gerstmann-straussler-scheinker disease/phosphatase

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A homozygous PIGO mutation associated with severe infantile epileptic encephalopathy and corpus callosum hypoplasia, but normal alkaline phosphatase levels.

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We describe two sisters from a consanguineous Arab family with global developmental delay, dystrophy, axial hypotonia, epileptic encephalopathy dominated by intractable complex partial seizures that were resistant to various anti-epileptic treatments. Dysmorphic features comprised low set ears,

Purple acid phosphatase of human brain macrophages in AIDS encephalopathy.

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Brains from AIDS patients with an HIV-induced encephalopathy but without opportunistic infections or indications for an inflammation were studied by immuno- and enzyme-histochemical methods. It was found that the macrophages of these brains expressed a lysosomal tartrate-resistant acid phosphatase

Transcriptome analyses of chronic traumatic encephalopathy show alterations in protein phosphatase expression associated with tauopathy.

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Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder that is associated with repetitive head injury and has distinctive neuropathological features that differentiate this disease from other neurodegenerative diseases. Intraneuronal tau aggregates, although they occur in

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

The cytochemistry of anoxic and anoxic-ischemic encephalopathy in rats. I. Alterations in neuronal lysosomes identified by acid phosphatase activity.

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Impaired brain glucose metabolism in cirrhosis without overt hepatic encephalopathy: a retrospective 18F-FDG PET/CT study.

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There are subclinical neurologic deficits in cirrhotic patients without overt hepatic encephalopathy. We aimed to use F-fluorodeoxyglucose PET/computed tomography to explore the impaired brain glucose metabolism of subclinical hepatic encephalopathy in

Behavioral and physiological sex differences observed in an animal model of fulminant hepatic encephalopathy in the rat.

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Hepatic encephalopathy is characterized by a number of neuropsychiatric and motor disturbances observed in patients with liver dysfunction. The purpose of this study is to fully characterize behavioral and physiological sex differences in an animal model of fulminant hepatic encephalopathy (FHE).

A neurotoxic alcohol exposure paradigm does not induce hepatic encephalopathy.

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Alcohol abuse is associated with neurological dysfunction, brain morphological deficits and frank neurotoxicity. Although these disruptions may be a secondary effect due to hepatic encephalopathy, no clear evidence of causality is available. This study examined whether a 72h period of alcohol

Methimazole alleviates hepatic encephalopathy in bile-duct ligated cirrhotic rats.

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BACKGROUND Acute or chronic liver damage may lead to hepatic encephalopathy. Previous studies have indicated the hemodynamic and hormonal mimicry between portal hypertension and hyperthyroidism. Furthermore, medically or surgically induced hypothyroidism has been found to be beneficial in

Measurement of serum alkaline phosphatase isozyme I in brain-damaged patients.

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The authors measured alkaline phosphatase isozyme I (ALP-I) in sera of 24 brain-damaged patients and four with disorders other than brain damage. The study population comprised three patients with postresuscitation encephalopathy, four with ruptured cerebral aneurysms, 14 with acute subdural

Unusually Low Serum Alkaline Phosphatase Activity in a Patient with Acute on Chronic Liver Failure and Hemolysis.

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A 28-year-old male with acute on chronic liver failure (ACLF) and hepatic encephalopathy had deranged liver function with curiously low level (0-15 IU/L) of serum alkaline phosphatase (ALP). Peripheral smear examination suggested hemolytic anemia. The finding of persistent low ALP, after ruling out

PIGO mutations in intractable epilepsy and severe developmental delay with mild elevation of alkaline phosphatase levels.

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Aberrations in the glycosylphosphatidylinositol (GPI)-anchor biosynthesis pathway constitute a subclass of congenital disorders of glycosylation, and mutations in seven genes involved in this pathway have been identified. Among them, mutations in PIGV and PIGO, which are involved in the late stages

Alkaline phosphatase as an early marker of hemolysis in newborns.

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BACKGROUND Early diagnosis and appropriate management of neonatal hyperbilirubinemia are very important in order to prevent bilirubin encephalopathy and kernicterus. Several diagnostic tests may be used for this purpose, including bilirubin level itself. The aim of the present study was to

Role of cyclooxygenase isoforms in encephalopathy of cirrhotic rats.

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BACKGROUND Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome secondary to acute or chronic liver failure. However, its pathophysiology remains obscure. Recently, we found that the inhibition of cyclooxygenase by indomethacin aggravated HE in rats with thioacetamide-induced acute

[Generation of sepsis encephalopathy patient-specific inducible pluripotent stem cells with urine cells].

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To recombine the induced pluripotent stem cells (iPSC) derived from the urine of septic encephalopathy (SE) patients, and provided a specificity cell model to explore the mechanism of the neuronal damage and treatment for SE patients.

METHODS

Urine of

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