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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAZV3thdvaaKklGBOHVbbzNZVRbFUQ7fTMd8ueDSP_Og0#_4 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAZV3thdvaaKklGBOHVbbzNZVRbFUQ7fTMd8ueDSP_Og0#_3 http://www.w3.org/ns/prov#value Meng et al. [23] conducted a study to determine whether co-exposure to smoke and LPS enhanced inflammatory response and other pathological effects related to COPD development in mice (Table 3). The most up-regulated genes in the three groups were Mmp12 (matrix metalloproteinase 12, 18.2-fold) in the smoke group, serum amyloid A1 in the LPS (242.4-fold), and LPS–smoke group (167.7- fold). Marco (macrophage receptor with collagenous structure) was also up-regulated by LPS (14.8-fold) and LPS–smoke (25.5-fold) groups. 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