Programming with heterogeneous structures: Manipulating XML data using bondi

Manipulating semistructured data, such as XML, does not fit well within conventional programming languages. A typical manipulation requires finding all occurrences of a structure matching a structured search pattern, whose context may be different in different places, and both aspects cause difficulty. If a special-purpose query language is used to manipulate XML, an interface to a more general programming environment is required, and this interface typically creates runtime overhead for type conversion. However, adding XML manipulation to a general-purpose programming language has proven difficult because of problems associated with expressiveness and typing. We show an alternative approach that handles many kinds of patterns within an existing strongly-typed general-purpose programming language called bondi. The key ideas are to express complex search patterns as structures of simple patterns, pass these complex patterns as parameters to generic data-processing functions and traverse heterogeneous data structures by a generalized form of pattern matching. These ideas are made possible by the language's support for pattern calculus, whose typing on structures and patterns enables path and pattern polymorphism. With this approach, adding a new kind of pattern is just a matter of programming, not language design. Copyright © 2006, Australian Computer Society, Inc

Estradiol induces apoptosis via activation of miRNA-23a and p53: implication for gender difference in liver cancer development

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Effect of nucleos(t)ide analogues therapy on HBsAg, intrahepatic HBV DNA and covalently closed circular DNA levels

BACKGROUND: We aimed to study 1) the effects of 1-year nucleos(t)ide analogue (NA) therapy on HBsAg and covalently closed circular DNA (cccDNA) levels; and 2) the possible use of HBsAg reduction as a marker for cccDNA reduction. METHODS: We recruited 124 NA-treated patients with ...postprin

Serum levels of IL-33 and soluble ST2 and their association with disease activity in systemic lupus erythematosus

BACKGROUND: IL-33 has recently been found to be the specific ligand of ST2, an IL-1 receptor family member that is selectively expressed on Th2 cells and mediates Th2 response. This study aimed to measure serum levels of soluble form of ST2 (sST2) and IL-33 in patients with systemic lupus erythematosus (SLE) and to examine its association with disease activity. METHODS: Seventy SLE patients were evaluated for disease activity determined by SLE disease activity index (SLEDAI), serological features (anti-dsDNA antibody, C3 and C4) and 57 patients were evaluated longitudinally on a second occasion. IL-33 and sST2 were measured by sandwich ELISA in the 127 SLE serum samples and compared to 28 age- and sex-matched healthy controls. RESULTS: Serum sST2 level was significantly higher in SLE patients with active disease (0.51+0.18 ng/mL) compared to those with inactive disease (0.42+0.08 ng/mL) [P=0.006] and to normal controls (0.36+0.13 ng/mL) [P<0.001]. sST2 level correlated significantly and positively with SLEDAI, level of anti-dsDNA antibody and prednisolone dosage and negatively with C3 and remained significantly predictive of active disease after adjustment for prednisolone use in logistic regression analysis (odds ratio=4.6, P=0.01). sST2 level was sensitive to change in disease activity in longitudinal evaluation and not influenced by age, gender, and renal function. Elevated serum IL-33 was comparable in frequency (4.3% vs 7.1%, P=0.62) and levels (P=0.53) between SLE patients and controls. CONCLUSION: Elevated serum sST2 level in SLE patients was found to correlate with disease activity and was sensitive to change, suggesting a potential role as surrogate marker of disease activity.published_or_final_versionThe 15th Medical Research Conference (15th MRC), Department of Medicine, University of Hong Kong, Hong Kong, 16 January 2010. In Hong Kong Medical Journal, 2010, v. 16 n. 1, suppl. 1, p. 46, abstract no. 7

Interleukin-1β increases the risk of gastric cancer through induction of aberrant DNA methylation in a mouse model

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Sequence Variations of Full-Length Hepatitis B Virus Genomes in Chinese Patients with HBsAg-Negative Hepatitis B Infection

BACKGROUND: The underlying mechanism of HBsAg-negative hepatitis B virus (HBV) infection is notoriously difficult to elucidate because of the extremely low DNA levels which define the condition. We used a highly efficient amplification method to overcome this obstacle and achieved our aim which was to identify specific mutations or sequence variations associated with this entity. METHODS: A total of 185 sera and 60 liver biopsies from HBsAg-negative, HBV DNA-positive subjects or known chronic hepatitis B (CHB) subjects with HBsAg seroclearance were amplified by rolling circle amplification followed by full-length HBV genome sequencing. Eleven HBsAg-positive CHB subjects were included as controls. The effects of pivotal mutations identified on regulatory regions on promoter activities were analyzed. RESULTS: 22 and 11 full-length HBV genomes were amplified from HBsAg-negative and control subjects respectively. HBV genotype C was the dominant strain. A higher mutation frequency was observed in HBsAg-negative subjects than controls, irrespective of genotype. The nucleotide diversity over the entire HBV genome was significantly higher in HBsAg-negative subjects compared with controls (p = 0.008) and compared with 49 reference sequences from CHB patients (p = 0.025). In addition, HBsAg-negative subjects had significantly higher amino acid substitutions in the four viral genes than controls (all p<0.001). Many mutations were uniquely found in HBsAg-negative subjects, including deletions in promoter regions (13.6%), abolishment of pre-S2/S start codon (18.2%), disruption of pre-S2/S mRNA splicing site (4.5%), nucleotide duplications (9.1%), and missense mutations in "alpha" determinant region, contributing to defects in HBsAg production. CONCLUSIONS: These data suggest an accumulation of multiple mutations constraining viral transcriptional activities contribute to HBsAg-negativity in HBV infection.published_or_final_versio

Estrogen represses anti-apoptotic genes expression via MiR-23a: contribution to sex differences in the development of hepatocellular carcinoma

This journal suppl. entitled: Abstract Issue: 23rd Annual Conference of APASL, March 12–15, 2014, Brisbane, AustraliaTopic: 11. Hepatocellular Carcinoma - Basic Science: abstract no. 667postprin

Inhibiting ERK Activation with CI-1040 Leads to Compensatory Upregulation of Alternate MAPKs and Plasminogen Activator Inhibitor-1 following Subtotal Nephrectomy with No Impact on Kidney Fibrosis

Extracellular-signal regulated kinase (ERK) activation by MEK plays a key role in many of the cellular processes that underlie progressive kidney fibrosis including cell proliferation, apoptosis and transforming growth factor β1-mediated epithelial to mesenchymal transition. We therefore assessed the therapeutic impact of ERK1/2 inhibition using a MEK inhibitor in the rat 5/6 subtotal nephrectomy (SNx) model of kidney fibrosis. There was a twentyfold upregulation in phospho-ERK1/2 expression in the kidney after SNx in Male Wistar rats. Rats undergoing SNx became hypertensive, proteinuric and developed progressive kidney failure with reduced creatinine clearance. Treatment with the MEK inhibitor, CI-1040 abolished phospho- ERK1/2 expression in kidney tissue and prevented phospho-ERK1/2 expression in peripheral lymphocytes during the entire course of therapy. CI-1040 had no impact on creatinine clearance, proteinuria, glomerular and tubular fibrosis, and α-smooth muscle actin expression. However, inhibition of ERK1/2 activation led to significant compensatory upregulation of the MAP kinases, p38 and JNK in kidney tissue. CI-1040 also increased the expression of plasminogen activator inhibitor-1 (PAI-1), a key inhibitor of plasmin-dependent matrix metalloproteinases. Thus inhibition of ERK1/2 activation has no therapeutic effect on kidney fibrosis in SNx possibly due to increased compensatory activation of the p38 and JNK signalling pathways with subsequent upregulation of PAI-1

Identification of Hepatitis B Virus DNA Polymerase Sequences to Predict Virological Response to Entecavir Therapy

Poster Presentations: Emerging / Infectious DiseasesConference Theme: Translating Health Research into Policy and Practice for Health of the Populationpublished_or_final_versio