Changing epidemiology of measles in Hong Kong from 1961 to 1990 - Impact of a measles vaccination program

With the use of measles vaccine since 1967, Hong Kong has experienced a low incidence of measles until a major outbreak in 1988. A shift in the distribution of susceptible children to older age groups was suddenly accelerated in the 1988 outbreak. The attack rate increased by 18.9-fold for children >10 years old, while that for those in the best-protected age group of 1-4 years was only 2.2-fold. Of the cases during that outbreak, 56.3% would have been considered preventable with the present vaccination regimen, and vaccine failures accounted for only 20.4% of the cases. Present control strategies aim at increasing the coverage rate rather than introducing a two- dose regimen, which may be necessary when vaccine failures account for a larger proportion of measles cases.published_or_final_versio

HIV-1 Tat dysregulation of KSHV induced immune response through the production of IL-8

Poster PresentationHuman immunodeficiency virus (HIV) causes acquired immunodeficiency syndrome (AIDS) and is a major health issue around the world. HIV is known to induce a number of pathological problems in AIDS patients via the transactivator (Tat) protein that is expressed and released by infected cells. One of the most important function of Tat is the dysregulation of the immune response. IL-8 is a chemokine known to be highly expressed in AIDS patients and Tat plays a major role in its production. IL-8 increases the HIV transmission and replication rate; and plays a role in Kaposi's sarcoma associated herpesvirus (KSHV) infection, which is a major opportunistic pathogen that AIDS patients are at risk to. KSHV is also known to induce the expression of IL-8 in patients, and IL-8 is known to assist tumour development by increasing angiogenesis. In our study, we investigated the role that Tat may have in manipulating the expression of IL-8 induced by KSHV in primary blood monocyte derived macrophages (PBMac). The results showed that pretreatment of PBMac with Tat inhibited the expression of IL-8 induced by KSHV by approximately 40%. We also found that Tat was able to inhibit the phosphorylation of STAT-1 induced by KSHV, and the inhibition of STAT-1 phosporylation was related to the expression of IL-8 induced by KSHV. In conclusion, we found that Tat was able to manipulate the expression of IL-8 induced by KSHV in macrophages, and this inhibition of IL-8 expression was regulated through the STAT-1 related pathways.published_or_final_versio

The role of oncogene in mycobacteria-induced antophagy in human macrophages

Poster PresentationMacrophages are the major immunocytes to initiate both innate and adaptive immune responses against Mycobacterium tuberculosis (Mtb), a causative agent of tuberculosis. Upon mycoabcteria infection, macrophages could eliminate the intracellular bacteria through different cell death pathways, including apoptosis and autophagy. c-Myc is a transcription factor that regulates a variety of target genes and control different cellular functions such as proliferation and immune resposnse. Recently, our group revealed that c-Myc has a potential role in regulating the antimicrobial responses in macrophages. Here we use BCG, a live attenuated strain of Mycobacterium bovis, which is similar to Mtb in antigenic composition, as a model to study the role of c-Myc in regulating mycobacteria-induced autophagy. We first investigated the role of c-Myc in BCG-induced LC3BII levels. Knocking down c-Myc by siRNA could decrease BCG-induced LC3BII levels. We found that BCG-induced autophagy is dependent on JNK and p38 and independent on PI3K or ERK pathways. And knocking down of c-Myc could significantly inhibit phosphorylation of p38. In conclusion, c-Myc may play a positive role in mycobacteria-induced autophagy in human macrophages.published_or_final_versio

Validation study of the Chinese Early Development Instrument (CEDI)

published_or_final_versio

The need of policies and legislative changes for tobacco control in Hong Kong: Letter of recommendations to Hong Kong Legislative Council

Recommendations on Anti-smoking Policy in Hong Kong, in response to the discussion on increasing tobacco taxation for the Legislative Council Subcommittee on Public Revenue Protection (Dutiable Commodities) Order 2011published_or_final_versio

Policy brief: Children left unattended at home in Hong Kong

Recommendations on Childhood Injury in Hong Kong, in response to the Child Fatality Review for the Legislative Council Welfare Services Panel Meetingpublished_or_final_versio

Bioactivity-guided identification and cell signaling technology to delineate the immunomodulatory effects of Panax ginseng on human promonocytic U937 cells

<p>Abstract</p> <p>Background</p> <p>Ginseng is believed to have beneficial effects against human diseases, and its active components, ginsenosides, may play critical roles in its diverse physiological actions. However, the mechanisms underlying ginseng's effects remain to be investigated. We hypothesize some biological effects of ginseng are due to its anti-inflammatory effects.</p> <p>Methods</p> <p>Human promonocytic U937 cells were used to investigate the immunomodulatory effects of ginseng following TNF-α treatment. A global gene expression profile was obtained by using genechip analysis, and specific cytokine expression was measured by quantitative RT-PCR and ELISA. HPLC was used to define the composition of ginsenosides in 70% ethanol-water extracts of ginseng. Activation of signalling kinases was examined by Western blot analysis.</p> <p>Results</p> <p>Seventy percent ethanol-water extracts of ginseng significantly inhibited the transcription and secretion of CXCL-10 following TNF-α stimulation. Nine ginsenosides including Rb₁, Rb₂, Rc, Rd, Re, Rf, Rg₁, Rg₃and Rh₁were identified in our extract by HPLC. Seven out of nine ginsenosides could significantly inhibit TNF-α-induced CXCL-10 expression in U937 cells and give comparable inhibition of CXCL-10 transcription to those with the extract. However, the CXCL-10 suppressive effect of individual ginsenosides was less than that of the crude extract or the mixture of ginsenosides. The CXCL-10 suppression can be correlated with the inactivation of ERK1/2 pathways by ginseng.</p> <p>Conclusion</p> <p>We showed ginseng suppressed part of the TNF-α-inducible cytokines and signalling proteins in promonocytic cells, suggesting that it exerts its anti-inflammatory property targeting at different levels of TNF-α activity. The anti-inflammatory role of ginseng may be due to the combined effects of ginsenosides, contributing in part to the diverse actions of ginseng in humans.</p

Proceedings of The First Current Topic in Infectious Diseases: Consensus Meeting on Conjugate Vaccines of the Center of Infection

Titles include: 1. Invasive Haemophilus Influenzae b Disease: Overview and Disease Burden in Hong Kong (YL LAU) ; 2. Overview and Disease Burden of Haemophilus Influenzae Type b in China (YH YANG) ; 3. Factors to Consider in the Routine Use of Hib in Hong Kong (THF TSANG) ; 4. Burden of Pneumococcal Disease in Hong Kong (CB CHOW) ; 5. Overview and Disease Burden of Streptococcus Pneumoniae in China (YH YANG) ; 6. Resistance in Pediatric Isolates of Pneumococci. Results from a Territorywide Carriage Study (SSS CHIU) ; 7. Serotype Distribution of Invasive and Noninvasive Strains of Pneumococci in Hong Kong (PL HO) ; 8. Overview of Conjugate Pneumococcal Vaccine: Serotype Coverage, Efficacy and Status of Usage in other Countries (SSY WONG)Conference Theme: The First Current Topic in Infectious Diseasespublished_or_final_versio

Early Life Socioeconomic Circumstance and Late Life Brain Hyperintensities : A Population Based Cohort Study

Funding: Image acquisition and image analysis for this study was funded by the Alzheimer's Research Trust (now Alzheimer's Research UK). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Acknowledgments The authors would like to thank the participants of the Aberdeen 1936 Birth Cohort (ABC36), without whom this research would not have been possible.Peer reviewedPublisher PD