Temperature as a modifier of the effects of fine particulate matter on acute mortality in Hong Kong

Interactions between particulate matter with aerodynamic diameter less than or equal to 2.5 μm (PM2.5) and temperature on mortality have not been well studied, and results are difficult to synthesize. We aimed to assess modification of temperature on the association between PM2.5 and cause-specific mortality by stratifying temperature into low, medium, and high stratum in Hong Kong, using data from 1999 to 2011. The mortality effects of PM2.5 were stronger in low temperature stratum than those in high. The excess risk (%) per 10 μg/m3 increase in PM2.5 at lag 0–1 in low temperature stratum were 0.94% (95% confidence interval: 0.65, 1.24) for all natural, 0.88% (0.38, 1.37) for cardiovascular, and 1.15% (0.51, 1.79) for respiratory mortality. We found statistically significant interaction of PM2.5 and temperature between low and high temperature stratum for all natural mortality. Our results suggested that temperature might modify mortality effects of PM2.5 in Hong Kong.postprin

Sputum elastase activity correlates with clinical parameters in steady state bronchiectasis

Conference Theme: Challenges to specialists in the 21st centurypublished_or_final_versio

Meta-analysis of adverse health effects due to air pollution in Chinese populations

BACKGROUND: Pooled estimates of air pollution health effects are important drivers of environmental risk communications and political willingness. In China, there is a lack of review studies to provide such estimates for health impact assessments. METHODS: We systematically searched the MEDLINE database using keywords of 80 major Chinese cities in Mainland China, Hong Kong and Taiwan on 30 June 2012, yielding 350 abstracts with 48 non-duplicated reports either in English or Chinese after screening. We pooled the relative risks (RR) per 10 μg/m(3) of particulate matter (PM(10)), nitrogen dioxide (NO(2)), sulphur dioxide (SO(2)) and ozone (O(3)). RESULTS: For short-term effects, the pooled RR (p < 0.05) ranges were: 1.0031 (PM(10)) to 1.0140 (NO(2)) for all-cause mortality, 1.0034 (cardiopulmonary, PM(10)) to 1.0235 (influenza and pneumonia, SO(2)) for 9 specific-causes mortality, 1.0021 (cardiovascular, PM(10)) to 1.0162 (asthma, O(3)) for 5 specific-causes hospital admissions. For birth outcomes, the RR (p < 0.05) ranged from 1.0051 (stillbirth, O(3)) to 1.1189 (preterm-birth, SO(2)) and for long-term effect on mortality from 1.0150 (respiratory, SO(2)) to 1.0297 (respiratory, NO(2)). Publication bias was absent (Egger test: p = 0.326 to 0.624). Annual PM(10) and NO(2) concentrations were inversely associated with RR of mortality (p = 0.017-0.028). CONCLUSIONS: Evidence on short-term effects of air pollution is consistent and sufficient for health impact assessment but that on long-term effects is still insufficient

Epstein-barr virus-encoded latent membrane protein 1 impairs G2 checkpoint in human nasopharyngeal epithelial cells through defective Chk1 activation

Nasopharyngeal carcinoma (NPC) is a common cancer in Southeast Asia, particularly in southern regions of China. EBV infection is closely associated with NPC and has long been postulated to play an etiological role in the development of NPC. However, the role of EBV in malignant transformation of nasopharyngeal epithelial cells remains enigmatic. The current hypothesis of NPC development is that premalignant nasopharyngeal epithelial cells harboring genetic alterations support EBV infection and expression of EBV genes induces further genomic instability to facilitate the development of NPC. The latent membrane protein 1 (LMP1) is a well-documented EBV-encoded oncogene. The involvement of LMP1 in human epithelial malignancies has been implicated, but the mechanisms of oncogenic actions of LMP1, particularly in nasopharyngeal cells, are unclear. Here we observed that LMP1 expression in nasopharyngeal epithelial cells impaired G2 checkpoint, leading to formation of unrepaired chromatid breaks in metaphases after γ-ray irradiation. We further found that defective Chk1 activation was involved in the induction of G2 checkpoint defect in LMP1-expressing nasopharyngeal epithelial cells. Impairment of G2 checkpoint could result in loss of the acentrically broken chromatids and propagation of broken centric chromatids in daughter cells exiting mitosis, which facilitates chromosome instability. Our findings suggest that LMP1 expression facilitates genomic instability in cells under genotoxic stress. Elucidation of the mechanisms involved in LMP1-induced genomic instability in nasopharyngeal epithelial cells will shed lights on the understanding of role of EBV infection in NPC development. © 2012 Deng et al.published_or_final_versio

Berberine induces autophagic cell death and mitochondrial apoptosis in liver cancer cells: The cellular mechanism

Extensive studies have revealed that berberine, a small molecule derived from Coptidis rhizoma (Huanglian in Chinese) and many other plants, has strong anti-tumor properties. To better understand berberine-induced cell death and its underlying mechanisms in cancer, we examined autophagy and apoptosis in the human hepatic carcinoma cell lines HepG2 and MHCC97-L. The results of this study indicate that berberine can induce both autophagy and apoptosis in hepatocellular carcinoma cells. Berberine-induced cell death in human hepatic carcinoma cells was diminished in the presence of the cell death inhibitor 3-methyladenine, or following interference with the essential autophagy gene Atg5. Mechanistic studies showed that berberine may activate mitochondrial apoptosis in HepG2 and MHCC97-L cells by increasing Bax expression, the formation of permeable transition pores, cytochrome C release to cytosol, and subsequent activation of the caspases 3 and 9 execution pathway. Berberine may also induce autophagic cell death in HepG2 and MHCC97-L cells through activation of Beclin-1 and inhibition of the mTOR-signaling pathway by suppressing the activity of Akt and up-regulating P38 MAPK signaling. This is the first study to describe the role of Beclin-1 activation and mTOR inhibition in berberine-induced autophagic cell death. These results further demonstrate the potential of berberine as a therapeutic agent in the emerging list of cancer therapies with novel mechanisms. © 2010 Wiley-Liss, Inc.postprin

Berberine Suppresses Cyclin D1 Expression through Proteasomal Degradation in Human Hepatoma Cells

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Dyslexia in Hong Kong : challenges and opportunities

Author name used in this publication: Cecilia W. P. Li-TsangAuthor name used in this publication: Pui Yee Grace Lung2011-2012 > Academic research: not refereed > Chapter in an edited book (author)Version of RecordPublishe

Outcome analysis of management of liver trauma: A 10-year experience at a trauma center

published_or_final_versio

Impact of G 2 checkpoint defect on centromeric instability

Centromeric instability is characterized by dynamic formation of centromeric breaks, deletions, isochromosomes and translocations, which are commonly observed in cancer. So far, however, the mechanisms of centromeric instability in cancer cells are still poorly understood. In this study, we tested the hypothesis that G 2 checkpoint defect promotes centromeric instability. Our observations from multiple approaches consistently support this hypothesis. We found that overexpression of cyclin B1, one of the pivotal genes driving G 2 to M phase transition, impaired G 2 checkpoint and promoted the formation of centromeric aberrations in telomerase-immortalized cell lines. Conversely, centromeric instability in cancer cells was ameliorated through reinforcement of G 2 checkpoint by cyclin B1 knockdown. Remarkably, treatment with KU55933 for only 2.5 h, which abrogated G 2 checkpoint, was sufficient to produce centromeric aberrations. Moreover, centromeric aberrations constituted the major form of structural abnormalities in G 2 checkpoint-defective ataxia telangiectasia cells. Statistical analysis showed that the frequencies of centromeric aberrations in G 2 checkpoint-defective cells were always significantly overrepresented compared with random assumption. As there are multiple pathways leading to G 2 checkpoint defect, our finding offers a broad explanation for the common occurrence of centromeric aberrations in cancer cells. © 2011 Macmillan Publishers Limited All rights reserved.postprin