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1

Campylobacter spp. - a significant microbiological hazard in food. II. Lesions and infection development, pathogenic mechanisms and complications

100%
Wysok B., Uradzinski J.
Polish Journal of Veterinary Sciences
|
2009
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tom 12
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nr 2
285-291
Infections with Campylobacter spp. occur as a result of consumption of live cells with food. In developing countries those infections are immensely common, particularly during early childhood and 5 to 10 cases can appear during the initial two years of life. The symptoms appear usually after 1-7 days from infection depending on the number of ingested cells and individual sensitivity. Characteristic symptoms of infections caused by Campylobacter spp. infrequently occurring jointly in the clinical form of the disease include: diarrhea, abdominal pain and increased temperature. In the majority of cases the disease is mild and lasts from 2 to 7 days. Usually Campylobacter are excreted with feces during a period of 7-21 days, sometimes even longer. Occasionally in the increased risk group dangerous complications may occur. They include: bacteremia, meningo-myelitis, neurological disturbances and reactive arthritis.
2
Content available remote

Role of COX inhibition in pathogenesis of NSAID-induced small intestinal damage

100%
Takeuchi K., Tanaka A., Ohno R., Yokota A.
Journal of Physiology and Pharmacology. Supplement
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2003
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tom 54
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nr 4
165-182
Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin decrease mucosal PGE2 production by inhibiting cyclooxygenase (COX) activity and produce damage in the small intestine. The development of intestinal lesions as induced by indomethacin was accompanied by increases in intestinal motility, enterobacterial invasion, and myeloperoxidase (MPO) as well as inducible nitric oxide synthase (iNOS) activity, together with the up-regulation of COX-2 and iNOS mRNA expression. Neither the selective COX-1 inhibitor, SC-560, nor the selective COX-2 inhibitor, rofecoxib, alone caused intestinal damage, but their combined administration produced lesions. SC-560, but not rofecoxib, caused intestinal hypermotility, bacterial invasion and the expression of COX-2 as well as iNOS mRNAs, yet the iNOS and MPO activity was increased only when rofecoxib was administered together with SC-560. Although SC-560 inhibited the PG production, the level of PGE2 was recovered, in a rofecoxib-dependent manner. The intestinal hypermotility response to indomethacin was prevented by both 16,16-dimethyl PGE2 and atropine but not ampicillin, yet all these agents inhibited not only the bacterial invasion but also the expression of COX-2 as well as the iNOS activity in the intestinal mucosa following indomethacin treatment, resulting in preventing the intestinal lesions. These results suggest that inhibition of COX-1, despite causing intestinal hypermotility, bacterial invasion and iNOS expression, up-regulates the expression of COX-2, and the PGE2 derived from COX-2 counteracts deleterious events caused by COX-1 inhibition and maintains the mucosal integrity. These sequences of events explain why intestinal damage occurs when both COX-1 and COX-2 are inhibited.
3

Pathogenetic mechanisms of atopic dermatitis

80%
Pastore S., Mascia F., Giustizieri M. L., Giannetti A., Girolomoni G.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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tom 48
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nr 6 Spec.Iss.
497-504
4
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Nitric oxide, superoxide radicals and mast cells in pathogenesis of indomethacin-induced small intestinal lesions in rats

80%
Konaka A., Nishijima M., Tanaka A., Kunikata T., Kato S., Takeuchi K.
Journal of Physiology and Pharmacology
|
1999
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tom 50
|
nr 1
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