The Australian Journal of Medical Science, May 1, 2004
Cardiac troponin I is a powerful tool to aid in the diagnosis of myocardial infarction and cardia... more Cardiac troponin I is a powerful tool to aid in the diagnosis of myocardial infarction and cardiac muscle damage, and is widely used in clinical practice. It is currently one of the best cardiac markers for a definitive diagnosis, with positive results being highly indicative of ...
The purpose of this study was to determine if the cardiac troponin I (cTnI) assay utilising Dade ... more The purpose of this study was to determine if the cardiac troponin I (cTnI) assay utilising Dade Behring's Dimension RxL was sensitive to heparin or ethylenediaminetetraacetic acid (EDTA) interference, and to ascertain if these additives influence cTnI recovery after storage at 2 - 8 C and -20 C. Seventy-three triplicate samples were analysed to compare cTnI values to those obtained in serum. Forty-five additional samples were used to examine sample stability. Serum, heparin plasma and EDTA plasma samples all show similar levels of imprecision at comparable cTnI concentrations. Heparin plasma samples were on average 0.017 g/L higher than the corresponding serum values. EDTA plasma samples were on average 0.185 g/L lower than the corresponding serum values. Across the grey area range of 0.10 - 1.50 g/L cTnI, heparin values were 0.021 g/L higher than serum, and EDTA values were 0.078 g/L higher. After storage at 2 - 8 C, heparin plasma samples showed a significant decrease in cTnI...
Introduction: Reactive oxygen species (ROS) are thought to play a central role in the genesis of ... more Introduction: Reactive oxygen species (ROS) are thought to play a central role in the genesis of arrhythmia. Mitochondria are the major source of cardiac ROS. Studies suggest ROS activates c-Src tyrosine kinase, which reduces Cx43 at the gap junctions by competing with Cx43 for binding to Zonula Occludence-1. We sought to determine the role of mitochondria oxidative stress in the genesis of ventricular arrhythmia in a manganese superoxide dismutase (MnSOD) knock out mouse model. We hypothesized that excess ROS in this model would activate c-Src and reduce Cx43 levels and that inhibition of c-Src would prevent Cx43 remodeling and the risk of arrhythmia. Method: Wild type and MnSOD+/- mice with and without treatment with the c-Src inhibitor PP1 (1.5 mg/kg IP three times/week x 2 weeks) were studied. Western blotting and immunohistochemistry staining for Cx43 were performed. Mitochondrial ROS was measured by confocal microscopy and flow cytometry from isolated cardiomyocytes using mito...
Information about reprints can be found online at: Reprints: document. Permissions and Rights Que... more Information about reprints can be found online at: Reprints: document. Permissions and Rights Question and Answer about this process is available in the located, click Request Permissions in the middle column of the Web page under Services. Further information Editorial Office. Once the online version of the published article for which permission is being requested is can be obtained via RightsLink, a service of the Copyright Clearance Center, not theCirculation Researchin Requests for permissions to reproduce figures, tables, or portions of articles originally publishedPermissions: by guest on April 29,
Connexins and pannexins form connexons, pannexons and membrane channels, which are critically inv... more Connexins and pannexins form connexons, pannexons and membrane channels, which are critically involved in many aspects of cardiovascular physiology. For that reason, a vast number of studies have addressed the role of connexins and pannexins in the arterial and venous systems as well as in the heart. Moreover, a role for connexins in lymphatics has recently also been suggested. This review provides an overview of the current knowledge regarding the involvement of connexins and pannexins in cardiovascular physiology.
1. Heart Rhythm. 2011 Nov 28. [Epub ahead of print] The Molecular Mechanisms of Gap Junction Remo... more 1. Heart Rhythm. 2011 Nov 28. [Epub ahead of print] The Molecular Mechanisms of Gap Junction Remodeling. Duffy HS. PMID: 22133632 [PubMed - as supplied by publisher].
The Australian Journal of Medical Science, May 1, 2004
Cardiac troponin I is a powerful tool to aid in the diagnosis of myocardial infarction and cardia... more Cardiac troponin I is a powerful tool to aid in the diagnosis of myocardial infarction and cardiac muscle damage, and is widely used in clinical practice. It is currently one of the best cardiac markers for a definitive diagnosis, with positive results being highly indicative of ...
The purpose of this study was to determine if the cardiac troponin I (cTnI) assay utilising Dade ... more The purpose of this study was to determine if the cardiac troponin I (cTnI) assay utilising Dade Behring's Dimension RxL was sensitive to heparin or ethylenediaminetetraacetic acid (EDTA) interference, and to ascertain if these additives influence cTnI recovery after storage at 2 - 8 C and -20 C. Seventy-three triplicate samples were analysed to compare cTnI values to those obtained in serum. Forty-five additional samples were used to examine sample stability. Serum, heparin plasma and EDTA plasma samples all show similar levels of imprecision at comparable cTnI concentrations. Heparin plasma samples were on average 0.017 g/L higher than the corresponding serum values. EDTA plasma samples were on average 0.185 g/L lower than the corresponding serum values. Across the grey area range of 0.10 - 1.50 g/L cTnI, heparin values were 0.021 g/L higher than serum, and EDTA values were 0.078 g/L higher. After storage at 2 - 8 C, heparin plasma samples showed a significant decrease in cTnI...
Introduction: Reactive oxygen species (ROS) are thought to play a central role in the genesis of ... more Introduction: Reactive oxygen species (ROS) are thought to play a central role in the genesis of arrhythmia. Mitochondria are the major source of cardiac ROS. Studies suggest ROS activates c-Src tyrosine kinase, which reduces Cx43 at the gap junctions by competing with Cx43 for binding to Zonula Occludence-1. We sought to determine the role of mitochondria oxidative stress in the genesis of ventricular arrhythmia in a manganese superoxide dismutase (MnSOD) knock out mouse model. We hypothesized that excess ROS in this model would activate c-Src and reduce Cx43 levels and that inhibition of c-Src would prevent Cx43 remodeling and the risk of arrhythmia. Method: Wild type and MnSOD+/- mice with and without treatment with the c-Src inhibitor PP1 (1.5 mg/kg IP three times/week x 2 weeks) were studied. Western blotting and immunohistochemistry staining for Cx43 were performed. Mitochondrial ROS was measured by confocal microscopy and flow cytometry from isolated cardiomyocytes using mito...
Information about reprints can be found online at: Reprints: document. Permissions and Rights Que... more Information about reprints can be found online at: Reprints: document. Permissions and Rights Question and Answer about this process is available in the located, click Request Permissions in the middle column of the Web page under Services. Further information Editorial Office. Once the online version of the published article for which permission is being requested is can be obtained via RightsLink, a service of the Copyright Clearance Center, not theCirculation Researchin Requests for permissions to reproduce figures, tables, or portions of articles originally publishedPermissions: by guest on April 29,
Connexins and pannexins form connexons, pannexons and membrane channels, which are critically inv... more Connexins and pannexins form connexons, pannexons and membrane channels, which are critically involved in many aspects of cardiovascular physiology. For that reason, a vast number of studies have addressed the role of connexins and pannexins in the arterial and venous systems as well as in the heart. Moreover, a role for connexins in lymphatics has recently also been suggested. This review provides an overview of the current knowledge regarding the involvement of connexins and pannexins in cardiovascular physiology.
1. Heart Rhythm. 2011 Nov 28. [Epub ahead of print] The Molecular Mechanisms of Gap Junction Remo... more 1. Heart Rhythm. 2011 Nov 28. [Epub ahead of print] The Molecular Mechanisms of Gap Junction Remodeling. Duffy HS. PMID: 22133632 [PubMed - as supplied by publisher].
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