Epidemiology of Acute Myocarditis/Pericarditis in Hong Kong Adolescents Following Comirnaty Vaccination

BACKGROUND: Age-specific incidence of acute myocarditis/pericarditis in adolescents following Comirnaty vaccination in Asia is lacking. This study aimed to study the clinical characteristics and incidence of acute myocarditis/pericarditis among Hong Kong adolescents following Comirnaty vaccination. METHODS: This is a population cohort study in Hong Kong that monitored adverse events following immunization through a pharmacovigilance system for COVID-19 vaccines. All adolescents aged between 12 and 17 years following Comirnaty vaccination were monitored under the COVID-19 vaccine Adverse Event Response and Evaluation Programme. The clinical characteristics and overall incidence of acute myocarditis/pericarditis in adolescents following Comirnaty vaccination were analysed. RESULTS: Between 14 June 2021 and 4 September 2021, 33 Chinese adolescents who developed acute myocarditis/pericarditis following Comirnaty vaccination were identified. 29 (87.88%) were males and 4 (12.12%) were females, with a median age of 15.25 years. 27 (81.82%) and 6 (18.18%) cases developed acute myocarditis/pericarditis after receiving the second and first dose, respectively. All cases are mild and required only conservative management.The overall incidence of acute myocarditis/pericarditis was 18.52 (95% Confidence Interval [CI], 11.67-29.01) per 100,000 persons vaccinated. The incidence after the first and second doses were 3.37 (95%CI 1.12-9.51) and 21.22 (95%CI 13.78-32.28 per 100,000 persons vaccinated, respectively. Among male adolescents, the incidence after the first and second doses were 5.57 (95% CI 2.38-12.53) and 37.32 (95% CI 26.98-51.25) per 100,000 persons vaccinated. CONCLUSIONS: There is a significant increase in the risk of acute myocarditis/pericarditis following Comirnaty vaccination among Chinese male adolescents, especially after the second dose

Association of markers of proinflammatory phenotype and beige adipogenesis with metabolic syndrome in Chinese centrally obese adults

201812 bcrcVersion of RecordPublishe

Association between sonographically measured mesenteric fat thickness and brachial artery flow-mediated dilation in Chinese young male adults

2016-2017 > Academic research: refereed > Publication in refereed journalbcmaVersion of RecordOthersDepartmental start-up fund (99TP) of the Hong Kong Polytechnic University.Publishe

A novel role of cdc-family gene PFTK1 in the control of liver cancer cell motility

Poster Session 17 - Signaling in Tumor Cell Migration and Invasion 2: abstract no. 5297Cancer metastasis remains a major cause of cancer morbidity and mortality in individuals diagnosed with hepatocellular carcinoma (HCC). We previously reported on regional chromosome 7q21-q22 gains in close association with HCC progression, and discerned a candidate proto-oncogene PFTK1 within this region by array-based CGH mapping. The PFTK1 protein, PFTAIRE protein kinase 1, is a novel member of the Cdc2-related serine/threonine protein kinases. Our earlier investigations by ectopic expression and gene knockdown of PFTK1 confirmed a functional role for the PFTAIRE protein kinase in the motile phenotype of HCC cells, yet the biological basis remained to be determined. The aims of this study are therefore to establish the clinicopathologic significance of PFTK1 in HCC, and to define the PFTK1-modulated mechanisms in the control of HCC cell motility. Recent Tissue Microarray Analysis (TMA) on 180 paired primary HCC and their adjacent non-tumoral liver suggested common up-regulated PFTK1 compared to non-malignant counterpart (76.1%; p<0.0001). Correlative analysis further indicated PFTK1 over-expression in association with advanced tumor grading (P<0.0001) and the presence of microvascular invasion (P=0.05). By 2D-PAGE coupled with mass spectrometry, comparative proteomic profiling for phosphorylated proteins in PFTK1-suppressed HCC cells highlighted 5 differentially down-regulated spots, which included β-actin (ACTB), transgelin2 (TAGLN2), heat shock protein 70, mitochondrial aldehyde dehydrogenase and 14-3-3 gamma protein. Western blot analysis further verified a consistent reduction on ACTB phosphorylation and the serine phosphorylation of the TAGLN2 protein in the absence of PFTK1 protein kinase. Immunofluorescence analysis for cytoskeletal organizations indicated marked reduction on the actin stress fibers in PFTK1 knockdown cells. In conclusion, our results suggested that PFTK1 can affect the actin cytoskeletal organization and thus a motile phenotype in HCC cells through phosphorylation of ACTB and TAGLN2.link_to_OA_fulltextThe 101st Annual Meeting of the American Association for Cancer Research (AACR 2010), Washington D.C., 17-21 April 2010. In AACR Meeting Abstracts, 201

Intelligent Variable Structure Control for Automated Guided Vehicle

Aiming at Automated Guided Vehicle (AGV) dynamic model characteristics, a Variable Structure Control based on genetic algorithm (GA) and least square-support vector machine (LS-SVM) was designed. Parameters, predetermined by conventional reaching law, were regulated by LS-SVM online. It was shown that system shattering is eliminated. Simulation results indicated that this method possesses the advantages of higher precision, greater adaptability and robustness, as compared to the conventional Variable Structure Control methods. © 2008 IEEE.link_to_subscribed_fulltex

A novel interplay between oncogenic PFTK1 protein kinase and tumor suppressor TAGLN2 in the control of liver cancer cell motility

The PFTK1 gene encodes a cdc2-related serine/threonine protein kinase that has been shown to confer cell migratory properties in hepatocellular carcinoma (HCC). However, the prognostic value and biological mechanism by which PFTK1 promotes HCC motility remain largely unknown. Here, we showed from tissue microarray that common upregulations of PFTK1 in primary HCC tumors (n133/180) correlated significantly with early age onset (≤40 years), advance tumor grading and presence of microvascular invasion (≤P0.05). To understand downstream phosphorylated substrate(s) of PFTK1, phospho-proteins in PFTK1 expressing and knockdown Hep3B cells were profiled by two-dimensional- polyacrylamide gel electrophoresis mass spectrometric analysis. Protein identification of differential spots revealed Β-actin (ACTB) and transgelin2 (TAGLN2) as the two most profound phosphorylated changes affected by PFTK1. We verified the presence of TAGLN2 serine phosphorylation and ACTB tyrosine phosphorylation. Moreover, reduced TAGLN2 and ACTB phosphorylations in PFTK1-suppressed Hep3B corresponded to distinct actin depolymerizations and marked inhibition on cell invasion and motility. Given that TAGLN2 is a tumor suppressor whose function has been ascribed in cancer metastasis, we examined if TAGLN2 is an intermediate substrate in the biological path of PFTK1. We showed in PFTK1-suppressed cells that knockdown of TAGLN2 over-rode the inhibitory effect on cell invasion and motility, and a recovery on actin polymerization was evident. Interestingly, we also found that unphosphorylated TAGLN2 in PFTK1-suppressed cells elicited strong actin-binding ability, a mechanism that possibly halts the actin cytoskeleton dynamics. Site-directed mutagenesis of TAGLN2 suggested that PFTK1 regulates the actin-binding affinity of TAGLN2 through the S83 and S163 residues, which if mutated can significantly affect HCC cell motility. Taken together, our data propose a novel, oncogene-tumor suppressor interplay, where oncogenic PFTK1 confers HCC cell motility through inactivating the actin-binding motile suppressing function of TAGLN2 via phosphorylation. © 2011 Macmillan Publishers Limited All rights reserved.link_to_subscribed_fulltex

Loss of brain-enriched miR-124 microRNA enhances stem-like traits and invasiveness of glioma cells

miR-124 is a brain-enriched microRNA that plays a crucial role in neural development and has been shown to be down-regulated in glioma and medulloblastoma, suggesting its possible involvement in brain tumor progression. Here, we show that miR-124 is down-regulated in a panel of different grades of glioma tissues and in all of the human glioma cell lines we examined. By integrated bioinformatics analysis and experimental confirmation, we identified SNAI2, which is often up-regulated in glioma, as a direct functional target of miR-124. Because SNAI2 has been shown to regulate stem cell functions, we examined the roles of miR-124 and SNAI2 in glioma cell stem-like traits. The results showed that overexpression of miR-124 and knockdown of SNAI2 reduced neurosphere formation, CD133 + cell subpopulation, and stem cell marker (BMI1, Nanog, and Nestin) expression, and these effects could be rescued by re-expression of SNAI2. Furthermore, enhanced miR-124 expression significantly inhibited glioma cell invasion in vitro. Finally, stable overexpression of miR-124 and knockdown of SNAI2 inhibited the tumorigenicity and invasion of glioma cells in vivo. These findings reveal, for the first time, that the tumor suppressor activity of miR-124 could be partly due to its inhibitory effects on glioma stem-like traits and invasiveness through SNAI2. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.link_to_subscribed_fulltex

'Light up' protein-protein interaction through bioorthogonal incorporation of a turn-on fluorescent probe into β-lactamase

202308 bckwAccepted ManuscriptOthersITC; NSFC; PolyU; The Society of Hong Kong Scholars; Chinese Academy of SciencesPublishe