galactosemias/phosphatase

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Using a Personal Glucose Meter and Alkaline Phosphatase for Point-of-Care Quantification of Galactose-1-Phosphate Uridyltransferase in Clinical Galactosemia Diagnosis.

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The personal glucose meter (PGM) was recently shown to be a general meter to detect many targets. Most studies, however, focus on transforming either target binding or enzymatic activity that cleaves an artificial substrate into the production of glucose. More importantly, almost all reports exhibit

Neonatal screening for galactosemia by quantitative analysis of hexose monophosphates using tandem mass spectrometry: a retrospective study.

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BACKGROUND Classic galactosemia (OMIM 230400) is an inherited disorder in the metabolism of galactose caused by deficiency of the enzyme galactose 1-phosphate uridyl transferase (EC 2.7.7.12). Galactosemia leads to accumulation of galactose and galactose 1-phosphate (gal-1-P) in blood and tissues

Galactose and galactose-1-phosphate spot test for galactosemia screening.

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A simple spot test to measure galactose and galactose-1-phosphate in blood-impregnated filter paper was studied as a screening test for galactosemia in the newborn. A 3-mm disc punched from blood-impregnated filter paper card was fixed with acetone-methanol and incubated in a reaction mixture

Bone metabolism in galactosemia.

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Classical galactosemia is an autosomal recessively inherited disorder of galactose metabolism. Treatment consists of life-long dietary restriction of galactose. Despite treatment, long-term complications occur such as a decreased bone mineral density (BMD). A decreased BMD might be the result of

Serum markers of bone turnover in children and adolescents with classic galactosemia.

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OBJECTIVE Classic galactosemia is an inherited metabolic disease resulting from galactose-1-phosphate uridyltransferase (GALT) deficiency. Dietary lactose exclusion reverses many clinical manifestations of acute phase of the disease. Unfortunately most of the patients, despite dietary treatment,

Galactose-1-phosphate in the pathophysiology of galactosemia.

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In galactosemia, galactose-1-phosphate (gal-1-P) is not properly metabolized and accumulates in the fetus and after birth in various tissues when lactose or galactose is ingested. Well-treated galactosemics retain a low level of red cell gal-1-P which increases after breaks of diet. The ester is an

Simultaneous quantitative estimation of galactose-1-phosphate and galactose in blood for the diagnosis of galactosemia.

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A new microfluorometrical simultaneous assay method of galactose-1-phosphate and galactose in blood discs was devised by use of alkaline phosphatase and beta-galactose dehydrogenase. Our method statistically corresponded well with the Kirkman's method. It can detect 1 X 10(-10) mole of minimal

Clinical significance of plasma galactose and erythrocyte galactose-1-phosphate measurements in transferase-deficient galactosemia and in individuals with below-normal transferase activity.

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We correlated the clinical symptoms of transferase-deficient galactosemia with the plasma galactose and erythrocyte galactose-1-phosphate concentrations in six galactosemic patients during dietary treatment, in a child before treatment, and in 12 individuals with below-normal erythrocyte

Microassay for screening newborns for galactosemia with use of a fluorometric microplate reader.

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We describe a microassay for measuring galactose (Gal) and galactose 1-phosphate (Gal-1-P) in dried blood spots. After a coupled enzyme reaction involving galactose dehydrogenase (GADH, EC 1.1.1.48) and alkaline phosphatase (AP, EC 3.1.3.1) in a microplate well, NADH fluorescence is measured by a

Assay of galactose-1-phosphate uridyl transferase in cultured amniotic cells for prenatal diagnosis of galactosaemia.

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We report studies designed to establish optimal conditions for the assay of amniotic cell galactose 1-phosphate uridyl transferase (Gal-PUT) for early prenatal diagnosis of galactosaemia. Methods based on linkage of the reaction to cause of non-specific reactions occurring even in the absence of

Salubrinal enhances eIF2α phosphorylation and improves fertility in a mouse model of Classic Galactosemia.

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Loss of galactose-1 phosphate uridylyltransferase (GALT) activity in humans results in Classic Galactosemia, and the GalT-deficient (GalT^-/-) mouse mimics the patient condition. GalT^-/- ovaries display elevated endoplasmic reticulum (ER) stress marker, BiP, and downregulated

[Bone alkaline phosphatase: characteristic and its clinical applications].

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Bone alkaline phosphatase (BALP) is one of the most frequently used biochemical markers of bone formation. The presented paper describes the enzyme's specificity, physiological values during normal growth and development as well as its clinical applications in various diseases. The main interest

Galactose-1-phosphatase in rat brain.

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A prominent galactose-1-phosphatase was isolated from rat brain and partially purified by chromatography on diethylaminoethyl-Sephacel, hydroxylapatite, and Sephacryl S-300 columns. The galactose-1-phosphatase was separated from alkaline phosphatase, and from two forms of glucose-1-phosphatase. The

Bone mineral density in patients with classic galactosaemia.

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BACKGROUND Diminished bone mineral density (BMD) is a well known complication in women with classic galactosaemia caused by premature ovarian failure. Diminished BMD in prepubertal patients of either sex has, however, only been reported once. OBJECTIVE To assess BMD in children with classic

Towards enhanced galactose utilization by Lactococcus lactis.

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Accumulation of galactose in dairy products due to partial lactose fermentation by lactic acid bacteria yields poor-quality products and precludes their consumption by individuals suffering from galactosemia. This study aimed at extending our knowledge of galactose metabolism in Lactococcus lactis,

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