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Related Concept Videos

Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid receptor...
Infection01:20

Infection

When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
Intestinal Obstruction II: Pathophysiology01:07

Intestinal Obstruction II: Pathophysiology

Intestinal obstruction triggers a series of physiological responses, starting with gas and fluid accumulation in the bowel segment proximal to the obstruction, leading to distension. This distended intestine compresses the diaphragm, hindering lung expansion and potentially leading to reduced respiratory effort, atelectasis, and pneumonia.To overcome the blockage, the gut intensifies contractions, causing colicky abdominal pain, nausea, and vomiting, which reduces fluid and food intake and...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...

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Related Experiment Video

Updated: Jun 3, 2026

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome
06:51

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Published on: July 28, 2023

Pathogenesis and prevention of necrotizing enterocolitis.

Jessie A Morgan1, Lauren Young, William McGuire

  • 1Centre for Reviews and Dissemination, Hull York Medical School, University of York, Heslington, York, UK.

Current Opinion in Infectious Diseases
|April 2, 2011
PubMed
Summary

Necrotizing enterocolitis (NEC) is a serious gastrointestinal disorder in preterm infants. While human milk feeding is protective, preventing NEC requires further research into probiotics and avoiding certain medications.

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Breast Milk Enhances Growth of Enteroids: An Ex Vivo Model of Cell Proliferation
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Breast Milk Enhances Growth of Enteroids: An Ex Vivo Model of Cell Proliferation

Published on: February 15, 2018

Related Experiment Videos

Last Updated: Jun 3, 2026

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome
06:51

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Published on: July 28, 2023

Breast Milk Enhances Growth of Enteroids: An Ex Vivo Model of Cell Proliferation
09:02

Breast Milk Enhances Growth of Enteroids: An Ex Vivo Model of Cell Proliferation

Published on: February 15, 2018

Area of Science:

  • Neonatalogy
  • Gastroenterology
  • Pediatric Surgery

Background:

  • Necrotizing enterocolitis (NEC) is the most frequent serious acquired gastrointestinal disorder in preterm infants.
  • It is a significant cause of mortality and morbidity, with risk inversely proportional to gestational age and birth weight.

Purpose of the Study:

  • To review recent advances in understanding NEC pathogenesis.
  • To consider implications for clinical practice and future research.

Main Methods:

  • Literature review of recent advances in NEC pathogenesis.
  • Analysis of risk factors and potential preventative interventions.

Main Results:

  • Key risk factors include prematurity, fetal growth restriction, formula feeding, rapid enteral feed advancement, and H2-receptor antagonist exposure.
  • Severe NEC and invasive infections are linked to acute morbidity, mortality, and adverse neurodevelopmental outcomes.

Conclusions:

  • Understanding NEC pathogenesis remains incomplete.
  • Limited evidence supports interventions beyond human milk feeding.
  • Prebiotics, probiotics, and avoiding H2-receptor antagonists show promise for NEC prevention and warrant further RCT evaluation.