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Team:Brasil-SP/TheIssue/OurSolution
From 2014.igem.org
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<h3 align="center">Our Solution</h3> | <h3 align="center">Our Solution</h3> | ||
<p><div align="justify"> Several studies support Cystatin C as the best biomarker of renal dysfunction when compared to classical biomarkers (urea nitrogen and serum creatinine), because Cystatin C is very sensitive to changes in GFR (SHLIPAK and DAY, 2013). However, the available methods to evaluate the levels of Cystatin C are often very expensive and inefficient, such as the immunofluorescence method (SHLIPAK and DAY, 2013). Our solution to this problem is to develop a genetic circuit to detect different levels of Cystatin C in the blood. When the detectable levels of Cystatin C are higher than the normal, it will lead us to diagnose CKD and other renal dysfunctions in early stages. The genetic circuit is shown in the Figure below and the input information is based on Cystatin C inhibitory activity against cysteine proteases, in this case, cathepsin S.</div></p> | <p><div align="justify"> Several studies support Cystatin C as the best biomarker of renal dysfunction when compared to classical biomarkers (urea nitrogen and serum creatinine), because Cystatin C is very sensitive to changes in GFR (SHLIPAK and DAY, 2013). However, the available methods to evaluate the levels of Cystatin C are often very expensive and inefficient, such as the immunofluorescence method (SHLIPAK and DAY, 2013). Our solution to this problem is to develop a genetic circuit to detect different levels of Cystatin C in the blood. When the detectable levels of Cystatin C are higher than the normal, it will lead us to diagnose CKD and other renal dysfunctions in early stages. The genetic circuit is shown in the Figure below and the input information is based on Cystatin C inhibitory activity against cysteine proteases, in this case, cathepsin S.</div></p> | ||
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<img src="https://static.igem.org/mediawiki/2014/f/fb/Detection_module.png" width="500" height="auto"/> | <img src="https://static.igem.org/mediawiki/2014/f/fb/Detection_module.png" width="500" height="auto"/> | ||
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| + | <p><div align="justify"> <b>Reference</b></div></p> | ||
<p><div align="justify"> SHLIPAK MG, DAY, EC. Biomarkers for incident CKD: a new framework for interpreting the literature. <b>Nature Review on Nephrology</b>, 2013, 9(8):478-83. doi: 10.1038/nrneph.2013.108.</div></p> | <p><div align="justify"> SHLIPAK MG, DAY, EC. Biomarkers for incident CKD: a new framework for interpreting the literature. <b>Nature Review on Nephrology</b>, 2013, 9(8):478-83. doi: 10.1038/nrneph.2013.108.</div></p> | ||
Revision as of 17:08, 12 October 2014
Our Solution
Several studies support Cystatin C as the best biomarker of renal dysfunction when compared to classical biomarkers (urea nitrogen and serum creatinine), because Cystatin C is very sensitive to changes in GFR (SHLIPAK and DAY, 2013). However, the available methods to evaluate the levels of Cystatin C are often very expensive and inefficient, such as the immunofluorescence method (SHLIPAK and DAY, 2013). Our solution to this problem is to develop a genetic circuit to detect different levels of Cystatin C in the blood. When the detectable levels of Cystatin C are higher than the normal, it will lead us to diagnose CKD and other renal dysfunctions in early stages. The genetic circuit is shown in the Figure below and the input information is based on Cystatin C inhibitory activity against cysteine proteases, in this case, cathepsin S.
<img src="
" width="500" height="auto"/>
Reference
SHLIPAK MG, DAY, EC. Biomarkers for incident CKD: a new framework for interpreting the literature. Nature Review on Nephrology, 2013, 9(8):478-83. doi: 10.1038/nrneph.2013.108.
