http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc#head http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc http://www.nanopub.org/nschema#hasAssertion http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc#assertion http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc http://www.nanopub.org/nschema#hasProvenance http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc#provenance http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc http://www.nanopub.org/nschema#hasPublicationInfo http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc#publicationInfo http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc http://www.w3.org/1999/02/22-rdf-syntax-ns#type http://www.nanopub.org/nschema#Nanopublication http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc#assertion http://rdf.disgenet.org/resource/gda/DGN584c63e3ec69f125f6e812dc0a464157 http://semanticscience.org/resource/SIO_000628 http://identifiers.org/ncbigene/2520 http://rdf.disgenet.org/resource/gda/DGN584c63e3ec69f125f6e812dc0a464157 http://semanticscience.org/resource/SIO_000628 http://linkedlifedata.com/resource/umls/id/C0333293 http://rdf.disgenet.org/resource/gda/DGN584c63e3ec69f125f6e812dc0a464157 http://www.w3.org/1999/02/22-rdf-syntax-ns#type http://semanticscience.org/resource/SIO_001123 http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc#provenance http://rdf.disgenet.org/resource/nanopub/NP420825.RAWGZ2duVnG4R9MpQt0PQUUPclllG98dFPokLBdtTpiwc#assertion http://purl.org/dc/terms/description [We conclude that 1) HP infected gastric ulcer margin coexpresses gastrin, its receptors (CCK(B)-R), and COX-2; 2) HP infection may be implicated in gastric ulceration via increased release of gastrin that could be responsible for the overexpression of COX-2 that in turn could help ulcer healing through the stimulation of mucosal cell growth, restoration of the glandular structure and angiogenesis in the ulcer area and 3) gastrin produced in HP infected antral mucosa seems to be involved in the induction of COX-2 and PG production by this enzyme and this may contribute to the ulcer healing.]. 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