Evidence map›Paper›PMID 39429164›Full record

ArticleHypertension (Dallas, Tex. : 1979)2024

Somatic

Alice Watson, Harriet Syme, Morris Brown

Abstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

3 authors.

Alice WatsonClinical Science and Services, Royal Veterinary College, London, United Kingdom (A.W., H.S.).ORCID 0009-0001-1048-6521
Harriet SymeClinical Science and Services, Royal Veterinary College, London, United Kingdom (A.W., H.S.).ORCID 0000-0002-0967-4031
Morris BrownClinical Pharmacology and Precision Medicine, Queen Mary University of London, United Kingdom (A.W., M.B.).ORCID 0000-0001-8409-1082

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrimary aldosteronism (PA) is a common cause of human hypertension. Somatic mutations in

methodsDNA and RNA extracted from tissue from 13 cats with unilateral aldosterone-secreting tumors, including 8 carcinomas and 5 adenomas, underwent whole genome sequencing, targeted Sanger sequencing, and RNA sequencing. Single-nucleotide substitution variants were filtered to select those with a predicted deleterious effect on protein function and a suspected role in aldosterone secretion.

resultsProbable functional somatic single-nucleotide polymorphisms (n=8) were found in 3 adenomas and 2 carcinomas. Mutations with predicted significant effects were identified in 2 genes also mutated in human PA;

conclusionsSimilar mutations were identified in cats to those found in humans. It is, therefore, likely that both species have shared underlying selection pressures for mutations that increase aldosterone secretion.

Indexed as

Aldosteronebeta CateninCalcium Channels, L-TypeGTP-Binding Protein alpha Subunits, Gq-G11HyperaldosteronismMutationAdenomaAdrenal Cortex NeoplasmsAnimalsCatsAldosteronebeta CateninCalcium Channels, L-TypeGTP-Binding Protein alpha Subunits, Gq-G11aldosteroneanimalshyperaldosteronismhypertensionmutation

Identifiers

PMID39429164
PMCPMC11578054

What Socratic 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 Socratic graph.