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Related Concept Videos

What is Monogastric Digestion?01:50

What is Monogastric Digestion?

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The human body contains a monogastric digestive system. In a monogastric digestive system, the stomach only contains one chamber in which it digests food. Several other animal species also have monogastric digestive systems, including pigs, horses, dogs, and birds. This chapter, however, focuses on the human digestive system.
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Mutagenicity and Carcinogenicity01:25

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Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
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Gastric Phase of Digestion01:26

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The gastric phase of digestion begins as soon as food enters the stomach. The incoming food bolus triggers neural and hormonal mechanisms, which last approximately 3 to 4 hours. During this phase, the stomach undergoes significant changes to prepare the food for further digestion and absorption.
When food enters the stomach, it stretches the stomach walls and activates stretch receptors. This triggers local reflexes of the enteric nervous system, mediated through the myenteric plexus. These...
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Mucosal Barrier of the Stomach01:25

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The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
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Gastritis-II: Pathophysiology01:17

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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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Gastritis II: Pathophysiology01:26

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The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
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Related Experiment Video

Updated: May 5, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
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Mutagenicity in gastric juice.

D L Morris, D Youngs, T J Muscroft

    Gut
    |July 1, 1984
    PubMed
    Summary

    Gastric ulcer, carcinoma, and post-gastric resection patients showed increased gastric juice mutagenicity. This mutagenicity correlated with higher gastric pH and bacterial counts, not histidine levels.

    Area of Science:

    • Gastroenterology
    • Microbiology
    • Oncology

    Background:

    • Mutagenicity in gastric juice is a potential risk factor for gastric diseases.
    • Previous studies have explored various factors influencing gastric mutagenicity.

    Purpose of the Study:

    • To investigate mutagenicity levels in gastric juice across different patient groups.
    • To identify factors correlating with elevated gastric mutagenicity.

    Main Methods:

    • Employed the Ames bacteriological test system to assess mutagenicity in gastric juice samples.
    • Analyzed samples from 228 patients, including controls, duodenal ulcer, gastric ulcer, carcinoma, and post-gastric resection groups.
    • Correlated mutagenicity with gastric juice pH, bacterial count, and histidine concentration.

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    Main Results:

    • Significantly increased mutagenicity was observed in patients with gastric ulcer (p < 0.002), carcinoma (p < 0.002), and after gastric resection (p < 0.01) compared to controls.
    • A transient increase in mutagenicity was noted after H2 antagonist ingestion (p < 0.002).
    • Mutagenicity levels strongly correlated with gastric juice pH and bacterial count.

    Conclusions:

    • Gastric juice mutagenicity is elevated in specific gastrointestinal conditions, including gastric ulcer, carcinoma, and post-gastric resection.
    • Gastric pH and bacterial load are key determinants of gastric mutagenicity.
    • Histidine levels do not appear to explain the observed mutagenicity.