Publications by authors named "H J Egberts"

Hypotension reduces cerebral O(2) supply, which may result in brain cell damage and loss of brain cell function in the near-term neonate. The aim is to elucidate 1) to what extent the functional disturbance of the cerebral cortex, as measured with electrocortical brain activity (ECBA), is related to cerebral cortical tissue damage, as estimated by MAP2; and 2) whether there is a relationship between the glutamate, nitric oxide (NO), cGMP pathway and the development of cerebral cortical tissue damage after hemorrhagic hypotension. Seven lambs were delivered at 131 d of gestation.

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Tight junctional structure and macromolecular permeability were tested in four three-week-old piglets, experimentally infected with the enterotoxigenic Escherichia coli (ETEC) strain O149 K91 K88. Histologically, only minor microscopic evidence of inflammation and little or no architectural changes in the jejunal mucosa were observed. A significant decrease in tight junctional strand numbers occurred, without a concomitant decrease in tight junctional depth.

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Macromolecular permeability of the small intestine was tested in four 3-week-old gnotobiotic pigs inoculated with porcine rotavirus strain RV277 (group A). Pigs were administered 125I-labeled polyvinylpyrrolidone (molecular weight [mol wt], 40,000) orally 1 day before and 2 and 24 hours after virus inoculation, and blood samples were obtained every 6 hours. Eight hours after rotavirus inoculation, pigs had watery diarrhea.

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In this study, the morphology of the glycocalyx of small intestinal enterocytes in the rat was investigated after the induction of mucosal atrophy by methotrexate (MTX) in 18 Wistar rats. On the 2nd, 4th and 6th day after the intraperitoneal administration of MTX, a group of 6 rats was sacrificed and tissue specimens taken at the level of the Treitz' ligament were post fixed in a mixture of 2.0% watery osmiumtetroxide and 1.

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Peroxisomes are ubiquitous organelles containing enzyme sequences for beta oxidation of fatty acids, synthesis of bile acids, and ether phospholipids. In the inherited peroxisomal diseases one or more enzymes are deficient in hepatic, renal, and fibroblast peroxisomes. We have examined peroxisomes by light and electron microscopy in 29 duodenal biopsy specimens (21 with normal mucosa) after staining for catalase activity, a marker enzyme.

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