Evidence map›Paper›PMID 38581378›Full record

ArticleJournal of biomechanical engineering2024

Assessment of Left Lung Remodeling With Magnetic Resonance Imaging in a Murine Model Following Exposure to Douglas Fir Smoke.

Jacqueline Matz, Mireia Perera Gonzalez, Peter Niedbalski, Hannah Kim, Ye Chen, Paola Sebastiani, Michael J Gollner, Chiara Bellini, Jessica M Oakes

Open access · greenAbstract read
In one paragraph

Article in Journal of biomechanical engineering, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 92% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 5 institutions in 2 countries.

Jacqueline Matz *Department of Bioengineering, Northeastern University, Boston, MA 02115.
Mireia Perera Gonzalez *Department of Bioengineering, Northeastern University, Boston, MA 02115.
Peter NiedbalskiPulmonary, Critical Care and Sleep Medicine, Kansas University Medical Center, Boston, MA 02115.
Hannah KimDepartment of Bioengineering, Northeastern University, Boston, MA 02115.
Ye ChenTufts Clinical and Translational Science Institute (CTSI), Tufts Medical Center, Boston, MA 02115.
Paola SebastianiInstitute for Clinical Research and Health Policy Studies (ICRHPS), Tufts Medical Center and Tufts University School of Medicine, Boston, MA 02115.
Michael J GollnerDepartment of Mechanical Engineering, University of California Berkeley, Berkeley, CA 94720.
Chiara BelliniDepartment of Bioengineering, Northeastern University, Boston, MA 02115.ORCID 0000-0003-0823-4613
Jessica M OakesDepartment of Bioengineering, Northeastern University, 360 Huntington Ave, Boston, MA 02115.ORCID 0000-0001-9669-0680
Northeastern University · USTufts Medical Center · USTufts University · USUniversity of California, Berkeley · USUniversity of Kansas · US

Funding

Cardiopulmonary Risk Assessment from Smoke Exposure at the Wildland Urban InterfaceR01ES033792 · NIEHS · NORTHEASTERN UNIVERSITY · PI Chiara Bellini · 2022 to 2026
$3.4M
NIEHS NIH HHS R01E5033792NIEHS NIH HHS R01 ES033792
6 · The paper itself

Abstract

Wildland firefighters (WLFFs) experience lung function decline due to occupational exposure to fire smoke. WLFFs typically do not wear respiratory personal protective equipment, and if they do, it is a simple bandana, which is not effective at filtering smoke. To pinpoint the biological underpinnings of abnormal respiratory function following 3-7 years of WLFF service, we exposed mice to Douglas fir smoke (DFS) over 8 weeks. Following exposure, we assessed changes in lung structure through Magnetic Resonance Imaging (MRI) and histological analysis, which was supported by immunohistochemistry staining. With MRI, we found that the signal decay time, T2*, from ultrashort echo time (UTE) images was significantly shorter in mice exposed to DFS compared to air controls. In addition, the variation in T2* was more heterogeneously distributed throughout the left lung in DFS-exposed mice, compared to air controls. As confirmed by histological analysis, shorter T2* was caused by larger parenchyma airspace sizes and not fibrotic remodeling. Destruction of the alveolar spaces was likely due to inflammation, as measured by an influx of CD68+ macrophages and destruction due to enhanced neutrophil elastase. In addition, measurements of airspace dimensions from histology were more heterogeneously distributed throughout the lung, corroborating the enhanced relative dispersion of T2*. Findings from this study suggest that the decline in lung function observed in WLFFs may be due to emphysema-like changes in the lung, which can be quantified with MRI.

Indexed as

LungMagnetic Resonance ImagingSmokeAirway RemodelingAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLSmokeemphysemasignal decay time constantwildland firefighterswildland fire smoke

Identifiers

PMID38581378
PMCPMC11080952
OpenAlexW4394013641

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.