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Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...
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Although digestion of proteins, carbohydrates, and lipids may begin in the stomach, it is completed in the intestine. The absorption of nutrients, water, and electrolytes from food and drink also occurs in the intestine. The intestines can be divided into two structurally distinct organs—the small and large intestines.
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Lumber defects, which can affect both the appearance and structural integrity of wood, include a variety of growth and manufacturing flaws. Growth defects such as knots and knotholes occur where branches were once attached to the tree trunk, with knotholes forming when these knots fall out. Other natural defects include decay and insect damage, which compromise the wood's strength and durability.
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The small intestine is primarily responsible for digestion and nutrient absorption. It spans from the pyloric sphincter to the ileocecal valve and connects to the large intestine.
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The large intestine is divided into three main regions: the cecum, colon, and rectum. Extending from the ileocecal valve to the anus, it frames the small intestine on three sides.
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The large intestine, a vital component of the gastrointestinal tract, is structured with four main layers: the mucosa, submucosa, muscularis, and serosa. Each layer performs a distinct role in facilitating the smooth functioning of the large intestine.
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Lethal small intestinal herniation through a congenital mesenteric defect.

Karen Heath1,2, Roger W Byard3,4

  • 1Forensic Science SA, GPO Box 2790, Adelaide, 5001, Australia.

Forensic Science, Medicine, and Pathology
|August 3, 2018
PubMed
Summary

A rare congenital mesenteric defect caused fatal small intestine strangulation in a child. Mesenteric lymphadenopathy, possibly linked to viral infections, may have complicated the presentation.

Keywords:
Congenital mesenteric defectHerniationMesenteric lymphadenopathySmall intestinal obstructionSudden death

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Area of Science:

  • Pediatric Surgery
  • Gastroenterology
  • Pathology

Background:

  • Congenital mesenteric defects are rare internal hernias with a high risk of strangulation.
  • Nonspecific symptoms in children can delay diagnosis, leading to rapid deterioration.
  • Mesenteric lymphadenopathy can potentially impede spontaneous reduction of hernias.

Observation:

  • A three-year-old boy with mild respiratory symptoms and vomiting collapsed and died.
  • Autopsy revealed strangulation of the small intestine due to a congenital mesenteric defect.
  • Enlarged mesenteric lymph nodes were noted, with positive testing for human metapneumovirus and enterovirus.

Findings:

  • The cause of death was strangulation of the small intestine through a congenital mesenteric defect.
  • The presence of mesenteric lymphadenopathy was associated with viral infections (human metapneumovirus and enterovirus).
  • The lymphadenopathy may have contributed to the intestinal entrapment and strangulation.

Implications:

  • This case highlights the critical importance of considering rare internal hernias in pediatric patients with sudden collapse.
  • Early recognition and surgical intervention are crucial for managing transmesenteric hernias to prevent catastrophic outcomes.
  • The potential role of viral-induced lymphadenopathy in precipitating intestinal entrapment warrants further investigation.