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hepatitis c/hypoxia
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Pagina 1 a partire dal 58 risultati
Hypoxia impairs anti-viral activity of natural killer (NK) cells but has little effect on anti-fibrotic NK cell functions in hepatitis C virus infection.
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OBJECTIVE
Natural killer (NK) cells have been shown to exert anti-viral as well as anti-fibrotic functions in hepatitis C virus (HCV) infection. Previous studies, however, analyzed NK cell functions exclusively under atmospheric oxygen conditions despite the fact that the liver microenvironment is
Hepatitis C virus core protein induces hypoxia-inducible factor 1α-mediated vascular endothelial growth factor expression in Huh7.5.1 cells.
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Hepatitis C virus (HCV) infection is one of the major causes of hepatocellular carcinoma (HCC). It has been demonstrated that the overexpression of angiogenic factors are associated with the maintenance of liver neoplasia. Hypoxia-inducible factor 1α (HIF-1α) and vascular endothelial growth factor
Hepatitis C virus core protein upregulates the expression of vascular endothelial growth factor via the nuclear factor-κB/hypoxia-inducible factor-1α axis under hypoxic conditions.
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OBJECTIVE
Hepatitis C virus (HCV) core protein critically contributes to hepatocarcinogenesis, which is often observed in liver cirrhosis. Since the liver cirrhosis microenvironment is affected by hypoxia, we focused on the possible driving force of HCV core protein on signal relay from
Hepatitis C virus stabilizes hypoxia-inducible factor 1alpha and stimulates the synthesis of vascular endothelial growth factor.
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Hepatitis C virus (HCV) infection is one of the major causes of chronic hepatitis, liver cirrhosis, which subsequently leads to hepatocellular carcinoma (HCC). The overexpression of the angiogenic factors has been demonstrated in HCC. In this study, we investigated the potential of HCV gene
Hepatitis C virus-linked mitochondrial dysfunction promotes hypoxia-inducible factor 1 alpha-mediated glycolytic adaptation.
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Hepatitis C virus (HCV) infection induces a state of oxidative stress by affecting mitochondrial-respiratory-chain activity. By using cell lines inducibly expressing different HCV constructs, we showed previously that viral-protein expression leads to severe impairment of mitochondrial oxidative
Retraction for Nasimuzzaman et al., "Hepatitis C Virus Stabilizes Hypoxia-Inducible Factor 1α and Stimulates the Synthesis of Vascular Endothelial Growth Factor"
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[Effects of HCV core protein on the expression of hypoxia-inducible factor 1 alpha and vascular endothelial growth factor].
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OBJECTIVE
To investigate the effect of core protein of hepatitis C virus (HCV) on the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF).
METHODS
Huh7.5.1 cells were transfected with plasmid flag2B-core carrying HCV core gene, expression of
[Clinical features of interstitial pneumonitis due to interferon alpha therapy for chronic hepatitis C].
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OBJECTIVE
To analyze the clinical features of interstitial pneumonitis (IP) associated with interferon therapy for chronic hepatitis C.
METHODS
We report the first case of IP in China resulting from pegylated interferon alpha-2a in combination with ribavirin for treatment of hepatitis C viral
Successful treatment of severe hepatitis C-associated pulmonary vasculitis in a liver transplant recipient.
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BACKGROUND
We report the clinical course of a patient who developed fever, hypoxia, and bilateral pulmonary infiltrates two and a half years after orthotopic liver transplantation (OLT) for cirrhosis due to hepatitis C. The patient had a history of hepatitis C-associated vasculitis manifested by
Low oxygen tension enhances hepatitis C virus replication.
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Low oxygen tension exerts a significant effect on the replication of several DNA and RNA viruses in cultured cells. In vitro propagation of hepatitis C virus (HCV) has thus far been studied under atmospheric oxygen levels despite the fact that the liver tissue microenvironment is hypoxic. In this
Hypoxia among patients on the liver-transplant waiting list.
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BACKGROUND
Hepatopulmonary syndrome is formed by a triad of liver disease, intrapulmonary vascular dilatation and changes in blood gases. This condition is present in 4-32% of patients with cirrhosis.
OBJECTIVE
To analyze the blood gas changes data of patients in liver-transplant waiting
[Pulmonary toxicity by pegylated interferon alpha-2a in a patient with chronic hepatitis C].
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The combination therapy with pegylated interferon alpha and ribavirin has increasingly prescribed for chronic hepatitis C. Although many side effects of interferon such as flu-like symptoms, gastrointestinal and neuropsychiatric symptoms are well known, only several cases of interferon-induced
Clearance of Hepatitis C Virus Prior to Lung Transplantation: A Case Report.
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Hepatitis C virus (HCV) continues to be considered a relative contraindication to lung transplantation due to concerns of progression of liver disease with the introduction of immunosuppression. Since the recent introduction of effective antiviral therapy for HCV, new approaches in the management of
Gene expression profiles associated with anaemia and ITPA genotypes in patients with chronic hepatitis C (CH-C).
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Anaemia is a common side effect of ribavirin (RBV) which is used for the treatment of hepatitis C. Inosine triphosphatase gene polymorphism (C to A) protects against RBV-induced anaemia. The aim of our study was to genotype patients for inosine triphosphatase gene polymorphism rs1127354 SNP (CC or
Is smoking a prognostic factor in patients with chronic hepatitis C?
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The progression of chronic liver diseases is characterized by a common histopathological pathway comprising fibrosis formation and distortion of hepatic architecture which are the hallmark of evolution to cirrhosis. Several factors are responsible for the severity and progression of chronic
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