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be potentially associated with the milder phenotype. One on chr.1, defined by marker D1Mit36, one on chr. 9 defined by marker D9Mit90, and one on chr. 10, defined by marker D10Mit14.\n\nConclusion\nPotential modifier regions were found that have a positive impact on the inflammatory phenotype of the CF mouse small intestine and animal survival. Identification of polymorphisms in specific genes in these regions should provide important new information about genetic modifiers of the CF intestinal phenotype.\n\nBackground\nCystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene [1]. Different mutations have a range of effects on the levels of CFTR protein and its proper functioning in epithelial transport of Cl- and HCO3- [2,3]. The severity of the pancreatic phenotype in human CF is well correlated with the extent of impaired CFTR function caused by specific mutations. Loss of CFTR function results in destruction of the exocrine tissue and eventual pancreatic insufficiency. 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    craft-ca-core-ex-dev

    {"project":"craft-ca-core-ex-dev","denotations":[{"id":"T702","span":{"begin":997,"end":1003},"obj":"UBERON:0000479"},{"id":"T703","span":{"begin":1017,"end":1027},"obj":"UBERON:0001264"},{"id":"T704","span":{"begin":1083,"end":1089},"obj":"UBERON:0000062"},{"id":"T705","span":{"begin":1104,"end":1111},"obj":"UBERON:0001005"},{"id":"T706","span":{"begin":1116,"end":1126},"obj":"UBERON:0000160"},{"id":"T707","span":{"begin":1165,"end":1169},"obj":"PR_EXT:000001044"},{"id":"T708","span":{"begin":1170,"end":1179},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T125","span":{"begin":63,"end":67},"obj":"GO_SO_EXT:chromosome"},{"id":"T126","span":{"begin":81,"end":87},"obj":"CHEBI_SO_EXT:molecular_indicator_or_label_or_marker_or_tag"},{"id":"T127","span":{"begin":104,"end":108},"obj":"GO_SO_EXT:chromosome"},{"id":"T128","span":{"begin":122,"end":128},"obj":"CHEBI_SO_EXT:molecular_indicator_or_label_or_marker_or_tag"},{"id":"T129","span":{"begin":149,"end":153},"obj":"GO_SO_EXT:chromosome"},{"id":"T130","span":{"begin":169,"end":175},"obj":"CHEBI_SO_EXT:molecular_indicator_or_label_or_marker_or_tag"},{"id":"T131","span":{"begin":271,"end":283},"obj":"GO_PATO_EXT:inflammatory_process_or_quality"},{"id":"T132","span":{"begin":304,"end":309},"obj":"NCBITaxon:10088"},{"id":"T133","span":{"begin":310,"end":325},"obj":"UBERON:0002108"},{"id":"T134","span":{"begin":330,"end":336},"obj":"NCBITaxon:33208"},{"id":"T135","span":{"begin":365,"end":378},"obj":"SO_EXT:polymorphism"},{"id":"T136","span":{"begin":391,"end":396},"obj":"SO_EXT:0000704"},{"id":"T137","span":{"begin":461,"end":468},"obj":"SO_EXT:0000704"},{"id":"T138","span":{"begin":489,"end":499},"obj":"UBERON:0000160"},{"id":"T678","span":{"begin":557,"end":566},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T679","span":{"begin":574,"end":625},"obj":"PR_EXT:000001044"},{"id":"T680","span":{"begin":590,"end":615},"obj":"GO:0055085"},{"id":"T681","span":{"begin":595,"end":603},"obj":"GO:0016020"},{"id":"T682","span":{"begin":616,"end":625},"obj":"GO_EXT:regulator"},{"id":"T683","span":{"begin":627,"end":631},"obj":"PR_EXT:000001044"},{"id":"T684","span":{"begin":633,"end":637},"obj":"SO_EXT:0000704"},{"id":"T685","span":{"begin":653,"end":662},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T686","span":{"begin":704,"end":708},"obj":"PR_EXT:000001044"},{"id":"T687","span":{"begin":709,"end":716},"obj":"CHEBI_PR_EXT:protein"},{"id":"T688","span":{"begin":747,"end":757},"obj":"UBERON:0000483"},{"id":"T689","span":{"begin":758,"end":774},"obj":"GO:0006821"},{"id":"T690","span":{"begin":758,"end":770},"obj":"_FRAGMENT"},{"id":"T691","span":{"begin":779,"end":784},"obj":"GO:0015701"},{"id":"T692","span":{"begin":771,"end":774},"obj":"CHEBI:17996"},{"id":"T693","span":{"begin":779,"end":784},"obj":"CHEBI:17544"},{"id":"T694","span":{"begin":812,"end":822},"obj":"UBERON:0001264"},{"id":"T695","span":{"begin":836,"end":841},"obj":"NCBITaxon:9606"},{"id":"T696","span":{"begin":892,"end":896},"obj":"PR_EXT:000001044"},{"id":"T697","span":{"begin":925,"end":934},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T698","span":{"begin":944,"end":948},"obj":"PR_EXT:000001044"},{"id":"T699","span":{"begin":969,"end":983},"obj":"_FRAGMENT"},{"id":"T700","span":{"begin":997,"end":1003},"obj":"GO:0016271"},{"id":"T701","span":{"begin":988,"end":996},"obj":"UBERON:0002330"}],"relations":[{"id":"R374","pred":"_lexicallyChainedTo","subj":"T691","obj":"T690"},{"id":"R375","pred":"_lexicallyChainedTo","subj":"T700","obj":"T699"}],"text":"to be potentially associated with the milder phenotype. One on chr.1, defined by marker D1Mit36, one on chr. 9 defined by marker D9Mit90, and one on chr. 10, defined by marker D10Mit14.\n\nConclusion\nPotential modifier regions were found that have a positive impact on the inflammatory phenotype of the CF mouse small intestine and animal survival. Identification of polymorphisms in specific genes in these regions should provide important new information about genetic modifiers of the CF intestinal phenotype.\n\nBackground\nCystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene [1]. Different mutations have a range of effects on the levels of CFTR protein and its proper functioning in epithelial transport of Cl- and HCO3- [2,3]. The severity of the pancreatic phenotype in human CF is well correlated with the extent of impaired CFTR function caused by specific mutations. Loss of CFTR function results in destruction of the exocrine tissue and eventual pancreatic insufficiency. On the other hand, the effects of CF on organs including the airways and intestines is less well correlated with specific CFTR mutations and their effects on C"}

    craft-ca-core-dev

    {"project":"craft-ca-core-dev","denotations":[{"id":"T610","span":{"begin":812,"end":822},"obj":"UBERON:0001264"},{"id":"T611","span":{"begin":836,"end":841},"obj":"NCBITaxon:9606"},{"id":"T612","span":{"begin":892,"end":896},"obj":"PR:000001044"},{"id":"T613","span":{"begin":944,"end":948},"obj":"PR:000001044"},{"id":"T614","span":{"begin":969,"end":983},"obj":"_FRAGMENT"},{"id":"T615","span":{"begin":997,"end":1003},"obj":"GO:0016271"},{"id":"T616","span":{"begin":988,"end":996},"obj":"UBERON:0002330"},{"id":"T617","span":{"begin":997,"end":1003},"obj":"UBERON:0000479"},{"id":"T618","span":{"begin":1017,"end":1027},"obj":"UBERON:0001264"},{"id":"T619","span":{"begin":1083,"end":1089},"obj":"UBERON:0000062"},{"id":"T620","span":{"begin":1104,"end":1111},"obj":"UBERON:0001005"},{"id":"T621","span":{"begin":1116,"end":1126},"obj":"UBERON:0000160"},{"id":"T622","span":{"begin":1165,"end":1169},"obj":"PR:000001044"},{"id":"T68","span":{"begin":304,"end":309},"obj":"NCBITaxon:10088"},{"id":"T69","span":{"begin":310,"end":325},"obj":"UBERON:0002108"},{"id":"T70","span":{"begin":330,"end":336},"obj":"NCBITaxon:33208"},{"id":"T71","span":{"begin":391,"end":396},"obj":"SO:0000704"},{"id":"T72","span":{"begin":461,"end":468},"obj":"SO:0000704"},{"id":"T73","span":{"begin":489,"end":499},"obj":"UBERON:0000160"},{"id":"T598","span":{"begin":574,"end":625},"obj":"PR:000001044"},{"id":"T599","span":{"begin":590,"end":615},"obj":"GO:0055085"},{"id":"T600","span":{"begin":595,"end":603},"obj":"GO:0016020"},{"id":"T601","span":{"begin":627,"end":631},"obj":"PR:000001044"},{"id":"T602","span":{"begin":633,"end":637},"obj":"SO:0000704"},{"id":"T603","span":{"begin":704,"end":708},"obj":"PR:000001044"},{"id":"T604","span":{"begin":747,"end":757},"obj":"UBERON:0000483"},{"id":"T605","span":{"begin":758,"end":774},"obj":"GO:0006821"},{"id":"T606","span":{"begin":758,"end":770},"obj":"_FRAGMENT"},{"id":"T607","span":{"begin":779,"end":784},"obj":"GO:0015701"},{"id":"T608","span":{"begin":771,"end":774},"obj":"CHEBI:17996"},{"id":"T609","span":{"begin":779,"end":784},"obj":"CHEBI:17544"}],"relations":[{"id":"R372","pred":"_lexicallyChainedTo","subj":"T607","obj":"T606"},{"id":"R373","pred":"_lexicallyChainedTo","subj":"T615","obj":"T614"}],"text":"to be potentially associated with the milder phenotype. One on chr.1, defined by marker D1Mit36, one on chr. 9 defined by marker D9Mit90, and one on chr. 10, defined by marker D10Mit14.\n\nConclusion\nPotential modifier regions were found that have a positive impact on the inflammatory phenotype of the CF mouse small intestine and animal survival. Identification of polymorphisms in specific genes in these regions should provide important new information about genetic modifiers of the CF intestinal phenotype.\n\nBackground\nCystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene [1]. Different mutations have a range of effects on the levels of CFTR protein and its proper functioning in epithelial transport of Cl- and HCO3- [2,3]. The severity of the pancreatic phenotype in human CF is well correlated with the extent of impaired CFTR function caused by specific mutations. Loss of CFTR function results in destruction of the exocrine tissue and eventual pancreatic insufficiency. On the other hand, the effects of CF on organs including the airways and intestines is less well correlated with specific CFTR mutations and their effects on C"}