GENETIC DETERMINANTS OF THROMBOSIS.

Charles J Lowenstein

Abstract read

In one paragraph

Article in Transactions of the American Clinical and Climatological Association, 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

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.

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

1 author.

Charles J LowensteinBALTIMORE, MARYLAND.

Funding

Population genomic variation, functional biology, and the risk of venous thrombosisR01HL134894 · NHLBI · UNIVERSITY OF WASHINGTON · PI LOWENSTEIN, CHARLES J, SMITH, NICHOLAS L · 2017 to 2020

$2.9M

Model system of oral contraceptive-induced VTE: integrating genomic, transcriptomic, and proteomic discovery with functional biologyR61HL141791 · NHLBI · UNIVERSITY OF ROCHESTER · PI LOWENSTEIN, CHARLES J, SMITH, NICHOLAS L · 2018 to 2019

$1.4M

NHLBI NIH HHS R01 HL134894NHLBI NIH HHS R61 HL141791

6 · The paper itself

Abstract

Venous thromboembolism (VTE) is a major cause of morbidity and mortality in the United States. VTE is caused by genetic and acquired conditions, but the genetic variants that increase the risk of VTE are not fully characterized. Recent genome-wide association studies (GWAS) have discovered novel genetic loci linked to VTE. Some of these loci have been characterized, uncovering new pathways that regulate VTE. Functional characterization of candidate genes discovered by GWAS may reveal new therapeutic targets to treat and prevent abnormal thrombosis or bleeding.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyBlood CoagulationHumansPhenotypeRisk FactorsThrombosisVenous Thromboembolism

Identifiers

PMID39135563

PMCPMC11316864

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.