Decentralization and marketization of education in China: challenges for migrant children and social harmony

Parallel Session II Governing the Asian Giants - Good Governance and Public Policy: Session on Managing Urban Development and Policy ResponsespostprintLaunch Conference for Journal of Asian Public Policy: "Governing the Asian Giants: The Search for Good Governance and Sustainable Development in China and India", Hong Kong, China, 29-30 March 2010

Ethnic differences in cardiovascular risk in rheumatic disease: Focus on Asians

Rheumatic diseases are associated with high cardiovascular morbidity and mortality. Considerable differences exist in the frequency of cardiovascular disease (CVD) risk factors and events among people of different ethnic origins, but little is known of the ethnic variations in the relative distribution of CVD risk factors and the degree of atherosclerosis in patients with rheumatic diseases. Understanding this variation will provide insight into the underlying pathogenesis of CVD in patients with rheumatic diseases, and aid in future studies of the detection and management of this complication. In general, although Asian patients seem to have fewer background CVD risk factors and are less affected by metabolic syndrome (MetS) than their non-Asian counterparts, those with rheumatic disease are equally as susceptible to CVD. Furthermore, it seems that systemic inflammation and mechanisms that do not involve conventional CVD risk factors and MetS have an important role in the development of atherosclerosis in patients with rheumatic diseases. Here we examine the frequency of conventional CVD risk factors and the prevalence of MetS in both Asian and non-Asian patients with selected rheumatic diseases. We also discuss the burden of CVD, as evaluated using various surrogate markers in these patients, and their overall CVD mortality rate. © 2011 Macmillan Publishers Limited. All rights reserved.postprin

Changes in urinary metabolomic profile during relapsing renal vasculitis

Current biomarkers of renal disease in systemic vasculitis lack predictive value and are insensitive to early damage. To identify novel biomarkers of renal vasculitis flare, we analysed the longitudinal urinary metabolomic profile of a rat model of anti-neutrophil cytoplasmic antibody (ANCA) vasculitis. Wistar-Kyoto (WKY) rats were immunised with human myeloperoxidase (MPO). Urine was obtained at regular intervals for 181 days, after which relapse was induced by re-challenge with MPO. Urinary metabolites were assessed in an unbiased fashion using nuclear magnetic resonance (NMR) spectroscopy, and analysed using partial least squares discriminant analysis (PLS-DA) and partial least squares regression (PLS-R). At 56 days post-immunisation, we found that rats with vasculitis had a significantly different urinary metabolite profile than control animals; the observed PLS-DA clusters dissipated between 56 and 181 days, and re-emerged with relapse. The metabolites most altered in rats with active or relapsing vasculitis were trimethylamine N-oxide (TMAO), citrate and 2-oxoglutarate. Myo-inositol was also moderately predictive. The key urine metabolites identified in rats were confirmed in a large cohort of patients using liquid chromatography-mass spectrometry (LC-MS). Hypocitraturia and elevated urinary myo-inositol remained associated with active disease, with the urine myo-inositol:citrate ratio being tightly correlated with active renal vasculitis

Delayed clearance of viral load and marked cytokine activation in severe cases of pandemic H1N1 2009 influenza virus infection

Background: Infections caused by the pandemic H1N1 2009 influenza virus range from mild upper respiratory tract syndromes to fatal diseases. However, studies comparing virological and immunological profile of different clinical severity are lacking. Methods: We conducted a retrospective cohort study of 74 patients with pandemic H1N1 infection, including 23 patients who either developed acute respiratory distress syndrome (ARDS) or died (ARDS-death group), 14 patients with desaturation requiring oxygen supplementation and who survived without ARDS (survived-withoutARDS group), and 37 patients with mild disease without desaturation (mild-disease group). We compared their pattern of clinical disease, viral load, and immunological profile. Results: Patients with severe disease were older, more likely to be obese or having underlying diseases, and had lower respiratory tract symptoms, especially dyspnea at presentation. The ARDS-death group had a slower decline in nasopharyngeal viral loads, had higher plasma levels of proinflammatory cytokines and chemokines, and were more likely to have bacterial coinfections (30.4%), myocarditis (21.7%), or viremia (13.0%) than patients in the survived-without-ARDS or the mild-disease groups. Reactive hemophagocytosis, thrombotic phenomena, lymphoid atrophy, diffuse alveolar damage, and multiorgan dysfunction similar to fatal avian influenza A H5N1 infection were found at postmortem examinations. Conclusions: The slower control of viral load and immunodysregulation in severe cases mandate the search for more effective antiviral and immunomodulatory regimens to stop the excessive cytokine activation resulting in ARDS and death. © 2010 by the Infectious Diseases Society of America. All rights reserved.published_or_final_versio

Total flavonoid fraction of the Herba epimedii extract suppresses urinary calcium excretion and improves bone properties in ovariectomised mice

2010-2011 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Pathophysiological mechanisms for the respiratory syncytial virus-reactive airway disease link

There is substantial epidemiological evidence supporting the concept that respiratory syncytial virus (RSV) lower respiratory tract infection in infancy may be linked to the development of reactive airway disease (RAD) in childhood. However, much less is known concerning the mechanisms by which this self-limiting infection leads to airway dysfunction that persists long after the virus is cleared from the lungs. A better understanding of the RSV–RAD link may have important clinical implications, particularly because prevention of RSV lower respiratory tract infection may reduce the occurrence of RAD later in life. Among the mechanisms proposed to explain the chronic sequelae of RSV infection is the interaction between the subepithelial neural network of the airway mucosa and the cellular effectors of inflammatory and immune responses to the virus. The body of clinical literature linking RSV and RAD is reviewed herein, as are the cellular and molecular mechanisms of neuroimmune interactions and neural remodeling that may underlie this link, and the possibility that preventing the infection may result in a decreased incidence of its chronic sequelae

Solution structure of a repeated unit of the ABA-1 nematode polyprotein allergen of ascaris reveals a novel fold and two discrete lipid-binding sites

Parasitic nematode worms cause serious health problems in humans and other animals. They can induce allergic-type immune responses, which can be harmful but may at the same time protect against the infections. Allergens are proteins that trigger allergic reactions and these parasites produce a type that is confined to nematodes, the nematode polyprotein allergens (NPAs). These are synthesized as large precursor proteins comprising repeating units of similar amino acid sequence that are subsequently cleaved into multiple copies of the allergen protein. NPAs bind small lipids such as fatty acids and retinol (Vitamin A) and probably transport these sensitive and insoluble compounds between the tissues of the worms. Nematodes cannot synthesize these lipids, so NPAs may also be crucial for extracting nutrients from their hosts. They may also be involved in altering immune responses by controlling the lipids by which the immune and inflammatory cells communicate. We describe the molecular structure of one unit of an NPA, the well-known ABA-1 allergen of Ascaris and find its structure to be of a type not previously found for lipid-binding proteins, and we describe the unusual sites where lipids bind within this structur

Gene mapping of familial amyotrophic lateral sclerosis

INTRODUCTION: Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disorder characterized by gradual death of motor neurons in cerebral cortex, brain stem, and spinal cord. The pathogenetic mechanism remains unclear for the vast majority of cases. About 10% of ALS cases are familial (FALS). Cu/Zn superoxide dismutase (SOD1) gene accounts for about 10% of autosomal dominant FALS and the gene(s) responsible for the rest of ALS/ FALS remain(s) to be found. METHOD: We recruited a large Chinese kindred without SOD1 mutation for linkage analysis. Peripheral blood samples were collected and DNA were extracted from peripheral lymphocyte. We screened the family with ~ 400 polymorphic microsatellite markers. The genotyping data were subjected to model-based and model-free linkage analysis. RESULT: Using MLINK of LINKAGE (Ver 5.2) package, we found a maximum LOD score of 4.357, ?[m=f]=0.0 at a microsatellite marker located at distal long arm of chromosome 8. Multipoint analysis by GENEHUNTER (Ver 1.2) revealed a maximum multipoint LOD score of 3.909 and NPL score 9.209. Haplotype analyses revealed a critical region which spanned 10.18-cM on chromosome 8. CONCLUSION: We identified a 10.18-cM critical FALS region on chromosome 8. Further analyses using positional cloning and candidate gene approach are indicated to delineate the underlying genetic defect for FALS in this family.published_or_final_versio