Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1971 to 1975, HBV-induced hepatitis was observed in 80 children. The diagnosis was based upon the detection in serum of HBsAg and/or the secondary occurrence of anti-HBs. Thirty-one patients presented with acute viral hepatitis, 16 with severe or fulminant hepatitis, 17 with chronic persistent hepatitis, 12 with chronic active hepatitis, and 4 were asymptomatic chronic carriers of HBsAg. Twenty-nine of 80 children were under one year of age (36%), the peak of frequency occurring from 2 to 5 months. The source of infection, determined in 27 of 29 infants, was administration of blood derivatives in 15 cases and contact with an HBsAg carrier mother in nine instances. In the latter type, the incubation time (103 days) was compartible with an oral route of infection, Persistent antigenemia occurred in only 3 of 29 patients. The overt type of disease developed by most infants, as well as the small number of patients who became HBsAg carriers, suggest that the carrier state, often encountered in neonatally infected infants in other countries, may be related to environmental or genetic factors rather than to immaturity of theimmune system.
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PMID:Hepatitis B in children. I. Analysis of 80 cases of acute and chronic hepatitis B. 61 70

The usual histologic pattern in acute viral hepatitis (AVH) includes cellular abnormalities predominantly in the perivenular (zone 3) hepatocytes and changes interpreted as representing regenerative activity in the periportal (zone 1) hepatocytes. Enzyme histochemical and ultrastructural studies of livers of 12 patients with AVH were undertaken to see whether these features support the concept of regeneration of hepatocytes in zone 1. The swollen hepatocytes in the perivenular areas were hydropic, with dilated or eccentric rough endoplasmic reticulum and decreased or vesicular smooth endoplasmic reticulum; correspondingly, the glucose-6-phosphatase activity (reflecting, when present, intact and functional endoplasmic reticulum) was markedly decreased. Succinic dehydrogenase and diphosphopyridine nucleotide diaphorase activities, representing mitochondrial enzymes, were limited to the perinuclear or pericanalicular cytoplasm of swollen hepatocytes. gamma-Glutamyl transpeptidase activity was increased. The periportal hydropic hepatocytes were small and arranged in clusters displacing sinusoids. Ultrastructurally, these hepatocytes had nearly normal organelles but scanty smooth endoplasmic reticulum. Activities of the enzymes glucose-6-phosphatase, succinic dehydrogenase, and diphosphopyridine nucleotide diaphorase were weak, although glycogen was abundant. gamma-Glutamyl transpeptidase activity was scanty in these hepatocytes. These findings from enzyme histochemical and electron microscopic studies could be interpreted as evidence of functional deterioration of perivenular swollen hepatocytes and relative functional immaturity of periportal hydropic clustered hepatocytes, suggesting regeneration of zone 1 hepatocytes.
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PMID:Acute viral hepatitis: morphologic and functional correlations in human livers. 669 43

Over one million people all over the world die every year due to the complications of HBV infections. This problem is particularly important in Asia, Africa and in the West Pacific region where HBV infection is widely spread (from 5-20% up to 80% of all infected people in the world). In these regions HBV infections are transmitted mostly perinatally or during early childhood. In North America and in West Europe where after introducing anti-HBV vaccinations less than 2% of the population is affected, infections are usually transmitted by intravenous drug abuse, sexual intercourse, or much less frequently by blood transfusions. The immaturity of immune system in young children is responsible for the fact that nearly 90% of HBV infections acquired in infancy and 40-70% of HBV infections before the age of 3 years, result in chronic viral hepatitis. Therefore, the choice of an efficient and safe therapy is one of the most important problems. In this paper current data concerning indications for treatment and side-effects of interferon-alpha and lamivudine therapy in children with chronic viral hepatitis type B are presented.
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PMID:[Chronic hepatitis B in children--is it still a real problem?]. 1860 86

The limited availability of experimental tumor models that faithfully mimic the progression of human tumors and their response to therapy remains a major bottleneck to the clinical translation and application of novel therapeutic principles. To address this challenge in hepatocellular carcinoma (HCC), one of the deadliest and most common cancers in the world, we developed and validated an inducible model of hepatocarcinogenesis in adult mice. Tumorigenesis was triggered by intravenous adenoviral delivery of Cre recombinase in transgenic mice expressing the hepatocyte-specific albumin promoter, a loxP-flanked stop cassette, and the SV40 large T-antigen (iAST). Cre recombinase-mediated excision of the stop cassette led to a transient viral hepatitis and resulted in multinodular tumorigenesis within 5 to 8 weeks. Tumor nodules with histologic characteristics of human HCC established a functional vasculature by cooption, remodeling, and angiogenic expansion of the preexisting sinusoidal liver vasculature with increasing signs of vascular immaturity during tumor progression. Treatment of mice with sorafenib rapidly resulted in the induction of vascular regression, inhibition of tumor growth, and enhanced overall survival. Vascular regression was characterized by loss of endothelial cells leaving behind avascular type IV collagen-positive empty sleeves with remaining pericytes. Sorafenib treatment led to transcriptional changes of Igf1, Id1, and cMet over time, which may reflect the emergence of potential escape mechanisms. Taken together, our results established the iAST model of inducible hepatocarcinogenesis as a robust and versatile preclinical model to study HCC progression and validate novel therapies.
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PMID:An inducible hepatocellular carcinoma model for preclinical evaluation of antiangiogenic therapy in adult mice. 2490 23