Evidence map›Paper›PMID 36748547›Full record

ArticleMicrobial genomics2022

A novel approach for combining the metagenome, metaresistome, metareplicome and causal inference to determine the microbes and their antibiotic resistance gene repertoire that contribute to dysbiosis.

Vitalii Stebliankin, Musfiqur Sazal, Camilo Valdes, Kalai Mathee, Giri Narasimhan

Open access · goldAbstract read
In one paragraph

Article in Microbial genomics, 2022. 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
0.3field-weighted citation impact, top 47% 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, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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

5 authors at 3 institutions in 1 country.

Vitalii StebliankinBioinformatics Research Group (BioRG), Knight Foundation School of Computing and Information Sciences, Florida International University, Miami, FL, USA.
Musfiqur SazalBioinformatics Research Group (BioRG), Knight Foundation School of Computing and Information Sciences, Florida International University, Miami, FL, USA.
Camilo ValdesBioinformatics Research Group (BioRG), Knight Foundation School of Computing and Information Sciences, Florida International University, Miami, FL, USA.
Kalai MatheeHerbert Wertheim College of Medicine, Florida International University, Miami, FL, USA.
Giri NarasimhanBioinformatics Research Group (BioRG), Knight Foundation School of Computing and Information Sciences, Florida International University, Miami, FL, USA.
Florida International University · USLawrence Livermore National Laboratory · USMicrosoft (United States) · US

Funding

Longitudinal Study of Vaginal Microbiota and Persistent Human Papillomavirus DetectionR15AI128714 · NIAID · FLORIDA INTERNATIONAL UNIVERSITY · PI MADHIVANAN, PURNIMA · 2017 to 2017
$440k
NIAID NIH HHS R15 AI128714
6 · The paper itself

Abstract

The use of whole metagenomic data to infer the relative abundance of all its microbes is well established. The same data can be used to determine the replication rate of all eubacterial taxa with circular chromosomes. Despite their availability, the replication rate profiles (metareplicome) have not been fully exploited in microbiome analyses. Another relatively new approach is the application of causal inferencing to analyse microbiome data that goes beyond correlational studies. A novel scalable pipeline called MeRRCI (Metagenome, metaResistome, and metaReplicome for Causal Inferencing) was developed. MeRRCI combines efficient computation of the metagenome (bacterial relative abundance), metaresistome (antimicrobial gene abundance) and metareplicome (replication rates), and integrates environmental variables (metadata) for causality analysis using Bayesian networks. MeRRCI was applied to an infant gut microbiome data set to investigate the microbial community's response to antibiotics. Our analysis suggests that the current treatment stratagem contributes to preterm infant gut dysbiosis, allowing a proliferation of pathobionts. The study highlights the specific antibacterial resistance genes that may contribute to exponential cell division in the presence of antibiotics for various pathogens, namely

Indexed as

Infant, PrematureMetagenomeAnti-Bacterial AgentsBacteriaBayes TheoremDrug Resistance, BacterialDysbiosisHumansInfantInfant, NewbornAnti-Bacterial Agentsantibacterial resistancecausal Bayesian networkmulti-omicsorigin of replicationpeak-to-trough ratio (PTR)

Identifiers

PMID36748547
PMCPMC9837561
OpenAlexW4313448109

What OpenQuestion holds

Textmetadata
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.