Effects of Tafamidis on Transthyretin Stabilization and Clinical Outcomes in Patients with Non-Val30Met Transthyretin Amyloidosis
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T. Tripp | D. Judge | G. Merlini | H. Schmidt | S. Perlini | V. Planté-Bordeneuve | L. Obici | J. Packman | D. Grogan | H. Schmidt
[1] R. Falk,et al. Tafamidis in transthyretin amyloid cardiomyopathy: effects on transthyretin stabilization and clinical outcomes. , 2015, Circulation. Heart failure.
[2] I. Merkies. Tafamidis for transthyretin familial amyloid polyneuropathy: A randomized, controlled trial , 2013, Neurology.
[3] Yukio Ando,et al. Guideline of transthyretin-related hereditary amyloidosis for clinicians , 2013, Orphanet Journal of Rare Diseases.
[4] F. Salvi,et al. Disease profile and differential diagnosis of hereditary transthyretin-related amyloidosis with exclusively cardiac phenotype: an Italian perspective. , 2013, European heart journal.
[5] R. Labaudinière,et al. Tafamidis, a potent and selective transthyretin kinetic stabilizer that inhibits the amyloid cascade , 2012, Proceedings of the National Academy of Sciences.
[6] B. Ericzon,et al. Long-term data from the Familial Amyloidotic Polyneuropathy World Transplant Registry (FAPWTR) , 2011, Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis.
[7] F. Salvi,et al. Transthyretin-related amyloidoses and the heart: a clinical overview , 2010, Nature Reviews Cardiology.
[8] H. Katus,et al. Serum levels of NT-proBNP as surrogate for cardiac amyloid burden: new evidence from gadolinium-enhanced cardiac magnetic resonance imaging in patients with amyloidosis , 2009, Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis.
[9] M. Borggrefe,et al. Diagnostic performance and cost effectiveness of measurements of plasma N-terminal pro brain natriuretic peptide in patients presenting with acute dyspnea or peripheral edema. , 2009, International journal of cardiology.
[10] C. Camargo,et al. Utility of amino-terminal pro-brain natriuretic peptide testing for prediction of 1-year mortality in patients with dyspnea treated in the emergency department. , 2006, Archives of internal medicine.
[11] Richard B Devereux,et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardio , 2005, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.
[12] S. Ikeda,et al. Ten years of experience with liver transplantation for familial amyloid polyneuropathy in Japan: outcomes of living donor liver transplantations. , 2005, Internal medicine.
[13] Peter J Dyck,et al. Monotonicity of nerve tests in diabetes: subclinical nerve dysfunction precedes diagnosis of polyneuropathy. , 2005, Diabetes care.
[14] R. Falk,et al. Definition of organ involvement and treatment response in immunoglobulin light chain amyloidosis (AL): A consensus opinion from the 10th International Symposium on Amyloid and Amyloidosis , 2005, American journal of hematology.
[15] A. Vinik,et al. The development and validation of the Norfolk QOL-DN, a new measure of patients' perception of the effects of diabetes and diabetic neuropathy. , 2005, Diabetes technology & therapeutics.
[16] C. Camargo,et al. The N-terminal Pro-BNP investigation of dyspnea in the emergency department (PRIDE) study. , 2005, The American journal of cardiology.
[17] B. Ericzon,et al. Ten years of international experience with liver transplantation for familial amyloidotic polyneuropathy: results from the familial amyloidotic polyneuropathy world transplant registry , 2004, Transplantation.
[18] O. Leone,et al. Combined heart and liver transplantation for familial amyloidotic polyneuropathy. , 2003, The Journal of thoracic and cardiovascular surgery.
[19] J. Kelly,et al. Prevention of Transthyretin Amyloid Disease by Changing Protein Misfolding Energetics , 2003, Science.
[20] Catherine E Costello,et al. Tabulation of human transthyretin (TTR) variants, 2003 , 2003, Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis.
[21] J. Kelly,et al. Sequence-dependent denaturation energetics: A major determinant in amyloid disease diversity , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[22] O. Suhr,et al. Long‐term follow‐up of survival of liver transplant recipients with familial amyloid polyneuropathy (Portuguese type) , 2002, Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society.
[23] J. Kelly,et al. Trans-Suppression of Misfolding in an Amyloid Disease , 2001, Science.
[24] M. Saraiva. Transthyretin amyloidosis: a tale of weak interactions , 2001, FEBS letters.
[25] M. Saraiva. Transthyretin mutations in hyperthyroxinemia and amyloid diseases , 2001, Human mutation.
[26] H. Ideta,et al. A novel compound heterozygote (FAP ATTR Arg104His/ATTR Val30Met) with high serum transthyretin (TTR) and retinol binding protein (RBP) levels. , 1999, Biochemical and biophysical research communications.
[27] P. Nihoyannopoulos,et al. Progressive cardiac amyloidosis following liver transplantation for familial amyloid polyneuropathy: implications for amyloid fibrillogenesis. , 1998, Transplantation.
[28] D. Lewis,et al. Progression of ventricular wall thickening after liver transplantation for familial amyloidosis. , 1997, Transplantation.
[29] W. Litchy,et al. Longitudinal assessment of diabetic polyneuropathy using a composite score in the Rochester Diabetic Neuropathy Study cohort , 1997, Neurology.
[30] A. Sousa,et al. Compound heterozygotes of transthyretin Met30 and transthyretin Met119 are protected from the devastating effects of familial amyloid polyneuropathy , 1996, Neuromuscular Disorders.
[31] W. Litchy,et al. Variables influencing neuropathic endpoints , 1995, Neurology.
[32] A Coda,et al. Structure of a complex of two plasma proteins: transthyretin and retinol-binding protein. , 1995, Science.
[33] G. Holmgren,et al. Malnutrition and gastrointestinal dysfunction as prognostic factors for survival in familial amyloidotic polyneuropathy , 1994, Journal of internal medicine.
[34] R. Falk,et al. Liver Transplantation as a Treatment for Familial Amyloidotic Polyneuropathy , 1994, Annals of Internal Medicine.
[35] G. Holmgren,et al. Biochemical effect of liver transplantation in two Swedish patients with familial amyloidotic polyneuropathy (FAP‐met30) , 1991, Clinical genetics.
[36] S. Araki,et al. Analyses of prealbumin mRNAs in individuals with familial amyloidotic polyneuropathy. , 1986, Journal of biochemistry.
[37] C. Blake,et al. Strjcture of human plasma prealbumin at 2-5 A resolution. A preliminary report on the polypeptide chain conformation, quaternary structure and thyroxine binding. , 1974, Journal of molecular biology.
[38] D. Small,et al. Transthyretin and familial amyloidotic polyneuropathy. Recent progress in understanding the molecular mechanism of neurodegeneration. , 2007, The FEBS journal.
[39] It Istituto Superiore di Sanit,et al. Definition of organ involvement and treatment response in immunoglobulin light chain amyloidosis (AL): a consensus opinion from th 10th International Symposium on Amyloid an Amyloidosis, Tours, France, 18-22 April 2004 , 2005 .
[40] S M Breathnach,et al. Amyloid and amyloidosis. , 1988, Journal of the American Academy of Dermatology.
[41] P. Coutinho,et al. Forty years of experience with type I amyloid neuropathy. Review of 483 cases , 1980 .
[42] O. M. Vinogradova,et al. [Familial amyloidosis]. , 1975, Klinicheskaia meditsina.