to North India.

Indexed as

Genetic Association StudiesAgedFemaleGene FrequencyGenotypeHumansIndiaMacular DegenerationMaleMiddle AgedPolymorphism, Single NucleotideToll-Like Receptor 3TLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID24682730
OpenAlexW2031571765

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.