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glucose 6 phosphatase/krvarenje

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Regulation of liver and kidney glucose-6-phosphatase gene expression in hemorrhage and resuscitation.

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The authors have recently demonstrated that increased gene expression of glucose-6-phosphatase (Glu-6-Pase) in hemorrhagic hypotension (HH) and following lactated Ringer's resuscitation (LR) is associated with a decrease in insulin and an increase in corticosterone concentrations. OBJECTIVE To
Decreased hepatic fructose 2,6-bisphosphate levels were observed in the early phase of hemorrhagic shock. The lower sugar bisphosphatae level was a result of increased phosphoenolpyruvate levels and decreased glucose-6-phosphate and fructose-6-phosphate levels. The decreased glucose-6-phosphate
The mRNA abundance of several hepatic glycolytic and gluconeogenic enzymes and blood hormone concentrations were determined in hemorrhagic hypotension-induced rats before and after resuscitation with lactated Ringer's. Northern blot analysis of total liver RNA after 30 min of hemorrhage showed

Histochemical investigation of hepatic adenosine triphosphatase and glucose-6-phosphatase activity in hemorrhagic shock.

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Effects of RU486 on Glu-6-pase gene expression in hemorrhage and resuscitation.

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To assess the role of glucocorticoid receptor antagonists and mediators released by Kupffer cells and other resident macrophages, we have used RU486 and gadolinium chloride to prevent the induction of glucose-6-phosphatase (Glu-6-Pase) gene expression in the liver following hemorrhagic shock (HS)

Infectious and bleeding complications in patients with glycogenosis Ib.

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Clinical, hematologic, and immunologic findings were reviewed in 21 patients with glycogenosis Ib. Fifteen of the patients suffered from moderate to severe bacterial infections. Ten patients had excessive epistaxis or bleeding from surgical sites, and eight suffered oral and anal mucosal ulceration.

Defective gamma-glutamyl carboxylase activity and bleeding in Rambouillet sheep.

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A flock of Rambouillet sheep was examined because of increased lamb mortality caused by ineffective hemostasis at parturition. Neonatal-affected lambs presented with inadequate hemostasis at the umbilicus, pale mucus membranes, and markedly prolonged activated clotting time. Affected lambs had
Immunization of rabbits with increasing doses of Cl. botulinum toxoid, type B, led to the development in the kidneys of a focal intracapillary productive glomerulonephritis, and also of productive endo- and perivasculites. Blood letting (in the amount of 1% of body weight) aggravated the

Glycogen Storage Disease type 1a - a secondary cause for hyperlipidemia: report of five cases.

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OBJECTIVE Glycogen storage disease type Ia (GSD Ia) is a rare metabolic disorder, caused by deficient activity of glucose-6-phosphatase-α. It produces fasting induced hypoglycemia and hepatomegaly, usually manifested in the first semester of life. Besides, it is also associated with growth delay,

A 20-year follow-up of a male patient with type Ia glycogen storage disease.

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Glycogen storage diseases (GSDs) or glycogenoses comprise several rare inherited diseases caused by abnormalities of the enzymes that regulate the synthesis or degradation of glycogen. We report on a male patient with type Ia GSD (GSD Ia) who was followed-up for more than 20 years. He had been

[Heterogeneous phenotypes in Chinese glycogen storage disease type Ia patients with homozygous G727T mutation].

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Glycogen storage disease (GSD) type Ia is an autosomal recessive disorder caused by a deficiency of glucose-6-phosphatase (G6Pase). The gene that encodes G6Pase was mapped to 17q21. The molecular genetic basis of GSD type Ia in the mainland Chinese population has not been explored. OBJECTIVE To

Induction of oxidative stress in liver and kidney of rats exposed to Nigerian bonny light crude oil.

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The local population of Niger-Delta in the Southern part of Nigeria have used bonny light crude oil (BLCO) as a remedy for various ailments and are exposed to some extent to this widespread environmental contaminant or its metabolites through the food chain. BLCO's hepatorenal toxicity was studied

A case of type Ia glycogen storage disease complicated by hepatic adenoma.

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A 31-year-old male patient with type Ia glycogen storage disease was admitted to our department complaining of general fatigue and right hypochondriac pain. He exhibited massive hepatomegaly with systemic hypoglycemia, lactic acidosis, hyperuricemia, hyperpyruvatemia and hyperlipemia. The failure of

[Clinical and biochemical alterations in rats treated with high doses of vitamin A].

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In the present work the effect of intramuscular administration of 30.000, 50.000 and 100.000 IU of vitamin A palmitate daily for seven days, respectively, on the liver enzyme activity in 45 white male Wistar rats, aged 12 weeks and weighing 180-200 g, have been studied. The group control was

Regression of hepatic adenomas in type Ia glycogen storage disease with dietary therapy.

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Individuals with type Ia glycogen storage disease (glucose-6-phosphatase deficiency) frequently develop hepatic adenomas. Potential complications involving these adenomas include malignant transformation and hemorrhage. Five of 9 patients with this disease had evidence of hepatic filling defects on
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