alpha 1-antitrypsin deficiency/carbohydrate

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Galactosamine-induced alpha 1-antitrypsin deficiency in rats. Alterations in plasma glycoproteins and alpha 1-antitrypsin carbohydrate composition.

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Administration of D-galactosamine (GalNH2) is known to produce alterations in plasma glycoprotein levels, including alpha 1-antitrypsin. The authors have studied the effects of GalNH2 on circulating protein bound carbohydrates and on the plasma concentrations of two alpha 1-antiproteases,

[Alpha 1-antitrypsin deficiency with histologic expression of metabolic disease of carbohydrates].

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A two months old male affected by alpha-1-AT PiZZ deficiency with severe transient neonatal cholestasis is presented. Two hepatic biopsies were practiced in neonatal period. There was no evidence of PAS positive globules, but an intense univacuolar steatosis and a rossetoid transformation of

Isolation and characterization of alpha 1-antitrypsin in PAS-positive hepatic granules from rats with experimental alpha 1-antitrypsin deficiency.

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Chronic galactosamine (GalNH2) administration in rats decreases plasma alpha 1-antitrypsin (AAT) levels to 10-50% of control levels and induces the formation of diastase-resistant, PAS-positive granules, which contain AAT in hepatocytes. This report describes the isolation and purification of

Characterization of alpha1-antitrypsin in the inclusion bodies from the liver in alpha 1-antitrypsin deficiency.

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alpha1-antitrypsin was isolated from periodic acid-Schiff-positive inclusion bodies from the hepatocytes of patients with alpha1-antitrypsin deficiency and further purified to enable more detailed chemical analysis. Amino acid and cyanogen bromide fragmentation studies showed a close similarity

[New aspects of the development of liver diseases – with special regard to the role of autophagy and microRNA]

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Autophagy plays an important role in the homeostasis of the cells and it may be upregulated in response to several types of stresses. Deregulation of autophagy is a key mechanism in the pathogenesis and progression of several liver diseases. Deficient autophagy can contribute to liver steatosis, to

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