Trial reportDigestive diseases and sciences1997
Transforming growth factor-alpha (TGF-alpha) levels in human proximal gastrointestinal epithelium. Effect of mucosal injury and acid inhibition.
Trial report in Digestive diseases and sciences, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed, 8 citations in OpenAlex.
- Novel mechanistic insights into ectodomain shedding of EGFR Ligands Amphiregulin and TGF-α: impact on gastrointestinal cancers driven by secondary bile acids.Cancer research · 2014Article
- Comparison of the antisecretory and antiulcer activity of epidermal growth factor, urogastrone and transforming growth factor alpha and its derivative in rodents in vivo.Molecular and cellular biochemistry · 2002Article
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
No grant is acknowledged in the PubMed record.
Abstract
TGF-alpha inhibits gastric acid secretion and may play an important role in epithelial repair. We quantitated regional levels of TGF-alpha in the human proximal gastrointestinal tract and determined whether they are affected by acid suppression or aspirin-induced injury. Ten healthy volunteers were studied. After baseline endoscopy with biopsy, five randomly received no treatment, aspirin, omeprazole, or cimetidine for one week. Endoscopy was repeated and prior unhealed biopsy sites quantitated. TGF-alpha levels were measured by RIA. Five additional subjects then completed an extended protocol of three weeks duration. All subjects were free of H. pylori infection. TGF-alpha levels in the antrum, 34.76 +/- 5.54 pg TGF-alpha/micrograms DNA were threefold higher than in the gastric body and duodenum (11.03 +/- 2.60 and 10.41 +/- 1.64 respectively, P < 0.01). The number of unhealed sites in the aspirin group was significantly greater than in the control or acid inhibition groups; however, TGF-alpha levels were not different from-the surrounding mucosa. TGF-alpha increased in the controls after biopsy; the increase was significant in the body at week 2 only. Aspirin significantly increased TGF-alpha levels in the gastric body and duodenum after one week. The rise in antral TGF-alpha appeared delayed and blunted by the aspirin treatment compared to control. There was no relationship between the number of visible biopsy sites, degree of aspirin-induced injury, and the TGF-alpha level. Acid suppression was associated with a significant increase in TGF-alpha in the gastric body and antrum at one week. Immunochemical staining did not demonstrate differences in proliferation in any treatment group compared to controls. TGF-alpha levels vary by location in the proximal gastrointestinal tract, with significantly greater levels in the antrum. After biopsy, TGF-alpha levels increase; short-term aspirin and acid inhibitors modulate this effect. Aspirin significantly impaired the healing of endoscopic biopsies in the antrum; however, this was not associated with changes in TGF-alpha levels. TGF-alpha levels did not change in response to acid secretory state. Further studies of mucosal levels of TGF-alpha in response to aspirin-induced injury in humans appear warranted.
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