A review of 10 children on continuous ambulatory peritoneal dialysis

The experience of continuous ambulatory peritoneal dialysis in children of the Queen Mary Hospital for the past 11 years was reviewed. Seven boys and three girls (aged 4.3 to 15.9 years) were treated for a mean of 27 months (range 5 to 58 months). There was significant biochemical improvement and patients led an active life on continuous ambulatory peritoneal dialysis. The commonest complications were peritonitis, occurring on average once per 10 patient-months and mostly due to Staphylococcus spp. The median catheter survival time was 30 months. There were two technique failures due to fungal peritonitis which necessitated transfer to haemodialysis due to fungal peritonitis. The only mortality was due to concurrent cardiac disease. This review supports that children with renal failure in Hong Kong can be maintained on long term dialysis with a reasonable quality of life. However, significant morbidity due to infective and mechanical complications still exists. Continuous ambulatory peitonitis dialysis remains a temporary treatment modality while patients are waiting for renal transplantation.published_or_final_versio

The effectiveness of low-dose desmopressin in improving hypothermia-induced impairment of primary haemostasis under influence of aspirin - a randomized controlled trial.

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Hepatoprotective Effects of Chinese Medicinal Herbs: A Focus on Anti-Inflammatory and Anti-Oxidative Activities

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CLUSTAG: Hierarchical clustering and graph methods for selecting tag SNPs

Summary: Cluster and set-cover algorithms are developed to obtain a set of tag single nucleotide polymorphisms (SNPs) that can represent all the known SNPs in a chromosomal region, subject to the constraint that all SNPs must have a squared correlation R 2 > C with at least one tag SNP, where C is specified by the user. © The Author 2004. Published by Oxford University Press. All rights reserved.published_or_final_versio

Combining functional and linkage disequilibrium information in the selection of tag SNPs

Summary: We have developed an online program, WCLUSTAG, for tag SNP selection that allows the user to specify variable tagging thresholds for different SNPs. Tag SNPs are selected such that a SNP with user-specified tagging threshold C will have a minimum R2 of C with at least one tag SNP. This flexible feature is useful for researchers who wish to prioritize genomic regions or SNPs in an association study. © 2007 Oxford University Press.postprin

Bioavailable testosterone predicts a lower risk of Alzheimer’s disease in older men: a 1-year cohort study

Oral Presentationpublished_or_final_versionThe 15th Annual Research Conference of the Department of Medicine, The University of Hong Kong, Hong Kong, 16 January 2010. In Hong Kong Medical Journal, 2010, v. 16, suppl. 1, p. 16, abstract no. 1

Highly pathogenic avian influenza H5N1 virus delays apoptotic responses via activation of STAT3

Highly pathogenic avian influenza (HPAI) H5N1 virus continues to pose pandemic threat, but there is a lack of understanding of its pathogenesis. We compared the apoptotic responses triggered by HPAI H5N1 and low pathogenic H1N1 viruses using physiologically relevant respiratory epithelial cells. We demonstrated that H5N1 viruses delayed apoptosis in primary human bronchial and alveolar epithelial cells (AECs) compared to H1N1 virus. Both caspase-8 and -9 were activated by H5N1 and H1N1 viruses in AECs, while H5N1 differentially up-regulated TRAIL. H5N1-induced apoptosis was reduced by TRAIL receptor silencing. More importantly, STAT3 knock-down increased apoptosis by H5N1 infection suggesting that H5N1 virus delays apoptosis through activation of STAT3. Taken together, we demonstrate that STAT3 is involved in H5N1-delayed apoptosis compared to H1N1. Since delay in apoptosis prolongs the duration of virus replication and production of pro-inflammatory cytokines and TRAIL from H5N1-infected cells, which contribute to orchestrate cytokine storm and tissue damage, our results suggest that STAT3 may play a previously unsuspected role in H5N1 pathogenesis.published_or_final_versio

Effect of WeiJia on carbon tetrachloride induced chronic liver injury

Aim: To study the effect of WeiJia on chronic liver injury using carbon tetrachloride (CCl 4) induced liver injury animal model. Methods: Wista r rats weighing 180-220g were randomly divided into three groups: normal control group (Group A), CCl 4 induced liver injury control group (Group B) and CCl 4 induction with WeiJia treatment group (Group C). Each group consisted of 14 rats. Liver damage and fibrosis was induced by subcutaneous injection with 40% CCl 4 in olive oil at 3 mL/kg body weight twice a week for eight weeks for Groups B and C rats whereas olive oil was used for Group A rats. Starting from the third week, Group C rats also received daily intraperitoneal injection of WeiJia at a dose of 1.25 μg/kg body weight. Animals were sacrificed at the fifth week (4 male, 3 female), and eighth week (4 male, 3 female) respectively. Degree of fibrosis were measured and serological markers for liver fibrosis and function including hyaluronic acid (HA), type IV collagen (CIV), γ-glutamyl transferase (γ-GT), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined. Alpha smooth muscle actin (α-SMA) and proliferating cell nuclear antigen (PCNA) immunohistochemistry were also performed. Results: CCl 4 induction led to the damage of liver and development of fibrosis in Group B and Group C rats when compared to Group A rats. The treatment of WeiJia in Group C rats could reduce the fibrosis condition significantly compared to Group B rats. The effect could be observed after three weeks of treatment and was more obvious after eight weeks of treatment. Serum HA, CIV, ALT, AST and γ-GT levels after eight weeks of treatment for Group C rats were 58±22 μg/L (P 0.05) respectively, similar to normal control group (Group A), but significantly different from CCl 4 induced liver injury control group (Group B). An increase in PCNA and decrease in α-SMA expression level was also observed. Conclusion: WeiJia could improve liver function and reduce liver fibrosis which might be through the inhibition of stellate cell activity. © 2006 The WJG Press. All rights reserved.published_or_final_versio

Competitive Binding Between Id1 and E2F1 to Cdc20 Regulates E2F1 Degradation and Thymidylate Synthase Expression to Promote Esophageal Cancer Chemoresistance

Purpose: Chemoresistance is a major obstacle in cancer therapy. We found that fluorouracil (5-FU)-resistant esophageal squamous cell carcinoma cell lines, established through exposure to increasing concentrations of 5-FU, showed upregulation of Id1, IGF2, and E2F1. We hypothesized that these genes may play an important role in cancer chemoresistance. Experimental Design: In vitro and in vivo functional assays were performed to study the effects of Id1–E2F1–IGF2 signaling in chemoresistance. Quantitative real-time PCR, Western blotting, immunoprecipitation, chromatin immunoprecipitation, and dual-luciferase reporter assays were used to investigate the molecular mechanisms by which Id1 regulates E2F1 and by which E2F1 regulates IGF2. Clinical specimens, tumor tissue microarray, and Gene Expression Omnibus datasets were used to analyze the correlations between gene expressions and the relationships between expression profiles and patient survival outcomes. Results: Id1 conferred 5-FU chemoresistance through E2F1-dependent induction of thymidylate synthase expression in esophageal cancer cells and tumor xenografts. Mechanistically, Id1 protects E2F1 protein from degradation and increases its expression by binding competitively to Cdc20, whereas E2F1 mediates Id1-induced upregulation of IGF2 by binding directly to the IGF2 promoter and activating its transcription. The expression level of E2F1 was positively correlated with that of Id1 and IGF2 in human cancers. More importantly, concurrent high expression of Id1 and IGF2 was associated with unfavorable patient survival in multiple cancer types. Conclusions: Our findings define an intricate E2F1-dependent mechanism by which Id1 increases thymidylate synthase and IGF2 expressions to promote cancer chemoresistance. The Id1–E2F1–IGF2 regulatory axis has important implications for cancer prognosis and treatment. ©2015 AACR.postprin