Evidence map›Paper›PMID 19149411›Full record

ArticleComparative medicine2008

Quantitative tomography of early-onset spontaneous AA amyloidosis in interleukin 6 transgenic mice.

Jonathan S Wall, Tina Richey, Amy Allen, Robert Donnell, Steve J Kennel, Alan Solomon

Open access · greenAbstract read
In one paragraph

Article in Comparative medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  7. The pattern recognition reagents RAGE VC1 and peptide p5 share common binding sites and exhibit specific reactivity with AA amyloid in mice.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2016
    Article
  8. A novel method for quantifying peripheral tissue amyloid load by using the radiolabeled amyloidophilic peptide, p5.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2013
    Article
  9. Systemic amyloidoses.Annual review of biochemistry · 2013
    Review
  10. Article
  11. Article
  12. Article
  13. Development and evaluation of agents for targeting visceral amyloid.Tijdschrift voor nu[c]leaire geneeskunde · 2011
    Article
  14. In vivo molecular imaging of peripheral amyloidosis using heparin-binding peptides.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  15. Article
  16. 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

6 authors at 1 institution in 1 country.

Jonathan S WallHuman Immunology and Cancer Program, Graduate School of Medicine, University of Tennessee, Knoxville, TN, USA. jwall@mc.utmck.edu
Tina Richey
Amy Allen
Robert Donnell
Steve J Kennel
Alan Solomon
University of Tennessee at Knoxville · US

Funding

SPECT/CT Imaging of Systemic AA-Amyloidosis in MiceR01EB000789 · NIBIB · UNIVERSITY OF TENNESSEE KNOXVILLE · PI WALL, JONATHAN S · 2002 to 2005
$3.8M
NIBIB NIH HHS EB00789NIBIB NIH HHS R01 EB000789
6 · The paper itself

Abstract

Mice that constitutively express the human interleukin 6 (huIL6) protein from a heritable transgene (H2-L(d)-IL-6) express high levels of the acute-phase reactant, serum amyloid protein A, a liver-derived apoprotein of high-density lipoprotein that is the precursor of AA amyloid. Typically at approximately 5 mo of age B6(C)- Tg(H2-L(d)-IL-6)Kish (H2/huIL-6) animals begin to develop splenic deposits of AA amyloid, which progress to involve the liver, kidney, and vasculature, ultimately resulting in death due to severe systemic AA amyloidosis at 8 to 9 mo of age. These mice provide a robust model in which to study novel therapeutic and diagnostic imaging agents for AA amyloidosis. We recently have noted a change in onset of spontaneous disease, as evidenced by 2 female transgenic mice that were found moribund at only 5 mo of age. Extensive hepatosplenic amyloid deposits in both mice were identified and quantified by single-photon emission computed tomography, which further revealed heterogeneous distribution of radiotracer in the spleen indicating a distinction between amyloid-laden red pulp and the disease-free lymphoid follicles. The AA nature of the deposits was evidenced immunohistochemically and by mass spectrometric analyses of extracted amyloid fibrils. Our studies have documented the manifestation of early-onset, severe, spontaneous AA amyloidosis in 2- to 5-mo-old H2/ huIL-6 mice; we hypothesize that this disease is due to genetic rather than environmental factors.

Indexed as

Age FactorsAmino Acid SequenceAmyloidosisAnimalsDisease Models, AnimalFemaleHumansInterleukin-6MaleMass SpectrometryMiceMice, TransgenicPeptide FragmentsRecombinant ProteinsSerum Amyloid A ProteinTomography, Emission-Computed, Single-PhotonIL6 protein, humanInterleukin-6Peptide FragmentsRecombinant ProteinsSerum Amyloid A Protein

Identifiers

PMID19149411
PMCPMC2710755
OpenAlexW1549746218

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.