Evidence map›Paper›PMID 32144123›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2020

NO-Releasing Nanoparticles Ameliorate Detrusor Overactivity in Transgenic Sickle Cell Mice via Restored NO/ROCK Signaling.

Serkan Karakus, Biljana Musicki, Mahantesh S Navati, Joel M Friedman, Kelvin P Davies, Arthur L Burnett

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Serkan KarakusThe James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins, University School of Medicine, Baltimore, Maryland (S.K., B.M., A.L.B.); and Departments of Physiology and Biophysics (M.S.N., J.M.F., K.P.D.) and Urology (K.P.D.), Albert Einstein College of Medicine, New York, New York skaraku2@jhmi.edu.ORCID 0000-0001-8913-5822
Biljana MusickiThe James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins, University School of Medicine, Baltimore, Maryland (S.K., B.M., A.L.B.); and Departments of Physiology and Biophysics (M.S.N., J.M.F., K.P.D.) and Urology (K.P.D.), Albert Einstein College of Medicine, New York, New York.
Mahantesh S NavatiThe James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins, University School of Medicine, Baltimore, Maryland (S.K., B.M., A.L.B.); and Departments of Physiology and Biophysics (M.S.N., J.M.F., K.P.D.) and Urology (K.P.D.), Albert Einstein College of Medicine, New York, New York.
Joel M FriedmanThe James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins, University School of Medicine, Baltimore, Maryland (S.K., B.M., A.L.B.); and Departments of Physiology and Biophysics (M.S.N., J.M.F., K.P.D.) and Urology (K.P.D.), Albert Einstein College of Medicine, New York, New York.
Kelvin P DaviesThe James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins, University School of Medicine, Baltimore, Maryland (S.K., B.M., A.L.B.); and Departments of Physiology and Biophysics (M.S.N., J.M.F., K.P.D.) and Urology (K.P.D.), Albert Einstein College of Medicine, New York, New York.
Arthur L BurnettThe James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins, University School of Medicine, Baltimore, Maryland (S.K., B.M., A.L.B.); and Departments of Physiology and Biophysics (M.S.N., J.M.F., K.P.D.) and Urology (K.P.D.), Albert Einstein College of Medicine, New York, New York.
Albert Einstein College of Medicine · US

Funding

Dysregulatory NOS Nexus for Erectile and Voiding DisordersR56DK114095 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI BURNETT, ARTHUR LOUIS · 2018 to 2018
$100k
NIDDK NIH HHS R56 DK114095
6 · The paper itself

Abstract

Sickle cell disease (SCD) is associated with overactive bladder (OAB). Detrusor overactivity, a component of OAB, is present in an SCD mouse, but the molecular mechanisms for this condition are not well-defined. We hypothesize that nitric oxide (NO)/ ras homolog gene family (Rho) A/Rho-associated kinase (ROCK) dysregulation is a mechanism for detrusor overactivity and that NO-releasing nanoparticles (NO-nps), a novel NO delivery system, may serve to treat this condition. Male adult SCD transgenic, combined endothelial NO synthases (eNOSs) and neuronal NOS (nNOS) gene-deficient (dNOS

Indexed as

Anemia, Sickle CellAnimalsMaleMiceMice, Inbred C57BLMice, TransgenicNanoparticlesNitric OxideNitric Oxide SynthasePhosphorylationrhoA GTP-Binding Proteinrho-Associated KinasesSignal TransductionUrinary Bladder, OveractiveNitric OxideNitric Oxide SynthaserhoA GTP-Binding ProteinRhoA protein, mouserho-Associated Kinases

Identifiers

PMID32144123
PMCPMC7160861
OpenAlexW3009208078

What Socratic 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 Socratic graph.