Evidence map›Paper›PMID 30273600›Full record

ArticleThe American journal of pathology2018

Colonoscopic-Guided Pinch Biopsies in Mice as a Useful Model for Evaluating the Roles of Host and Luminal Factors in Colonic Inflammation.

David C Montrose, Xi K Zhou, Erin M McNally, Erika Sue, Hanhan Wang, Ryohei Nishiguchi, Akanksha Verma, Olivier Elemento, Kenneth W Simpson, Peiying Yang and 2 more

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

Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 91% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. 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 at 4 institutions in 1 country.

David C MontroseDepartment of Medicine, Weill Cornell Medicine, New York, New York. Electronic address: dam2040@med.cornell.edu.
Xi K ZhouDepartment of Healthcare Policy and Research, Weill Cornell Medicine, New York, New York.
Erin M McNallyDepartment of Medicine, Weill Cornell Medicine, New York, New York.
Erika SueDepartment of Medicine, Weill Cornell Medicine, New York, New York.
Hanhan WangDepartment of Healthcare Policy and Research, Weill Cornell Medicine, New York, New York.
Ryohei NishiguchiDepartment of Medicine, Weill Cornell Medicine, New York, New York.
Akanksha VermaDepartment of Physiology and Biophysics, Weill Cornell Medicine, New York, New York.
Olivier ElementoDepartment of Physiology and Biophysics, Weill Cornell Medicine, New York, New York.
Kenneth W SimpsonDepartment of Clinical Sciences, Cornell University College of Veterinary Medicine, Ithaca, New York.
Peiying YangDepartment of Palliative, Rehabilitation and Integrative Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Timothy HlaVascular Biology Program, Boston Children's Hospital, Boston, Massachusetts; Department of Surgery, Harvard Medical School, Boston, Massachusetts.
Andrew J DannenbergDepartment of Medicine, Weill Cornell Medicine, New York, New York. Electronic address: ajdannen@med.cornell.edu.
Cornell University · USWeill Cornell Medicine · USBoston Children's Hospital · USThe University of Texas MD Anderson Cancer Center · US

Funding

Mechanisms of sphingolipid signaling in vascular health and diseaseR35HL135821 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI HLA, TIMOTHY TUN · 2017 to 2023
$6.3M
National Heart, Lung, and Blood Institute R35 HL135821NHLBI NIH HHS R35 HL135821
6 · The paper itself

Abstract

Colonic inflammation, a hallmark of inflammatory bowel disease, can be influenced by host intrinsic and extrinsic factors. There continues to be a need for models of colonic inflammation that can both provide insights into disease pathogenesis and be used to investigate potential therapies. Herein, we tested the utility of colonoscopic-guided pinch biopsies in mice for studying colonic inflammation and its treatment. Gene expression profiling of colonic wound beds after injury showed marked changes, including increased expression of genes important for the inflammatory response. Interestingly, many of these gene expression changes mimicked those alterations found in inflammatory bowel disease patients. Biopsy-induced inflammation was associated with increases in neutrophils, macrophages, and natural killer cells. Injury also led to elevated levels of sphingosine-1-phosphate (S1P), a bioactive lipid that is an important mediator of inflammation mainly through its receptor, S1P

Indexed as

Disease Models, AnimalMicrobiotaAnimalsAnti-Bacterial AgentsBiopsyCells, CulturedColonColonoscopyFemaleGene Expression ProfilingInflammationInflammatory Bowel DiseasesIntestinal MucosaLysophospholipidsMaleMiceAnti-Bacterial AgentsLysophospholipidsReceptors, LysosphingolipidS1pr1 protein, mouseSphingosinesphingosine 1-phosphateSphingosine-1-Phosphate Receptors

Identifiers

PMID30273600
PMCPMC6334259
OpenAlexW2893349519

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.