Evidence map›Paper›PMID 39919185›Full record

ArticleScience advances2025

Inflammatory responses to acute carbon monoxide poisoning and the role of plasma gelsolin.

Awadhesh K Arya, Kinjal Sethuraman, Jaylyn Waddell, Yong Sung Cha, Yuanyuan Liang, Veena M Bhopale, Abid R Bhat, Zuha Imtiyaz, Alik Dakessian, Yoonsuk Lee and 1 more

Abstract read
In one paragraph

Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

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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

11 authors.

Awadhesh K AryaDepartment of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-2142-4924
Kinjal SethuramanDepartment of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Jaylyn WaddellDepartment of Pediatrics, University of Maryland School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-7372-8682
Yong Sung ChaDepartment of Emergency Medicine and Research Institute of Hyperbaric Medicine and Science, Yonsei University Wonju College of Medicine, Wonju, Republic of Korea.ORCID 0000-0001-9897-4273
Yuanyuan LiangDepartment of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD, USA.
Veena M BhopaleDepartment of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-5057-1739
Abid R BhatDepartment of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-4476-1189
Zuha ImtiyazDepartment of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.ORCID 0000-0001-6927-8623
Alik DakessianDepartment of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.ORCID 0000-0003-2031-8465
Yoonsuk LeeDepartment of Emergency Medicine and Research Institute of Hyperbaric Medicine and Science, Yonsei University Wonju College of Medicine, Wonju, Republic of Korea.ORCID 0000-0003-0404-7255
Stephen R ThomDepartment of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.ORCID 0000-0002-3533-6124

Funding

Inflammatory changes and glymphatic dysfunction in carbon monoxide neuropathologyR01NS122855 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI STEPHEN RAYMOND THOM · 2022 to 2026
$2.9M
NINDS NIH HHS R01 NS122855
6 · The paper itself

Abstract

The mechanism for neurological deficits from carbon monoxide (CO) poisoning is unclear. In a series of 150 patients with CO poisoning, we found marked elevations of blood-borne inflammatory filamentous (F-) actin-coated microparticles (MPs), neutrophil activation, and a 90% reduction in the normal level of plasma gelsolin (pGSN), a protein capable of lysing F-actin-coated MPs. This led to studies in a murine model where the same events occur and cause neuroinflammation with cognitive dysfunction. All events are recapitulated when F-actin MPs are injected intravenously, which establishes a blood-to-brain-to-blood inflammatory cycle that persists for weeks. All changes, including cognitive dysfunction, can be abrogated by an injection of human recombinant pGSN within 2 weeks after CO poisoning. These findings demonstrate that CO-induced neurological injury has an inflammatory etiology. Because of MP-mediated communications between the brain and systemic circulation, CO-induced cognitive deficits may be reversible with a pharmaceutical intervention.

Indexed as

Carbon Monoxide PoisoningGelsolinInflammationActinsAnimalsDisease Models, AnimalFemaleHumansMaleMiceActinsGelsolin

Identifiers

PMID39919185
PMCPMC11804920

What OpenQuestion holds

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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.