Evidence map›Paper›PMID 21266772›Full record

ArticleThe Journal of clinical investigation2011

Thrombotic thrombocytopenic purpura: reducing the risk?

Michael C Berndt, Robert K Andrews

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2011. 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 39% 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, 7 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Michael C BerndtBiomedical Diagnostics Institute, Dublin City University, and Royal College of Surgeons in Ireland, Dublin, Ireland. michael.berndt@dcu.ie
Robert K Andrews
Australian Centre for HIV and Hepatitis Virology Research · AUDublin City University · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

von Willebrand factor (vWF) has a key role in initiating platelet aggregation, and thereby thrombus formation, that is dependent on its ability to form appropriately sized multimers. Ultralarge multimers promote the formation of the microvascular thrombi that are hallmarks of the life-threatening condition thrombotic thrombocytopenic purpura (TTP). In this issue of the JCI, Chen et al. show that the drug N-acetylcysteine (NAC) can decrease the size of vWF multimers in vitro and in vivo, resolving thrombi in mice. These data suggest that NAC could potentially be used to treat thrombotic conditions such as TTP.

Indexed as

AcetylcysteineADAM ProteinsADAMTS13 ProteinAnimalsHumansMembrane GlycoproteinsMicePlatelet AggregationPlatelet Glycoprotein GPIb-IX ComplexPurpura, Thrombotic ThrombocytopenicThrombosisvon Willebrand FactorAcetylcysteineADAM ProteinsADAMTS13 ProteinADAMTS13 protein, humanadhesion receptorMembrane GlycoproteinsPlatelet Glycoprotein GPIb-IX Complexvon Willebrand Factor

Identifiers

PMID21266772
PMCPMC3026753
OpenAlexW2096861228

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.