Evidence map›Paper›PMID 26585380›Full record

ArticleThe Journal of heredity2016

Serum Amyloid A Protein Concentration in Blood is Influenced by Genetic Differences in the Cheetah (Acinonyx jubatus).

Ashley D Franklin, Anne Schmidt-Küntzel, Karen A Terio, Laurie L Marker, Adrienne E Crosier

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of heredity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

3 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. 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 2 countries.

Ashley D FranklinFrom the Animal Sciences Department, University of Maryland College Park, College Park, MD 20742, USA (Franklin); Center for Species Survival, Smithsonian Conservation Biology Institute, 1500 Remount Road, Front Royal, VA 22630, USA (Franklin and Crosier); Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel and Marker); Life Technologies Conservation Genetics Laboratory, Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel); University of Illinois Zoological Pathology Program, Maywood, IL 60153, USA (Terio). ashley.franklin@pdza.org.
Anne Schmidt-KüntzelFrom the Animal Sciences Department, University of Maryland College Park, College Park, MD 20742, USA (Franklin); Center for Species Survival, Smithsonian Conservation Biology Institute, 1500 Remount Road, Front Royal, VA 22630, USA (Franklin and Crosier); Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel and Marker); Life Technologies Conservation Genetics Laboratory, Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel); University of Illinois Zoological Pathology Program, Maywood, IL 60153, USA (Terio).
Karen A TerioFrom the Animal Sciences Department, University of Maryland College Park, College Park, MD 20742, USA (Franklin); Center for Species Survival, Smithsonian Conservation Biology Institute, 1500 Remount Road, Front Royal, VA 22630, USA (Franklin and Crosier); Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel and Marker); Life Technologies Conservation Genetics Laboratory, Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel); University of Illinois Zoological Pathology Program, Maywood, IL 60153, USA (Terio).
Laurie L MarkerFrom the Animal Sciences Department, University of Maryland College Park, College Park, MD 20742, USA (Franklin); Center for Species Survival, Smithsonian Conservation Biology Institute, 1500 Remount Road, Front Royal, VA 22630, USA (Franklin and Crosier); Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel and Marker); Life Technologies Conservation Genetics Laboratory, Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel); University of Illinois Zoological Pathology Program, Maywood, IL 60153, USA (Terio).
Adrienne E CrosierFrom the Animal Sciences Department, University of Maryland College Park, College Park, MD 20742, USA (Franklin); Center for Species Survival, Smithsonian Conservation Biology Institute, 1500 Remount Road, Front Royal, VA 22630, USA (Franklin and Crosier); Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel and Marker); Life Technologies Conservation Genetics Laboratory, Cheetah Conservation Fund, PO Box 1755, Otjiwarongo, Namibia (Schmidt-Küntzel); University of Illinois Zoological Pathology Program, Maywood, IL 60153, USA (Terio).
Smithsonian Conservation Biology Institute · USUniversity of Maryland, College Park · USCheetah Conservation Fund · NA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic amyloid A (AA) amyloidosis is a major cause of morbidity and mortality among captive cheetahs. The self-aggregating AA protein responsible for this disease is a byproduct of serum amyloid A (SAA) protein degradation. Transcriptional induction of the SAA1 gene is dependent on both C/EBPβ and NF-κB cis-acting elements within the promoter region. In cheetahs, 2 alleles exist for a single guanine nucleotide deletion in the putative NF-κB binding site. In this study, a novel genotyping assay was developed to screen for the alleles. The results show that the SAA1A (-97delG) allele is associated with decreased SAA protein concentrations in the serum of captive cheetahs (n = 58), suggesting genetic differences at this locus may be affecting AA amyloidosis prevalence. However, there was no significant difference in the frequency of the SAA1A (-97delG) allele between individuals confirmed AA amyloidosis positive versus AA amyloidosis negative at the time of necropsy (n = 48). Thus, even though there is evidence that having more copies of the SAA1A (-97delG) allele results in a potentially protective decrease in serum concentrations of SAA protein in captive cheetahs, genotype is not associated with this disease within the North American population. These results suggest that other factors are playing a more significant role in the pathogenesis of AA amyloidosis among captive cheetahs.

Indexed as

AcinonyxAmyloidosisAnimalsAnimals, WildAnimals, ZooBinding SitesCatsFemaleGene FrequencyGenetics, PopulationGenetic VariationGenotypeGenotyping TechniquesImmunoglobulin Light-chain AmyloidosisMaleNF-kappaB-Inducing KinaseNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesSerum Amyloid A ProteinAcute phase responseamyloidosischeetahgenetic typing of insertion/deletionserum amyloid A.

Identifiers

PMID26585380
PMCPMC5994965
OpenAlexW2175657961

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.