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Báo cáo y học: "Quantitative analysis of interferon alpha receptor subunit 1 and suppressor of cytokine signaling 1 gene transcription in blood cells of patients with chronic hepatitis C"

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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Quantitative analysis of interferon alpha receptor subunit 1 and suppressor of cytokine signaling 1 gene transcription in blood cells of patients with chronic hepatitis C | Sedeno-Monge et al. Virology Journal 2010 7 243 http www.virologyj.eom content 7 1 243 VIROLOGY JOURNAL RESEARCH Open Access Quantitative analysis of interferon alpha receptor subunit 1 and suppressor of cytokine signaling 1 gene transcription in blood cells of patients with chronic hepatitis C Virginia Sedeno-Monge1 2 4 Gerardo Santos-Lopez1 Rosa C Rocha-Gracia2 Daniel Meléndez-Mena3 Alberto Ramirez-Mata1 Verónica Vallejo-Ruiz1 Julio Reyes-Leyva1 Abstract Background Interferon IFN -a receptor 1 ifnarl and suppressor of cytokine signaling 1 socsl transcription levels were quantified in peripheral blood mononuclear cells PBMC of 59 patients infected with hepatitis C virus HCV and 17 non-infected individuals. Samples were obtained from patients infected with HCV that were either untreated or treated with IFN-a2 plus ribavirin for 1 year and divided into responders and non-responders based on viral load reduction 6 months after treatment. Ifnarl and socsl transcription was quantified by real-time RT-PCR and the fold difference 2- CT with respect to hprt housekeeping gene was calculated. Results Ifnarl transcription increased significantly in HCV-infected patients either untreated 3.26 0.31 responders 3.1 0.23 and non-responders 2.18 0.23 with respect to non-infected individuals 1 0.34 P 0.005 . Ifnarl transcription increased significantly P 0.003 in patients infected with HCV genotypes 1a 4.74 0.25 and 1b 2.81 0.25 but not in 1a1b 1.58 0.21 . No association was found of Ifnarl transcription with disease progress initial viral load or other clinical factors. With respect to socsl transcription values were similar for non-infected individuals 1 0.28 and untreated patients 0.99 0.41 but increased in responders 2.81 0.17 and non-responder patients 1.67 0.41 . Difference between responder and non-responder patients was not statistically significant. Socsl transcription increased in patients infected with HCV genotypes 1a and 1b 2.87 0.45 and 2.22 0.17 respectively but not

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