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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesions in the peritoneal cavity have been implicated in the cause of intestinal obstruction and infertility, but their role in the aetiology of chronic pelvic pain is unclear. Nerves have been demonstrated in human pelvic adhesions, but the presence of pain-conducting fibres has not been established. The purpose of this study was to use an animal model to examine the growth of nerves during adhesion formation at various times following injury and to characterize the types of fibres present. Adhesions were generated in mice by injuring the surface of the caecum and adjacent abdominal wall, with apposition. At 1-8 weeks post-surgery, adhesions were processed and nerve fibres characterized histologically, immunohistochemically, and ultrastructurally. Peritoneal adhesions had consistently formed by 1 week after surgery and from 2 weeks onwards, all adhesions contained some nerve fibres which were synaptophysin, calcitonin gene-related peptide, and substance P-immunoreactive, and were seen to originate from the caecum. By 4 weeks post-surgery, nerve fibres were found to originate from both the caecum and the abdominal wall, and as demonstrated by acetylcholinesterase histochemistry, many traversed the entire adhesion. Ultrastructural analysis showed both myelinated and non-myelinated nerve fibres within the adhesion. This study provides the first direct evidence for the growth of sensory nerve fibres within abdominal visceral adhesions in a murine model and suggests that there may be nerve fibres involved in the conduction of pain stimuli.
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PMID:Growth of nerve fibres into murine peritoneal adhesions. 1105 24

The cell adhesion and neurite outgrowth-promoting function of acetylcholinesterase has been localised to the area of the peripheral anionic site. In order to precisely determine the site involved, we used synthetic peptides representing sequences of the peripheral anionic site and its surrounds, and investigated their binding to a panel of monoclonal antibodies that inhibit cell adhesion/neurite outgrowth and/or to recognise the peripheral anionic site. Binding to laminin-1 and collagen IV was also investigated. A relationship between recognition of the sequence 37-50, representing a surface loop adjacent to the peripheral anionic site, and the degree of inhibition of cell adhesion was observed; both laminin-1 and collagen IV also bound this loop with high affinity. Neurite outgrowth on coverslips coated with this peptide was similar to those coated with acetylcholinesterase itself. Adhesion-inhibiting antibodies also recognised the omega loop 69-96, as did laminin-1 and collagen IV. Laminin also bound the sequences 55-66 and 340-353, recognised by the antibodies to varying degrees, but collagen did not. All these peptides were able to promote neurite outgrowth to some degree. No binding to the amyloid-binding omega loop 275-304 by the ligands was observed, nor did the antibodies recognise this consistently. No relationship was observed between the degree of inhibition of acetylcholinesterase and inhibition of neurite outgrowth by the antibodies from which we conclude that the neurite outgrowth function is non-cholinergic. In conclusion, we have identified a specific conformational structure on acetylcholinesterase, comprising adjacent surface loops between residues 37-50 and 69-96, with additional involvement of the sequences 55-66 and 340-353, that mediates cell adhesion and neurite outgrowth.
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PMID:Identification of a structural site on acetylcholinesterase that promotes neurite outgrowth and binds laminin-1 and collagen IV. 1517 27