Evidence map›Paper›PMID 28940111›Full record

ArticleLipids2017

Hyperuricemia is Associated with Increased Apo AI Fractional Catabolic Rates and Dysfunctional HDL in New Zealand Rabbits.

Miriam Martínez-Ramírez, Cristóbal Flores-Castillo, L Gabriela Sánchez-Lozada, Rocío Bautista-Pérez, Elizabeth Carreón-Torres, José Manuel Fragoso, José Manuel Rodriguez-Pérez, Fernando E García-Arroyo, Victoria López-Olmos, María Luna-Luna and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Lipids, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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  5. 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

13 authors at 1 institution in 2 countries.

Miriam Martínez-RamírezDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
Cristóbal Flores-CastilloDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
L Gabriela Sánchez-LozadaNephrology Department, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City, Mexico.
Rocío Bautista-PérezDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
Elizabeth Carreón-TorresDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
José Manuel FragosoDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
José Manuel Rodriguez-PérezDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
Fernando E García-ArroyoNephrology Department, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City, Mexico.
Victoria López-OlmosDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
María Luna-LunaDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
Gilberto Vargas-AlarcónDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico.
Martha FrancoNephrology Department, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City, Mexico.
Oscar Pérez-MéndezDepartment of Molecular Biology, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano 1, Sección XVI, 14080, Mexico City, Mexico. opmendez@yahoo.com.
Instituto Nacional de Cardiología · MX

Funding

Consejo Nacional de Ciencia y Tecnología Project No. 132473
6 · The paper itself

Abstract

The potential cause-effect relationship between uric acid plasma concentrations and HDL functionality remains elusive. Therefore, this study aimed to explore the effect of oxonic acid (OA)-induced hyperuricemia on the HDL size distribution, lipid content of HDL subclasses, and apo AI turnover, as well as HDL functionality in New Zealand white rabbits. Experimental animals received OA 750 mg/kg/day by oral gavage during 21 days. The HDL-apo AI fractional catabolic rate (FCR) was determined by exogenous labeling with

Indexed as

AnimalsApolipoprotein A-IAryldialkylphosphataseDisease Models, AnimalHumansHyperuricemiaLipoproteins, HDLOxonic AcidRabbitsApolipoprotein A-IAryldialkylphosphataseLipoproteins, HDLOxonic AcidCoronary heart diseaseLipoprotein metabolismRenal failureRisk factorsUricemia

Identifiers

PMID28940111
OpenAlexW2759507609

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.