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Interferon-γ is a therapeutic target molecule for prevention of postoperative adhesion formation

Overview of attention for article published in Nature Medicine, March 2008
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (81st percentile)
  • Average Attention Score compared to outputs of the same age and source

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Citations

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48 Mendeley
Title
Interferon-γ is a therapeutic target molecule for prevention of postoperative adhesion formation
Published in
Nature Medicine, March 2008
DOI 10.1038/nm1733
Pubmed ID
Authors

Hisashi Kosaka, Tomohiro Yoshimoto, Takayuki Yoshimoto, Jiro Fujimoto, Kenji Nakanishi

Abstract

Intestinal adhesions are bands of fibrous tissue that connect the loops of the intestine to each other, to other abdominal organs or to the abdominal wall. Fibrous tissue formation is regulated by the balance between plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (tPA), which reciprocally regulate fibrin deposition. Several components of the inflammatory system, including cytokines, chemokines, cell adhesion molecules and neuropeptide substance P, have been reported to participate in adhesion formation. We have used cecal cauterization to develop a unique experimental mouse model of intestinal adhesion. Mice developed severe intestinal adhesion after this treatment. Adhesion development depended upon the interferon-gamma (IFN-gamma) and signal transducer and activator of transcription-1 (STAT1) system. Natural killer T (NKT) cell-deficient mice developed adhesion poorly, whereas they developed severe adhesion after reconstitution with NKT cells from wild-type mice, suggesting that NKT cell IFN-gamma production is indispensable for adhesion formation. This response does not depend on STAT4, STAT6, interleukin-12 (IL-12), IL-18, tumor necrosis factor-alpha, Toll-like receptor 4 or myeloid differentiation factor-88-mediated signals. Wild-type mice increased the ratio of PAI-1 to tPA after cecal cauterization, whereas Ifng(-/-) or Stat1(-/-) mice did not, suggesting that IFN-gamma has a crucial role in the differential regulation of PAI-1 and tPA. Additionally, hepatocyte growth factor, a potent mitogenic factor for hepatocytes, strongly inhibited intestinal adhesion by diminishing IFN-gamma production, providing a potential new way to prevent postoperative adhesions.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 48 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 2 4%
Unknown 46 96%

Demographic breakdown

Readers by professional status Count As %
Researcher 13 27%
Other 6 13%
Student > Ph. D. Student 6 13%
Student > Bachelor 4 8%
Professor > Associate Professor 4 8%
Other 7 15%
Unknown 8 17%
Readers by discipline Count As %
Medicine and Dentistry 18 38%
Agricultural and Biological Sciences 12 25%
Biochemistry, Genetics and Molecular Biology 5 10%
Immunology and Microbiology 3 6%
Unknown 10 21%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 7. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 26 December 2023.
All research outputs
#4,144,328
of 22,660,862 outputs
Outputs from Nature Medicine
#4,937
of 8,452 outputs
Outputs of similar age
#13,872
of 80,248 outputs
Outputs of similar age from Nature Medicine
#29
of 60 outputs
Altmetric has tracked 22,660,862 research outputs across all sources so far. Compared to these this one has done well and is in the 80th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 8,452 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 96.3. This one is in the 39th percentile – i.e., 39% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 80,248 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 81% of its contemporaries.
We're also able to compare this research output to 60 others from the same source and published within six weeks on either side of this one. This one is in the 40th percentile – i.e., 40% of its contemporaries scored the same or lower than it.