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dc.contributor.authorTarnow, Inge
dc.contributor.authorMichelson, Alan D.
dc.contributor.authorFrelinger, Andrew L. III
dc.contributor.authorLinden, Matthew Dean
dc.contributor.authorLi, YouFu
dc.contributor.authorFox, Marsha L.
dc.contributor.authorBarnard, Marc R.
dc.contributor.authorO'Sullivan, Brian P.
dc.date2022-08-11T08:10:14.000
dc.date.accessioned2022-08-23T17:00:27Z
dc.date.available2022-08-23T17:00:27Z
dc.date.issued2007-05-29
dc.date.submitted2012-01-11
dc.identifier.citation<p>Thromb Res. 2007;121(2):159-62. Epub 2007 May 29. <a href="http://dx.doi.org/10.1016/j.thromres.2007.04.004">Link to article on publisher's site</a></p>
dc.identifier.issn0049-3848 (Linking)
dc.identifier.doi10.1016/j.thromres.2007.04.004
dc.identifier.pmid17532368
dc.identifier.urihttp://hdl.handle.net/20.500.14038/43800
dc.description.abstractINTRODUCTION: We have previously demonstrated platelet hyperreactivity in cystic fibrosis (CF) patients. Carriers of one CF mutation (heterozygotes) have been shown to have abnormalities related to the presence of only one-half the normal amount of CF transmembrane conductance regulator protein. Platelet hyperreactivity in CF heterozygotes would be an important cardiovascular risk factor, since approximately 1 in 25 Caucasians is a CF carrier. MATERIALS AND METHODS: We used highly sensitive assays of platelet activation to assess the difference between 16 CF heterozygotes and 16 age- and sex-matched healthy controls without CF mutations. RESULTS: We found no difference in platelet activation between CF heterozygotes and controls. CONCLUSIONS: The 50% reduction in the CF transmembrane conductance regulator protein in heterozygotes is insufficient to cause platelet activation.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17532368&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/j.thromres.2007.04.004
dc.subjectAdult
dc.subjectCase-Control Studies
dc.subjectCystic Fibrosis
dc.subjectCystic Fibrosis Transmembrane Conductance Regulator
dc.subjectFemale
dc.subject*Heterozygote
dc.subjectHumans
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectPlatelet Activation
dc.subjectPlatelets
dc.subjectCystic fibrosis
dc.subjectFlow cytometry
dc.subjectCystic fibrosis carriers
dc.subjectPlatelet function
dc.subjectAllergy and Immunology
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectCongenital, Hereditary, and Neonatal Diseases and Abnormalities
dc.subjectDigestive System Diseases
dc.subjectGenetic Phenomena
dc.subjectHematology
dc.subjectInvestigative Techniques
dc.subjectPediatrics
dc.subjectRespiratory Tract Diseases
dc.titleCystic fibrosis heterozygotes do not have increased platelet activation
dc.typeJournal Article
dc.source.journaltitleThrombosis research
dc.source.volume121
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/peds_pulmonary/16
dc.identifier.contextkey2441376
html.description.abstract<p>INTRODUCTION: We have previously demonstrated platelet hyperreactivity in cystic fibrosis (CF) patients. Carriers of one CF mutation (heterozygotes) have been shown to have abnormalities related to the presence of only one-half the normal amount of CF transmembrane conductance regulator protein. Platelet hyperreactivity in CF heterozygotes would be an important cardiovascular risk factor, since approximately 1 in 25 Caucasians is a CF carrier.</p> <p>MATERIALS AND METHODS: We used highly sensitive assays of platelet activation to assess the difference between 16 CF heterozygotes and 16 age- and sex-matched healthy controls without CF mutations.</p> <p>RESULTS: We found no difference in platelet activation between CF heterozygotes and controls.</p> <p>CONCLUSIONS: The 50% reduction in the CF transmembrane conductance regulator protein in heterozygotes is insufficient to cause platelet activation.</p>
dc.identifier.submissionpathpeds_pulmonary/16
dc.contributor.departmentDepartment of Pediatrics
dc.source.pages159-62


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