Evidence map›Paper›PMID 8070900›Full record

ArticleInflammation1994

Decreased production of nitric oxide by human neutrophils during septic multiple organ dysfunction syndrome. Comparison with endotoxin and cytokine effects on normal cells.

M C Carreras, S D Catz, G A Pargament, C G Del Bosco, J J Poderoso

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Inflammation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

4 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Cytokine-treated human neutrophils contain inducible nitric oxide synthase that produces nitration of ingested bacteria.Proceedings of the National Academy of Sciences of the United States of America · 1996
    Article
  4. Oxidative stress in rodent closed duodenal loop pancreatitis.International journal of pancreatology : official journal of the International Association of Pancreatology · 1996
    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

5 authors at 1 institution in 1 country.

M C CarrerasLaboratory of Oxygen Metabolism, University Hospital School of Medicine, University of Buenos Aires, Argentina.
S D Catz
G A Pargament
C G Del Bosco
J J Poderoso
University of Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The objective of this study was to determine nitric oxide (NO) and superoxide anion release (O-2) by neutrophils (PMNs) in the septic multiple organ dysfunction syndrome (MODS) and to compare them with the response of normal cells to lipopolysaccharide (LPS) and cytokines. NO production was measured by the release of nitrites in the medium, its maximal production rate by a modified oxyhemoglobin assay and O-2 by standard methods. Normal cells were incubated with LPS, gamma interferon (IFN-gamma), or tumor necrosis factor (TNF-alpha) alone or in combination. Results showed that PMN release of both NO and O-2 was reduced in septic samples; in contrast, an association of LPS, IFN-gamma, and TNF-alpha promoted maximal NO release by normal cells (40-50%). We conclude that while interaction of normal PMNs with cytokines increases NO and O-2 release, progression of sepsis to a multiple organ dysfunction impairs these responses in both functions.

Indexed as

AdultAgedAnionsBacterial InfectionsCytokinesEndotoxinsFemaleHumansMaleMiddle AgedNeutrophilsNitric OxideOxygen ConsumptionSuperoxidesAnionsCytokinesEndotoxinsNitric OxideSuperoxides

Identifiers

PMID8070900
OpenAlexW2020876412

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.