hepatomegaly/protease

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HIV protease inhibitor induces fatty acid and sterol biosynthesis in liver and adipose tissues due to the accumulation of activated sterol regulatory element-binding proteins in the nucleus.

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The mechanism by which human immunodeficiency virus (HIV) protease inhibitor therapy adversely induces lipodystrophy and hyperlipidemia has not been defined. This study explored the mechanism associated with the adverse effects of the prototype protease inhibitor ritonavir in mice. Ritonavir

Impaired activity of plasma von Willebrand factor-cleaving protease may predict the occurrence of hepatic veno-occlusive disease after stem cell transplantation.

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Hepatic veno-occlusive disease (VOD) is a life-threatening complication after stem cell transplantation (SCT), characterized by thrombus formation in hepatic venules leading to a symptom triad of hyperbilirubinemia, hepatomegaly, and ascites. Multifactorial defects in the hemostatic system may

Cysteine protease inhibitors block schistosome hemoglobin degradation in vitro and decrease worm burden and egg production in vivo.

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Schistosome parasites utilize hemoglobin as a major protein source for their metabolism. Degradation of hemoglobin has been hypothesized to be mediated by both cysteine and aspartyl proteases secreted into the lumen of the parasite intestine. We now show that two distinct types of irreversible

Prognostic value of protease activated receptor-1 in children with acute lymphoblastic leukemia.

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BACKGROUND Acute Lymphoblastic leukemia (ALL) is a malignant disorder of lymphoid progenitor cells that proliferate and replace the normal hematopoietic cells of the bone marrow. Protease-activated receptors (PARs) comprise a family of trans-membrane G-protein coupled receptors. Protease-activated

A syndrome of lipoatrophy, lactic acidaemia and liver dysfunction associated with HIV nucleoside analogue therapy: contribution to protease inhibitor-related lipodystrophy syndrome.

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BACKGROUND Lipodystrophy (LD; peripheral lipoatrophy, central adiposity) hyperlipidaemia and insulin resistance often complicate protease inhibitor-containing antiretroviral therapy. Lipoatrophy and abdominal distension were observed in protease inhibitor-naive nucleoside analogue reverse

[Alpha 1-antitrypsin deficiency in childhood].

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Alpha-1-antitrypsin is a blood glycoprotein synthesized in the liver. It is a protease inhibitor of the serpine group and has a specific action for elastase. Alpha-1-antitrypsin electrophoresis shows about 20 phenotypes, the normal one being PiM. The allele PiZ is usually responsible for liver or

Diagnosis of alpha-1-antitrypsin deficiency in bleeding disorder-related neonatal death.

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Alpha-1-antitrypsin (AAT) deficiency is a rare genetic disorder characterized by hepatitis in neonates, childhood and adulthood (protease inhibitor (PI)*ZZ) and emphysema with or without hepatitis (PI*ZZ)/(PI*SS,SZ or null) in adulthood. We report the case of a female neonate born at 40 weeks of

Acute hepatitis and bleeding possibly induced by zidovudine and ritonavir in an infant with HIV infection.

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Acute hepatitis led to abnormal coagulopathy, bleeding, and death in a nonhemophiliac infant infected with the human immunodeficiency virus, possibly due to zidovudine or ritonavir or both. Acute hepatitis during ritonavir treatment and episodes of spontaneous bleeding have been reported in patients

Localization of Tubulin from the Carcinogenic Human Liver Fluke, Opisthorchis viverrini.

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BACKGROUND Opisthorchiasis caused by Opisthorchis viverrini, is of considerable public health importance in Southeast Asia, particularly in Lao People's Democratic Republic and Thailand. The infection is associated with a number ofhepatobiliary diseases including cholangitis, obstructive jaundice,

[Alpha-antitrypsin deficiency in infancy].

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Clinical, histological (including electron-microscopic), immunohistochemical and genetic studies were performed on two infants with alpha1-antitrypsin deficiency. The clinical picture was one of neonatal biliary stasis. Liver biopsies revealed multiple cytoplasmic acidophilic bodies within many

Ethanol administration alters the proteolytic activity of hepatic lysosomes.

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Protein accumulation in liver cells contributes to alcohol-induced hepatomegaly and is the result of an ethanol-elicited deceleration of protein catabolism (Alcohol Clin Exp Res 13:49, 1989). Because lysosomes are active in the degradation of most hepatic proteins, the present studies were conducted

The effect of prenatal highly active antiretroviral therapy on the transmission of congenital and perinatal/early postnatal cytomegalovirus among HIV-infected and HIV-exposed infants.

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BACKGROUND Before highly active antiretroviral therapy (HAART), congenital cytomegalovirus (CMV) rates were higher among human immunodeficiency virus (HIV)-exposed infants than unexposed infants. This study examines congenital and perinatal/early postnatal (P/EP) CMV among HIV-exposed infants pre-

Does the mutation of the SERPINA1 gene contribute to liver damage and cholestasis in patients with diagnosed cystic fibrosis? preliminary study.

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Mutation of the SERPINA1 gene is present in about 2% of patients with cystic fibrosis but is more common and accounts for about 5% in patients with cystic fibrosis and co-existing liver lesions. The SERPINA1 gene is responsible for the synthesis of a serine protease inhibitor. The protein related

Liver disease associated with alpha1-antitrypsin deficiency in childhood.

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Liver disease in children with alpha1-antitrypsin deficiency and protease inhibitor type ZZ does not necessarily carry a bad prognosis. Fourteen of our 18 patients presented with the neonatal hepatitis syndrome and four had hepatomegaly without jaundice. Although four patients have died of cirrhosis

[Hereditary alpha 1-antitrypsin deficiency and infantile cirrhosis of the liver].

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A report on 9 cases of infantile hepatopathy and cirrhosis of the liver respectively in cases of hereditary autosome-recessive alpha 1-antitrypsin deficiency (alpha 1-ATM). The genetic variants of the serum-protease-inhibitor (Pi) alpha 1-antitrypsin (alpha 1-AT) were examined by means of

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