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hepatic encephalopathy/tyrosine
L'enllaç es desa al porta-retalls
Pàgina 1 des de 136 resultats
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
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
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,
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
The effects of hemoperfusion using coated charcoal or tyrosinase artificial cells on middle molecules and tyrosine in brain and serum of hepatic coma rats.
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Hypoosmotic swelling increases protein tyrosine nitration in cultured rat astrocytes.
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Astrocyte swelling is observed in different types of brain injury. We studied a potential contribution of swelling to protein tyrosine nitration (PTN) by using cultured rat astrocytes exposed to hypoosmotic (205 mosmol/L) medium. Hypoosmolarity (2 h) increases total PTN by about 2-fold in 2 h. The
Plasma GABA-like activity in rats with hepatic encephalopathy is due to GABA and taurine.
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Significant discrepancy exists between radioreceptor and high-performance liquid chromatographic estimates of plasma GABA concentrations in animal models of hepatic encephalopathy. A possible explanation for this discrepancy is the presence in plasma of a substance that can inhibit [3H]-GABA binding
[Cerebral manifestations in the hepatic coma syndrome (author's transl)].
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The pathogenesis of hepatic encephalopathy has been investigated in a two-stage devascularization model in the rat with portavacal shunt and hepatic artery ligation. There is a significant increase in brain octopamine and phenylethanolamine and a decrease in brain norepinephrine (NE) 6 to 9 hours
Mesocaval and distal splenorenal shunts: effect on hepatic function, hepatic hemodynamics, and portal systemic encephalopathy.
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The effect of the mesocaval interposition shunt (n = 12) and the distal splenorenal shunt (n = 9) on the wedged hepatic venous pressure, the estimated hepatic blood flow, quantitative hepatic function, and the rate of portal systemic encephalopathy was evaluated in 21 patients who had bled from
Reduced TH expression and α-synuclein accumulation contribute towards nigrostriatal dysfunction in experimental hepatic encephalopathy.
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The present work examines α-synuclein expression in the nigrostriatal system of a rat chronic hepatic encephalopathy model induced by portacaval anastomosis (PCA). There is evidence that dopaminergic dysfunction in disease conditions is strongly associated with such expression. Possible
Citrulline as a diagnostic parameter and a major amino acid constituent of cerebrospinal fluid in hepatic coma.
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Free amino acids of cerebrospinal fluid and serum in hepatic coma have been studied. Citrulline was found to form about 80% of the total free amino acids in cerebrospinal fluid, whereas serum contained slightly higher levels of tyrosine, methionine, phenylalanine and glutamine. The higher level of
Human cerebral free amino acids in hepatic coma.
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Free amino acids and some related compounds in autopsy specimens of different human brain areas have been determined by column chromatography. Only in patients with hepatic coma could a significant difference in the contents of tyrosine and lysine between caudate nucleus and N. amygdalae be found.
Deranged tyrosine metabolism in cirrhosis.
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In normal individuals, the main route for tyrosine degradation is the hepatic pathway tyrosine→4-hydroxyphenylpyruvic acid→homogentisic acid→CO(2). Quantitatively minor pathways, in large part extrahepatic, are: tyrosine→tyramine→octopamine and tyrosine→dopa→catecholamines.In cirrhosis, the main
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