Array CGH testing in prenatal diagnosis: a promising new service with improved diagnostic yield and shortened reporting time

Eletronic Presentation: abstract no. 904Conference Theme: Enhancing Health - 協作同心‧醫澤社群INTRODUCTION: Array Comparative Genomic Hybridization (aCGH) with genome-wide coverage has proved to be valuable for postnatal and prenatal studies. Traditionally, prenatal diagnosis of chromosomal abnormalities has relied on conventional cytogenetics which required cell culture and chromosome analysis under micro…postprin

Clinical and electrophysiological features in Chinese patients with Kennedy's disease

Kennedy's disease is a X-linked neuromuscular disorder caused by an expanded trinucleotide repeat in the androgen receptor gene. To ascertain the clinical diagnosis of Kennedy's disease in a Chinese population, we used a rapid, accurate PCR-based sizing method for the CAG repeat allelotype. The clinical and electrophysiological features of affected patients are described. The CAG repeats ranged from 43 to 53 and were inversely correlated with the age of onset (r=-0.63; P<0.005). © 2004 Elsevier B.V. All rights reserved.link_to_subscribed_fulltex

Induction of proinflammatory cytokines in primary human macrophages by influenza A virus (H5N1) is selectively regulated by IFN regulatory factor 3 and p38 MAPK

The hyperinduction of proinflammatory cytokines and chemokines such as TNF-α, IFN-β, and CCL2/MCP-1 in primary human macrophages and respiratory epithelial cells by the highly pathogenic avian influenza H5N1 is believed to contribute to the unusual severity of human H5N1 disease. Here we show that TNF-α, IFN-β, and IFN-λ1 are the key mediators directly induced by the H5N1 virus in primary human macrophages. In comparison with human influenza (H1N1), the H5N1 virus more strongly activated IFN regulatory factor 3 (IRF3). IRF3 knockdown and p38 kinase inhibition separately and in combination led to a substantial reduction of IFN-β, IFN-λ1, and MCP-1 but only to a partial reduction of TNF-α. IRF3 translocation was independent of p38 kinase activity, indicating that IRF3 and p38 kinase are distinct pathways leading to cytokine production by H5N1 virus. We conclude that IRF3 and p38 kinase separately and predominantly contribute to H5N1-mediated induction of IFN-β, IFN-λ1, and MCP-1 but only partly control TNF-α induction. A more precise identification of the differences in the regulation of TNF-α and IFN-β could provide novel targets for the design of therapeutic strategies for severe human H5N1 influenza and also for treating other causes of acute respiratory distress syndrome. Copyright © 2009 by The American Association of Immunologists, Inc.link_to_subscribed_fulltex

Induction of proinflammatory cytokines in primary human macrophages by influenza A virus (H5N1) is selectively regulated by IFN regulatory factor 3 and p38 MAPK

The hyperinduction of proinflammatory cytokines and chemokines such as TNF-α, IFN-β, and CCL2/MCP-1 in primary human macrophages and respiratory epithelial cells by the highly pathogenic avian influenza H5N1 is believed to contribute to the unusual severity of human H5N1 disease. Here we show that TNF-α, IFN-β, and IFN-λ1 are the key mediators directly induced by the H5N1 virus in primary human macrophages. In comparison with human influenza (H1N1), the H5N1 virus more strongly activated IFN regulatory factor 3 (IRF3). IRF3 knockdown and p38 kinase inhibition separately and in combination led to a substantial reduction of IFN-β, IFN-λ1, and MCP-1 but only to a partial reduction of TNF-α. IRF3 translocation was independent of p38 kinase activity, indicating that IRF3 and p38 kinase are distinct pathways leading to cytokine production by H5N1 virus. We conclude that IRF3 and p38 kinase separately and predominantly contribute to H5N1-mediated induction of IFN-β, IFN-λ1, and MCP-1 but only partly control TNF-α induction. A more precise identification of the differences in the regulation of TNF-α and IFN-β could provide novel targets for the design of therapeutic strategies for severe human H5N1 influenza and also for treating other causes of acute respiratory distress syndrome. Copyright © 2009 by The American Association of Immunologists, Inc.link_to_subscribed_fulltex

The role of interferon regulatory factor 3 and p38 in influenza a virus induced pro-inflammatory cytokines

The hyperinduction of pro-inflammatory cytokines and chemokines such as TNF-α, IFN-β, and CCL2/MCP-1 in primary human macrophages by the highly pathogenic avian influenza H5N1 is believed to contribute to the unusual severity of human H5N1 disease. Here we show that TNF-α and IFN-β are the key mediators directly induced by the H5N1 virus in primary human macrophages. In comparison to human influenza (H1N1), the H5N1 virus more strongly activated interferon regulatory factor 3 (IRF3). IRF3 knock-down and p38 kinase inhibition separately and in combination led to a dramatic reduction of IFN-β and MCP-1 but only to a partial reduction of TNF-α. IRF3 translocation was independent of p38 activity indicating that IRF3 and p38 are distinct pathways leading to cytokine production by H5N1 virus. We conclude that IRF3 and p38 kinase separately and predominantly contribute to H5N1-mediated hyper-induction of IFN-β and MCP-1 but only partly control TNF-α induction. A more precise identification of the differences in the regulation of TNF-α and IFN-β may provide novel strategies for the design of therapeutic strategies for severe human H5N1 influenza and also for treating other causes of acute respiratory disease syndrome.abstractThe 7th Joint Conference of the International Cytokine Society and the International Society for Interferon and Cytokine Research, Montreal, Quebec, 12–16 October 2008. In Cytokine, 2008, v. 43 n. 3, p. 25

Array CGH evaluation for prenatal diagnosis in Hong Kong

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