Evidence map›Paper›PMID 32756554›Full record

ArticlePloS one2020

Serum discrimination and phenotype assessment of coronary artery disease patents with and without type 2 diabetes prior to coronary artery bypass graft surgery.

James R Hocker, Megan Lerner, Stan A Lightfoot, Marvin D Peyton, Jess L Thompson, Subrato Deb, Mathew Reinersman, R Jane Hanas, Russel G Postier, Barish H Edil and 2 more

Abstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

12 authors.

James R HockerDepartment of Biochemistry and Molecular Biology The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Megan LernerDepartment of Surgery The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Stan A LightfootDepartment of Medicine The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Marvin D PeytonDepartment of Surgery The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Jess L ThompsonDepartment of Surgery The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Subrato DebDepartment of Surgery The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Mathew ReinersmanDepartment of Surgery The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
R Jane HanasDepartment of Biochemistry and Molecular Biology The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Russel G PostierDepartment of Surgery The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Barish H EdilDepartment of Surgery The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Harold M BurkhartDepartment of Surgery The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Jay S HanasDepartment of Biochemistry and Molecular Biology The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.ORCID 0000-0003-1922-5333

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes Mellitus (DM) accelerates coronary artery disease (CAD) and atherosclerosis, the causes of most heart attacks. The biomolecules involved in these inter-related disease processes are not well understood. This study analyzes biomolecules in the sera of patients with CAD, with and without type (T) 2DM, who are about to undergo coronary artery bypass graft (CABG) surgery. The goal is to develop methodology to help identify and monitor CAD patients with and without T2DM, in order to better understand these phenotypes and to glean relationships through analysis of serum biomolecules. Aorta, fat, muscle, and vein tissues from CAD T2DM patients display diabetic-related histologic changes (e.g., lipid accumulation, fibrosis, loss of cellularity) when compared to non-diabetic CAD patients. The patient discriminatory methodology utilized is serum biomolecule mass profiling. This mass spectrometry (MS) approach is able to distinguish the sera of a group of CAD patients from controls (p value 10-15), with the CAD group containing both T2DM and non-diabetic patients. This result indicates the T2DM phenotype does not interfere appreciably with the CAD determination versus control individuals. Sera from a group of T2DM CAD patients however are distinguishable from non-T2DM CAD patients (p value 10-8), indicating it may be possible to examine the T2DM phenotype within the CAD disease state with this MS methodology. The same serum samples used in the CAD T2DM versus non-T2DM binary group comparison were subjected to MS/MS peptide structure analysis to help identify potential biochemical and phenotypic changes associated with CAD and T2DM. Such peptide/protein identifications could lead to improved understanding of underlying mechanisms, additional biomarkers for discriminating and monitoring these disease conditions, and potential therapeutic targets. Bioinformatics/systems biology analysis of the peptide/protein changes associated with CAD and T2DM suggested cell pathways/systems affected include atherosclerosis, DM, fibrosis, lipogenesis, loss of cellularity (apoptosis), and inflammation.

Indexed as

AdultAgedBiomarkersBlood ProteinsCase-Control StudiesCoronary Artery BypassCoronary Artery DiseaseCross-Sectional StudiesDiabetes Mellitus, Type 2Diabetic AngiopathiesFemaleHumansMaleMiddle AgedPhenotypeRetrospective StudiesBiomarkersBlood Proteins

Identifiers

PMID32756554
PMCPMC7527241

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Registered trials

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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.