Results 151 to 160 of about 10,856 (192)
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Transthyretin Mass Determination for Detection of Transthyretin Familial Amyloid
2009The concentration range of plasma proteins exceeds the dynamic range of any single analytical method. It has been estimated that the concentration range of serum proteins exceeds ten orders of magnitude (1). Because of this, prior immunoselection of even abundant proteins facilitates the relative nonquantitative observations required to show structural
John F, O'Brien, H Robert, Bergen
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Monoclonal antibodies to transthyretin
Scandinavian Journal of Clinical and Laboratory Investigation, 1986Monoclonal antibodies (mabs) have been raised against human transthyretin (hTTR). The protein was isolated by an affinity chromatography procedure using Sepharose-hRBP and BALB/c mice were immunized. Following fusion with SP 2/0 myeloma cells, 26 single cell clones producing antibodies against hTTR were isolated.
V P, Collins +3 more
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Acoramidis: A New Transthyretin Stabilizer for Transthyretin Amyloid Cardiomyopathy
Annals of PharmacotherapyObjective: The objective of the study was to review acoramidis, a new transthyretin stabilizer, for treatment of transthyretin amyloid cardiomyopathy by means of pharmacology, efficacy, and safety. Data sources: An Embase, PubMed, and ...
Taylor Clark +4 more
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Transthyretin Cardiac Amyloidosis
Current Cardiology Reports, 2017Transthyretin (TTR)-related cardiac amyloidosis is a progressive infiltrative cardiomyopathy that mimics hypertensive, hypertrophic heart disease and may go undiagnosed. Transthyretin-derived amyloidosis accounts for 18% of all cases of cardiac amyloidosis.
Anit K, Mankad, Keyur B, Shah
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Tafamidis for transthyretin amyloidosis
Drugs of Today, 2012Tafamidis meglumine (Vyndaqel®, Pfizer) is a novel, first-in-class drug for the treatment of transthyretin familial amyloid polyneuropathy (TTR-FAP), a rare neurodegenerative disorder characterized by progressive sensory, motor and autonomic impairment that is ultimately fatal.
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Nursing, 2020
Abstract: Cardiac amyloidosis is a poorly understood cause of heart failure and is often undiagnosed. Recent advances in diagnostic testing and understanding of the disease have enhanced the ability of clinicians to detect this disease and provide patients with appropriate treatment.
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Abstract: Cardiac amyloidosis is a poorly understood cause of heart failure and is often undiagnosed. Recent advances in diagnostic testing and understanding of the disease have enhanced the ability of clinicians to detect this disease and provide patients with appropriate treatment.
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Transthyretin amyloid cardiomyopathy
Ugeskrift for LægerTransthyretin amyloidosis (ATTR-CM) is an infiltrative cardiomyopathy caused by the deposition of amyloid fibrils, leading to heart failure, arrhythmias, and increased mortality. ATTR-CM prevalence is rising. The first disease-modifying drugs have been approved and implemented in Denmark.
Sie Kronborg, Fensman +3 more
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Computational Studies on Transthyretin
Current Medicinal Chemistry, 2012Among the 23 different fibril proteins described in human amyloidosis, transthyretin is associated with the most common hereditary form of the disease and its knowledge is corroborated through about 150 crystal structures in addition to thousands of small ligands tested as fibril formation inhibitors. In spite of the large amount of available data, the
ORTORE, GABRIELLA MARIA PIA +1 more
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Cardiac transthyretin amyloidosis
Heart, 2012Cardiac amyloidosis of transthyretin fibril protein (ATTR) type is an infiltrative cardiomyopathy characterised by ventricular wall thickening and diastolic heart failure. Increased access to cardiovascular magnetic resonance imaging has led to a marked increase in referrals to our centre of Caucasian patients with wild-type ATTR (senile systemic ...
Jason N, Dungu +3 more
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Pathogenesis of transthyretin amyloidosis
Amyloid, 2012Current dogma for transthyretin (TTR) pathogenesis is that mutations in TTR alter its structure such that the tetramer becomes unstable and prone to release of monomer which then becomes the putative building block of the fibril. This hypothesis is supported by thermodynamic data showing decreased stability of mutant TTR tetrameric proteins and ...
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