gerstmann-straussler-scheinker disease/tyrosine

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Astrocyte swelling and protein tyrosine nitration in hepatic encephalopathy.

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Hepatic encephalopathy (HE) is a neuropsychiatric syndrome during the course of acute or chronic liver disease. It is functional in nature, potentially reversible and precipitated by rather heterogeneous factors. Current evidence suggests that HE is the consequence of a low grade chronic glial edema

Protein tyrosine nitration in hyperammonemia and hepatic encephalopathy.

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Hepatic encephalopathy is seen as a clinical manifestation of a chronic low grade cerebral edema, which is thought to trigger disturbances of astrocyte function, glioneuronal communication, and finally HE symptoms. In cultured astrocytes, hypoosmotic swelling triggers a rapid oxidative stress

Decarboxylation to tyramine: an important route of tyrosine metabolism in dogs with experimental hepatic encephalopathy.

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Tyrosine metabolism via decarboxylation to tyramine was evaluated in dogs with functional end-to-side portacaval shunt. It was found that the endogenous plasma levels of both tyrosine and tyramine increased steadily after the construction of the shunt. These elevations became more pronounced when

A new tyrosine hydroxylase genotype associated with early-onset severe encephalopathy.

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We describe a boy affected by an early-onset severe encephalopathy (stagnation of psychomotor development, paroxysmal dystonic postures and movements of limbs, hypokinesia) due to tyrosine hydroxylase deficiency. High blood prolactin and low homovanillic acid in cerebrospinal fluid suggested the

Slow neurodegeneration and transmissible spongiform encephalopathies/prion diseases. Hypothesis: a cycle involving repeated tyrosine kinase A activation could drive the development of TSEs.

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Neurons are specialised non-mitogenic cells. They cannot be replaced after damage, but most survive the lifetime of the individual. This is achieved by a very specialised process of repair and regeneration. During this process, a phase of degeneration in the distal end of the damaged neuron occurs

Brain phenylalanine and tyrosine levels and hepatic encephalopathy induced by CCl4 in rats.

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The correlation between the levels of brain aromatic amino acids and hepatic encephalopathy induced by CCl4 was investigated in rats. CCl4 (1.0 ml/kg three times per week for over 10 weeks) caused hyperammonemia and hepatic encephalopathy in rats. The brain levels of aromatic amino acids, especially

CNS Modulation of adrenal tyrosine hydroxylase in Parkinson's disease and metabolic encephalopathies.

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Tyrosine hydroxylase (TH) activity was assayed radioenzymatically in various regions of post-mortem brains of human individuals without neurologic disorders (controls), with Parkinson's disease, senile dementia, hypertensive encephalopathy, hepatic and diabetic coma, liver cirrhosis without coma,

Elevated dopamine induces minimal hepatic encephalopathy by activation of astrocytic NADPH oxidase and astrocytic protein tyrosine nitration.

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BACKGROUND We previously demonstrated that dopamine (DA) overload may be a key mechanism behind development of minimal hepatic encephalopathy (MHE) in rats. It has been shown that low-grade cerebral oedema and oxidative stress play important roles in the pathogenesis of MHE. In the current study,

Disruption of Striatal-Enriched Protein Tyrosine Phosphatase Signaling Might Contribute to Memory Impairment in a Mouse Model of Sepsis-Associated Encephalopathy.

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Sepsis-associated encephalopathy (SAE) is a potentially irreversible acute cognitive dysfunction with unclear mechanism. Striatal-enriched protein tyrosine phosphatase (STEP) is a brain-specific phosphatase which normally opposes synaptic strengthening by regulating key signaling molecules involved

Early Recognition and Management of Posterior Reversible Encephalopathy Syndrome: A Newly Recognized Complication in Patients Receiving Tyrosine Kinase Inhibitors.

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BACKGROUND Adult patients with cancer receiving antineoplastic, targeted, and other immunosuppressive therapies are at risk for severe side effects. Studies link posterior reversible encephalopathy syndrome (PRES) with immunosuppressants used for patients undergoing transplantation, as well as

Tyrosine hydroxylase deficiency causes progressive encephalopathy and dopa-nonresponsive dystonia.

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Tyrosine hydroxylase (TH) is the key enzyme in the biosynthesis of the catecholamines dopamine, epinephrine, and norepinephrine. Recessively inherited deficiency of TH was recently identified and incorporated into recent concepts of genetic dystonias as the cause of recessive Dopa-responsive

3-nitro-tyrosine as a peripheral biomarker of minimal hepatic encephalopathy in patients with liver cirrhosis.

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OBJECTIVE Between 30 and 50% of the cirrhotic patients who do not show symptoms of clinical hepatic encephalopathy (HE) present minimal hepatic encephalopathy (MHE), with mild cognitive impairment. MHE impairs the quality of life, increases the risk of suffering accidents, predicts the appearance of

Atypical Posterior Reversible Encephalopathy Syndrome due to Oral Tyrosine Kinase Inhibitor Cabozantinib: First Case Report

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We report here a rare case of atypical posterior reversible encephalopathy syndrome (PRES) due to oral tyrosine kinase inhibitor cabozantinib. No case reports of such have been found in our literature search. The patient, a 70-year-old female with metastatic renal cell cancer on oral tyrosine kinase

Can the tyrosine kinase inhibitors trigger metabolic encephalopathy in cirrhotic patients?

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BACKGROUND Sorafenib is the standard treatment of advanced hepatocarcinoma (HCC) in cirrhotic patients with preserved liver function. It shares many adverse effects with other tyrosine-kinase (TK) inhibitors and antiangiogenic drugs. TK inhibitors could have a direct toxicity on CNS, both by

Posterior reversible encephalopathy syndrome (PRES) induced by pazopanib, a multi-targeting tyrosine kinase inhibitor, in a patient with soft-tissue sarcoma: case report and review of the literature.

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Posterior reversible encephalopathy syndrome (PRES) is a clinical entity characterized by acute neurological symptoms such as severe headache, seizures, and visual disturbance, and by typical reversible lesion on brain magnetic resonance (MR) images. Since PRES is thought to be caused by vascular

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