0000000000415921
AUTHOR
G. Tarantino
PRE-SERVICE TEACHER FORMATION: EXAMPLES OF PEDAGOGIC ACTIVITIES BY USING ICT TOOLS
Retinol-binding protein 4 (RBP4) : a new marker of G1 HCV-induced steatosis
INSULIN RESISTANCE AND SEVERITY OF FIBROSIS IN HCV GENOTYPE 1 CHRONIC HEPATITIS.
THE PHYSICS OF THE AIRCRAFT PILOTAGE
Teacher’s Education Using The Project Approach: Modeling the Airplane Flight Using ICT Based Strategies”
Elastic Waves: Common Representations and Related Teaching/Learning Sequences
In vivo liver expression of TLR2, TLR3 and TLR7 in chronic hepatitis C
The role of innate immune response mediated by Toll-like receptors in HCV infection, is not yet well understood and there is a lack of data regarding liver tissue expression of these molecules in chronic hepatitis C (CHC). Our study is aimed to investigate ex vivo, liver expression of TLR2, TLR3 and TLR7, which are more involved in the immune-pathogenesis of CHC, and to explore possible correlations with features of disease. We obtained liver biopsies and collected peripheral blood mononuclear cells (PBMC) from 23 consecutive patients with CHC and from 6 patients of control, without liver disease, undergoing surgery for cholecystectomy. The levels of TLRs mRNA in the samples were determined…
Insulin resistance and diabetes increase fibrosis in the liver of patients with genotype 1 HCV infection.
OBJECTIVES: Metabolic factors may affect the course of chronic hepatitis C (CHC). Insulin resistance (IR) determines steatosis, but its direct role in affecting progression of hepatic fibrosis is less clear. We aimed to assess whether increasing degrees of IR, up to overt diabetes, are linked to steatosis and higher stages of fibrosis in patients with CHC resulting from genotype 1 HCV (G1-HCV). METHODS: Two hundred one consecutive patients with G1-HCV infection were evaluated by liver biopsy and anthropometric and metabolic measurements, including IR, by the homeostasis model assessment (HOMA). Nondiabetic patients were defined as insulin resistant if HOMA-IR was >2.7. All biopsies were …