Evidence map›Paper›PMID 29930915›Full record

ArticleFrontiers in cellular and infection microbiology2018

Upregulation of P2Y

Virginie Bondu, Casey Bitting, Valerie L Poland, Joshua A Hanson, Michelle S Harkins, Sarah Lathrop, Kurt B Nolte, Daniel A Lawrence, Tione Buranda

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Therapeutic potential for P2YPurinergic signalling · 2023
    Review
  7. Article
  8. Early Dry Eye Disease Onset in a NOD.H-2h4 Mouse Model of Sjögren's Syndrome.Investigative ophthalmology & visual science · 2022
    Article
  9. suPAR to Risk-Stratify Patients With Malaria.Frontiers in immunology · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Orthohantavirus Pathogenesis and Cell Tropism.Frontiers in cellular and infection microbiology · 2020
    Review
  16. Review
  17. 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

9 authors at 2 institutions in 1 country.

Virginie BonduDepartment of Pathology, University of New Mexico School of Medicine, Albuquerque, NM, United States.
Casey BittingDepartment of Pathology, University of New Mexico School of Medicine, Albuquerque, NM, United States.
Valerie L PolandOffice of the Medical Investigator, University of New Mexico School of Medicine, Albuquerque, NM, United States.
Joshua A HansonDepartment of Pathology, University of New Mexico School of Medicine, Albuquerque, NM, United States.
Michelle S HarkinsDivision of Infectious Disease, Pulmonary, Critical Care, and Sleep, Department of Internal Medicine, School of Medicine, University of New Mexico, Albuquerque, NM, United States.
Sarah LathropDepartment of Pathology, University of New Mexico School of Medicine, Albuquerque, NM, United States.
Kurt B NolteDepartment of Pathology, University of New Mexico School of Medicine, Albuquerque, NM, United States.
Daniel A LawrenceDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, United States.
Tione BurandaDepartment of Pathology, University of New Mexico School of Medicine, Albuquerque, NM, United States.
University of New Mexico · USUniversity of Michigan–Ann Arbor · US

Funding

Unraveling the role of tPA in the neurovascular unitR01HL055374 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Antonetti, Daniel A Lawrence · 1995 to 2026
$8.6M
NHLBI NIH HHS R01 HL055374
6 · The paper itself

Abstract

Sin Nombre virus (SNV) causes hantavirus cardiopulmonary pulmonary syndrome (HCPS) with the loss of pulmonary vascular endothelial integrity, and pulmonary edema without causing cytopathic effects on the vascular endothelium. HCPS is associated primarily with a dysregulated immune response. We previously found occult signs of hemostatic imbalance in the form of a sharp >30-100 fold increase in the expression of plasminogen activator inhibitor type 1 (PAI-1), in serial blood plasma draws of terminal stage-patients. However, the mechanism of the increase in PAI-1 remains unclear. PAI-1 is a primary inhibitor of fibrinolysis caused by tissue plasminogen activator (tPA) and urokinase plasminogen activator plasma (uPA). Here, we investigate factors that contribute to PAI-1 upregulation during HCPS. Using zymography, we found evidence of PAI-1-refractory uPA activity and no tPA activity in plasma samples drawn from HCPS patients. The sole prevalence of uPA activity suggested that severe inflammation drove PAI-1 activity. We have recently reported that the P2Y

Indexed as

Hantavirus InfectionsUp-RegulationAdultAgedCapillary PermeabilityFemaleFibrinolysisHantavirus Pulmonary SyndromeHumansImmunohistochemistryInflammationLeukocytesLungMaleMiddle AgedNew MexicoPlasminogen Activator Inhibitor 1PLAT protein, humanReceptors, Purinergic P2Y2SERPINE1 protein, humanTissue Plasminogen ActivatorUrokinase-Type Plasminogen ActivatorHantatvirus cardiopulmonary syndromeHCPSimmunohistochemistryintegrin activationP2Y2RPAI-1uPAzymography

Identifiers

PMID29930915
PMCPMC6001748
OpenAlexW2802971089

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.