ArticleThe Journal of surgical research2013
Endotoxin-induced changes in phospholipid dynamics of the stomach.
Article in The Journal of surgical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Cardiolipins Act as a Selective Barrier to Toll-Like Receptor 4 Activation in the Intestine.Applied and environmental microbiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe gastric mucosa is protected in part by a hydrophobic layer of phosphatidylcholine (PC) that overlies the mucus gel on the stomach. Endotoxin treatment (i.e., lipopolysaccharide [LPS]) results in an apparent disruption of this layer, as evidenced by a reduction in surface hydrophobicity and an increase in transmural permeability. The current studies compared PC and lyso-PC levels in mucus and gastric mucosa before and after LPS treatment, and examined potential mechanisms for surface phospholipid changes.
methodsRats were administered LPS (5 mg//kg, intraperitoneally) and samples were collected after 5 h for analysis of PC and its primary degradant, lyso-PC, in the loosely and firmly adherent mucus layers and the mucosa. The dependence of LPS-induced effects on gastric alkalinization, PC synthetic activity, and intestinal reflux material was assessed.
resultsThe gastric contents after LPS, which also contained duodenal reflux material, had greatly increased amounts of PC and lyso-PC. The firmly adherent mucus layer was unchanged. The gastric mucosa after LPS revealed significant reductions of PC levels and no change in lyso-PC content. These phospholipid changes were not caused by alkalinization of the stomach or altered PC synthesis. Prevention of duodenogastric reflux by pylorus ligation blocked the LPS-induced increase in luminal lyso-PC and the reduction in mucosal PC.
conclusionsLPS appears to induce a release of PC from gastric mucosa into the lumen, along with degradation of PC to lyso-PC, without an effect on PC synthesis. Component(s) of intestinal reflux material appear to be required for these effects. The lowered PC levels in gastric mucosa after LPS may contribute to reduced barrier properties of this tissue.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.