polyneuropathies/tyrosine

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Progression of cardiomyopathy and neuropathy after liver transplantation in a patient with familial amyloidotic polyneuropathy caused by tyrosine-77 transthyretin variant.

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Identifikohuni Regjistrohu

Familial amyloidotic polyneuropathy is an inherited form of amyloidosis associated with a mutant form of a protein called transthyretin. The Methionine-30 variant is the most frequent mutation observed. This disorder is caused by deposition of this protein as amyloid in several organs, such as the

The Bruton tyrosine kinase inhibitor ibrutinib improves anti-MAG antibody polyneuropathy.

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To assess whether neuropathy with anti-myelin-associated glycoprotein (MAG) antibody may improve after treatment with ibrutinib, an oral inhibitor of Bruton tyrosine kinase, we prospectively treated with ibrutinib a cohort of 3 patients with anti-MAG neuropathy and Waldenström

Impaired neurotrophin-3 signaling in a TrkAII mutant associated with hereditary polyneuropathy.

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Mutations of the neurotrophin receptor tyrosine kinase TrkA (NTRK1) cause congenital sensory neuropathy with insensitivity to pain and anhydrosis (CIPA), also called hereditary sensory and autonomous neuropathy type IV (HSAN IV). The neuronal splice variant of TrkA, TrkAII, binds two neurotrophin

[Finnish amyloid polyneuropathy in a French patient].

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Identifikohuni Regjistrohu

BACKGROUND Finnish amyloid variety is a rare familial amiloidosis polyneuropathy essentially observed in Finland. It concerns about six hundred people in the world in which five hundred reside in Finland. METHODS We report a case of a 58-year-old French woman with a 10-year history of lattice cornea

A novel variant of transthyretin (Tyr114 to Cys) deduced from the nucleotide sequences of gene fragments from familial amyloidotic polyneuropathy in Japanese sibling cases.

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A to G transversion was identified in exon 4 of transthyretin gene in familial amyloidotic polyneuropathy in two sibling cases living in Osaka. This transversion led to the replacement of tyrosine by cysteine residue at codon 114 of 127 residue molecule. This identification was achieved by randomly

Diagnosis of familial amyloidotic polyneuropathy in France.

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Two cases of familial amyloidotic polyneuropathy (FAP) in a French family are reported. Clinical onset was in the fifth and sixth decades with decreased sensation in the lower limbs followed by involvement of the upper extremities. Motor changes appeared later and evolved to restrict ambulation.

Immunization in familial amyloidotic polyneuropathy: counteracting deposition by immunization with a Y78F TTR mutant.

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The mechanism of amyloid formation in familial amyloidotic polyneuropathy (FAP), a hereditary disorder associated with mutant transthyretin (TTR), is still unknown. It is generally believed that altered conformations exposing cryptic regions are intermediary steps in this mechanism. A TTR

Concurrent chronic motor axonal polyneuropathy and synaptic impairment of neuromuscular junction.

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Identifikohuni Regjistrohu

Polyneuropathies may exhibits clinical, electrophysiologic signs of neuromuscular junction impairment. Distal motor nerve terminals and neuromuscular junction contain pre or postsynaptically specific targets for circulating autoantibodies, if present in neuropathies. Motor nerve terminal blockade

[Biomarkers of the development and progression of diabetic polyneuropathy]

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Objective: To study the diagnostic potential of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGFA) and their high affinity receptors (TrkB, VEGFR2) in the development and progression of diabetic

Familial amyloid polyneuropathy associated with the transthyretin Cys114 gene in a Japanese kindred.

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Identifikohuni Regjistrohu

A Japanese kindred with dominantly inherited amyloid polyneuropathy, commonly called familial amyloid polyneuropathy (FAP), has been identified. Amyloid protein was transthyretin (TTR) related and the patients were heterozygous for the mutant gene encoding TTR with a single amino acid substitution

Transthyretin-related familial amyloid polyneuropathy: evaluation of CSF enhancement on serial T1-weighted and fluid-attenuated inversion recovery images following intravenous contrast administration.

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OBJECTIVE CSF enhancement on MR images after intravenous administration of gadolinium chelate, which mimics subarachnoid hemorrhage, has been reported. The purpose of this study was to determine whether CSF enhancement can be seen on serial MR images following administration of contrast material in

Familial amyloid polyneuropathy: receptor for advanced glycation end products-dependent triggering of neuronal inflammatory and apoptotic pathways.

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Identifikohuni Regjistrohu

Familial amyloid polyneuropathy (FAP) is a neurodegenerative disorder associated with extracellular deposition of mutant transthyretin (TTR) amyloid fibrils, particularly in the peripheral nervous system. We have hypothesized that binding of TTR fibrils to the receptor for advanced glycation end

Dasatinib-associated reversible demyelinating peripheral polyneuropathy in a case of chronic myeloid leukemia.

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Identifikohuni Regjistrohu

Tyrosine kinase inhibitors (TKIs) are essential for the treatment of chronic myeloid leukemia (CML). Adverse effects of dasatinib have been reported; however, few reports have highlighted the association between dasatinib and demyelinating peripheral neuropathy (DPN). We report a patient with CML

[Pathophysiology of restless legs syndrome].

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Restless legs syndrome (RLS) is a sensorimotor disorder that is frequently associated with periodic leg movements (PLMS). RLS is generally considered to be a central nervous system (CNS)-related disorder although no specific lesion has been found to be associated with the syndrome. Reduced

Suramin disrupts insulin-like growth factor-II (IGF-II) mediated autocrine growth in human SH-SY5Y neuroblastoma cells.

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Identifikohuni Regjistrohu

Suramin, traditionally used in the treatment of trypanosomiasis, is under investigation in the treatment of cancer. One side effect that limits its use is the onset of a sensorimotor polyneuropathy. In order to investigate the mechanism by which suramin induces polyneuropathy, we examined its

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