Evidence map›Paper›PMID 34944741›Full record

ArticleBiomedicines2021

C3d Elicits Neutrophil Degranulation and Decreases Endothelial Cell Migration, with Implications for Patients with Alpha-1 Antitrypsin Deficiency.

Laura T Fee, Debananda Gogoi, Michael E O'Brien, Emer McHugh, Michelle Casey, Ciara Gough, Mark Murphy, Ann M Hopkins, Tomás P Carroll, Noel G McElvaney and 1 more

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

Article in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Neutrophils, Fast and Strong.Biomedicines · 2022
    Article
  3. 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

11 authors at 1 institution in 1 country.

Laura T FeeAlpha-1 Foundation Ireland, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.
Debananda GogoiIrish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.
Michael E O'BrienIrish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.
Emer McHughIrish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.
Michelle CaseyIrish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.
Ciara GoughIrish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.
Mark MurphyIrish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.ORCID 0000-0001-5624-1338
Ann M HopkinsDepartment of Surgery, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.ORCID 0000-0003-2836-6584
Tomás P CarrollAlpha-1 Foundation Ireland, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.
Noel G McElvaneyIrish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.
Emer P ReevesIrish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, D02 YN77 Dublin, Ireland.ORCID 0000-0002-1922-0447
Royal College of Surgeons in Ireland · IE

Funding

Alpha-1 Foundation 615848
6 · The paper itself

Abstract

Alpha-1 antitrypsin (AAT) deficiency (AATD) is characterized by increased risk for emphysema, chronic obstructive pulmonary disease (COPD), vasculitis, and wound-healing impairment. Neutrophils play a central role in the pathogenesis of AATD. Dysregulated complement activation in AATD results in increased plasma levels of C3d. The current study investigated the impact of C3d on circulating neutrophils. Blood was collected from AATD (

Indexed as

alpha-1 antitrypsinalpha-1 antitrypsin deficiencycomplement component 3ddegranulationlactoferrinmyeloperoxidaseneutrophil elastaseneutrophils

Identifiers

PMID34944741
PMCPMC8698851
OpenAlexW4200553578

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.