Evidence map›Paper›PMID 32183316›Full record

Trial reportNutrients2020

Plasma Levels of the Bioactive Sphingolipid Metabolite S1P in Adult Cystic Fibrosis Patients: Potential Target for Immunonutrition?

Emina Halilbasic, Elisabeth Fuerst, Denise Heiden, Lukasz Japtok, Susanne C Diesner, Michael Trauner, Askin Kulu, Peter Jaksch, Konrad Hoetzenecker, Burkhard Kleuser and 2 more

Open access · goldAbstract readClinical TrialComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Article
  3. Involvement of Ceramide Metabolism in Cerebral Ischemia.Frontiers in molecular biosciences · 2022
    Review
  4. Article
  5. Review
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

12 authors at 2 institutions in 2 countries.

Emina HalilbasicDivision of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-4878-1470
Elisabeth FuerstInstitute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Denise HeidenInstitute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, 1090 Vienna, Austria.
Lukasz JaptokInstitute of Nutritional Science, Faculty of Mathematics and Natural Science, University of Potsdam, 14558 Nuthetal, Germany.
Susanne C DiesnerDepartment of Pediatrics and Adolescent Medicine, Medical University of Vienna, 1090 Vienna, Austria.
Michael TraunerDivision of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, 1090 Vienna, Austria.
Askin KuluDivision of Thoracic Surgery, Department of Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Peter JakschDivision of Thoracic Surgery, Department of Surgery, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-4635-3242
Konrad HoetzeneckerDivision of Thoracic Surgery, Department of Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Burkhard KleuserInstitute of Nutritional Science, Faculty of Mathematics and Natural Science, University of Potsdam, 14558 Nuthetal, Germany.ORCID 0000-0002-1888-9595
Lili Kazemi-ShiraziDivision of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, 1090 Vienna, Austria.
Eva UntersmayrInstitute of Pathophysiology and Allergy Research, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-1963-499X
Medical University of Vienna · ATUniversity of Potsdam · DE

Funding

Austrian Science Fund KLI 284
6 · The paper itself

Abstract

Recent research has linked sphingolipid (SL) metabolism with cystic fibrosis transmembrane conductance regulator (CFTR) activity, affecting bioactive lipid mediator sphingosine-1-phosphate (S1P). We hypothesize that loss of CFTR function in cystic fibrosis (CF) patients influenced plasma S1P levels. Total and unbound plasma S1P levels were measured in 20 lung-transplanted adult CF patients and 20 healthy controls by mass spectrometry and enzyme-linked immunosorbent assay (ELISA). S1P levels were correlated with CFTR genotype, routine laboratory parameters, lung function and pathogen colonization, and clinical symptoms. Compared to controls, CF patients showed lower unbound plasma S1P, whereas total S1P levels did not differ. A positive correlation of total and unbound S1P levels was found in healthy controls, but not in CF patients. Higher unbound S1P levels were measured in ΔF508-homozygous compared to ΔF508-heterozygous CF patients (

Indexed as

Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorHeterozygoteHomozygoteIntestinal DiseasesLung TransplantationLysophospholipidsAdultFemaleHumansLungMaleMiddle AgedSphingosineCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorLysophospholipidsSphingosinesphingosine 1-phosphatecystic fibrosishigh density lipoproteinsimmunonutritionintestinesphingolipidssphingosine-1-phosphateΔF508 mutation

Identifiers

PMID32183316
PMCPMC7146441
OpenAlexW3011809788

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.