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Solucionariodekletenikpdf12

solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
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solucionariodekletenikpdf12
solucionariodekletenikpdf12
solucionariodekletenikpdf12
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solucionariodekletenikpdf12
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solucionariodekleten

https://colab.research.google.com/drive/1ObcjOXYlle4L8vbXvQGtAFByPF-woxsQ
https://colab.research.google.com/drive/1vFsVavyPl7G-BltbDMaJaBh-mNyfL1rh
https://colab.research.google.com/drive/1aFcbUqTAAxOnrp0EKvwZqPY8X060gRNU
https://colab.research.google.com/drive/1Gaxu2MTFetC75XOTKb9G4pNdOnFKutpv
https://colab.research.google.com/drive/12WCESePTUI7lzYBdGNNebPAe0cW1-DYF

A:

There are no unicode characters in your title.
I tried this:
$#&A patient with hypertrophic obstructive cardiomyopathy associated with a novel R811C mutation in the myosin binding protein C gene.
Hypertrophic cardiomyopathy is a heterogeneous autosomal dominant heart muscle disease characterized by disproportionate hypertrophy of the left ventricle that may be associated with diastolic dysfunction and sudden cardiac death. Most mutations of the myosin binding protein C (MYBPC3) gene have been reported to be associated with hypertrophic cardiomyopathy. We describe a patient with MYBPC3-related hypertrophic cardiomyopathy associated with a novel point mutation in exon 13, R811C, in the myosin binding protein C gene in a 57-year-old woman. Clinically, she exhibited left ventricular outflow tract obstruction (tricuspid valve pressure gradient: 52 mm Hg), and echocardiography demonstrated a large left ventricular mass with both systolic and diastolic dysfunction. To investigate the mechanism of sudden cardiac death, we examined the expression of mutated MYBPC3 in isolated mouse cardiomyocytes using adenovirus infection. The mutant protein was expressed at higher levels than wild-type MYBPC3 (pSt. Augustine, Florida

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