Evidence map›Paper›PMID 36254341›Full record

ArticleClinical and translational allergy2022

Determining biomarkers for evaluation and diagnosis of hereditary angioedema.

Umesh Singh, Jonathan A Bernstein

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational allergy, 2022. 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
0.9field-weighted citation impact, top 24% 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, 6 citations in OpenAlex.

  1. The journal of allergy and clinical immunology. Global · 2026
    Article
  2. Article
  3. 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

2 authors at 1 institution in 1 country.

Umesh SinghUniversity of Cincinnati College of Medicine Cincinnati Ohio USA.ORCID https://orcid.org/0000-0003-1830-6262
Jonathan A BernsteinUniversity of Cincinnati College of Medicine Cincinnati Ohio USA.
University of Cincinnati Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rationale: Kallikrein-bradykinin-forming cascade is known to cause hereditary angioedema (HAE) acute angioedema (AE) attacks. Further research of HAE attacks is needed to explain disease heterogeneity, predict treatment response and identify biomarkers for monitoring HAE attacks. Differential expression of the microvascular endothelial cell-surface receptors for example, g-C1qR, cytokeratin-1, and plasminogen-activator-urokinase-receptor (PLAUR) were hypothesized as biomarkers of AE attacks. Method: To understand HAE attacks, the differentially expressed genes (DEGs) in RNAseq and mi-RNAseq data of total RNA extracted from skin biopsies of lesional versus non-lesional skin collected during and between attacks in Type-1 HAE patients ( Results: PLAUR gene, encoding urokinase-type plasminogen activator (u-PAR), was constitutively over-expressed in HAE-Type-1 versus non-HAE controls suggestive of overactive u-PAR-mediated signaling via binding to Factor-XII. Baseline PLAUR expression was associated with severe AE ( Conclusion: Angiopoetin-activated

Indexed as

biomarkersdifferentially expressed genesHAE attacksHAE with normal C1 inhibitorhereditary angioedemaheterogeneityIL‐1b, beta1/beta3‐integrinIL‐6immunologyimmunotherapykallikrein‐bradykininotherPLAUR geneRNAseq

Identifiers

PMID36254341
PMCPMC9557132
OpenAlexW4304842674

What OpenQuestion holds

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LicenceCC BY
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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.