n acetyl beta d glucosaminidase/hypoxia

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Netilmicin effect on urinary retinol binding protein (RBP) and N-acetyl-beta-D-glucosaminidase (NAG) in preterm newborns with and without anoxia.

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The study aim was to evaluate urinary excretion of Retinol Binding Protein (RBP), compared with urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), in preterm infants with anoxia and netilmicin treatment. Urinary RBP and NAG were evaluated in 83 preterm newborns divided in 4 groups: 37

The effect of polycythemia and hypoxia on urinary N-acetyl-beta-D-glucosaminidase activity in newborns.

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Urinary N-acetyl-beta-D-glucosaminidase activity was assayed in fullterm and preterm polycythemic neonates, in preterm infants with hypoxia, and in healthy newborns. There were no significant differences between fullterm and preterm babies or between appropriate for gestational age and small for

Selected biochemical variables in a model of neonatal anoxia in rats.

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OBJECTIVE To assess the time course of biochemical responses to neonatal anoxia. METHODS Neonatal anoxia was induced by placing 2-day-old rat pups into a glass chamber with 100% N(2) atmosphere, T=36.5 degrees C, for 20 minutes. The samples of serum, brain, lungs and liver were taken after 10

Effect of hypoxia on renal prostaglandin E2 production in human and rat neonates.

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Effect of hypoxia on renal prostaglandin E2 (PGE2) production was shown in asphyxic newborn infants and experimental hypoxic rats. In asphyxic infants, at postnatal day 1, the urinary excretion of PGE2 in severe asphyxia (1.00 +/- 0.19 pg/kg/min, n = 10) was lower than that of the mild asphyxia

Urinary N-acetyl-beta-D-glucosaminidase activity in healthy, polycythemic and hypoxic neonates.

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The authors investigated the urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in the case of 101 normal healthy and 20 polycythemic newborns and prematures, and 50 prematures suffering from hypoxia on the 1st, 2nd, 4th, 14th, and 28th day after birth. The obtained activities were referred to

N-Acetyl-beta-D-glucosaminidase in urine of patients with renal disease, and after renal transplants and surgery.

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The isoenzyme forms of N-acetyl-beta-D-glucosaminidase (NAG) have been studied in the urine of patients with renal disease, those with stable and rejecting renal transplants, and after surgery. Besides the increase in total urinary NAG excretion as an indicator of renal damage, changes were shown in

[Histochemical and biochemical study of radiation injury of the kidneys in gas hypoxia].

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A radioprotective effect of hypoxia was studied in kidney radiation. The use of hypoxic respiratory mixture containing 8% oxygen (the normal content is 21%) enhances kidney resistance to local single and fractionated irradiation. Determination of renal activity of succinate dehydrogenase, lactate

[Urinary N-acetyl-beta-D-glucosaminidase activity in healthy, polycythemic and hypoxic newborn infants].

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Urinary N-acetyl-beta-D-glucosaminidase (NAG) activity was assayed in 20 polycythemic newborns and prematures, together with 50 prematures suffering from hypoxia on the 1st, 2nd, 4th, 14th, and 28th day after birth. The enzyme was also assayed in 101 healthy newborns which provided normal reference

Acute and severe hypobaric hypoxia-induced muscle oxidative stress in mice: the role of glutathione against oxidative damage.

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This study intended to analyze: (1) the effects of acute and severe hypoxia exposure on skeletal muscle oxidative stress and oxidative damage markers; (2) the protective role of the antioxidant glutathione against oxidative damage; and (3) the expression of heat shock protein 70 kDa (HSP70) induced

The diagnostic role of urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in the detection of renal tubular impairment.

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The kidney function can be assessed by a number of methods. The urinary excretion of enzymes, in particular N-acetyl-beta-D-glucosaminidase (NAG), is considered a relatively simple, cheap, fast and non-invasive method in the detection and follow-up of renal tubular function under various conditions.

Renal tubular function and urinary N-acetyl-β-d-glucosaminidase and kidney injury molecule-1 levels in asthmatic children.

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BACKGROUND Asthma is a chronic inflammatory disorder of the airways which results in chronic hypoxia. Chronic hypoxia and inflammation can affect renal tubular function. OBJECTIVE The aim of this study was to investigate renal tubular function and early kidney injury molecules such as urinary

Randomized clinical trial of the effects of methylprednisolone on renal function after major vascular surgery.

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BACKGROUND Perioperative renal dysfunction following abdominal aortic aneurysm (AAA) repair is multifactorial and may involve hypotension, hypoxia and ischaemia-reperfusion injury. Studies of cardiac and hepatic transplant surgery have demonstrated beneficial effects on renal function of high-dose

Effect of melatonin on biochemical variables induced by phenytoin in organs of mothers, foetuses and offsprings of rats.

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The present pre- and postnatal study was carried out to investigate the effect of melatonin (MEL), a potent antioxidant, on biochemical variables in the in vivo model of intrauterine hypoxia in rats. Chronic hypoxia was induced pharmacologically by the administration of the anticonvulsant phenytoin

Cytoprotective effect of ulinastatin, a Kunitz-type protease inhibitor, on hypoxic injury in L2 cells treated with antimycin A via stabilization of lysosomal fragility.

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The cytoprotective effect of ulinastatin, a Kunitz-type protease inhibitor, was studied in L2 cells treated with antimycin A, which induces depletion of cellular adenosine triphosphate (ATP), so-called <hypoxia>>. Antimycin A treatment with 2 microM significantly elevated the release of

Urinary kidney injury molecules in children with febrile seizures.

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OBJECTIVE Hypoxia occurs following convulsions, and hypoxia is one of the most common causes of acute renal damage. The aim of this study was to investigate urinary levels of kidney injury molecules, including neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl-β-D-glucosaminidase (NAG), and

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