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1. SARS-CoV-2 variants divergently infect and damage cardiomyocytes in vitro and in vivo

Author

Mok, Bobo Wing-Yee, Kwok, Maxwell, Li, Hung Sing, Ling, Lowell, Lai, Angel, Yan, Bin, Law, Cherie Tsz-Yiu, Yeung, Chui Him, Zhang, Anna Jinxia, Tam, Rachel Chun-Yee, Kukic, Anja, Cremin, Conor J., Zhang, Yajie, Long, Teng, Kang, Zhisen, Luo, Ruibang, Leung, Kam Tong, Li, Albert M., Lui, Grace, Tsui, Stephen Kwok-Wing, Chan, Jasper Fuk-Woo, To, Kelvin Kai-Wang, Chan, Paul K. S., Yan, Bryan P., Chen, Honglin, and Poon, Ellen Ngar-Yun

Published
2024
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5. Temporal Control of the WNT Signaling Pathway During Cardiac Differentiation Impacts Upon the Maturation State of Human Pluripotent Stem Cell Derived Cardiomyocytes

Author

Tsoi, Chantelle, primary, Deng, Ruixia, additional, Kwok, Maxwell, additional, Yan, Bin, additional, Lee, Carrie, additional, Li, Hung Sing, additional, Ma, Chloe Ho Yi, additional, Luo, Ruibang, additional, Leung, Kam Tong, additional, Chan, Godfrey Chi-Fung, additional, Chow, Larry Ming-cheung, additional, and Poon, Ellen N., additional

Published
2022
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8. Remdesivir induces persistent mitochondrial and structural damage in human induced pluripotent stem cell-derived cardiomyocytes.

Author

Kwok, Maxwell, Lee, Carrie, Li, Hung Sing, Deng, Ruixia, Tsoi, Chantelle, Ding, Qianqian, Tsang, Suk Ying, Leung, Kam Tong, Yan, Bryan P, and Poon, Ellen N

Subjects
*CORONAVIRUS disease treatment, *REMDESIVIR, *COVID-19, *MITOCHONDRIA, *ADENOSINE triphosphate, *PRODRUGS
Abstract

Aims Remdesivir is a prodrug of an adenosine triphosphate analogue and is currently the only drug formally approved for the treatment of hospitalized coronavirus disease of 2019 (COVID-19) patients. Nucleoside/nucleotide analogues have been shown to induce mitochondrial damage and cardiotoxicity, and this may be exacerbated by hypoxia, which frequently occurs in severe COVID-19 patients. Although there have been few reports of adverse cardiovascular events associated with remdesivir, clinical data are limited. Here, we investigated whether remdesivir induced cardiotoxicity using an in vitro human cardiac model. Methods and results Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were exposed to remdesivir under normoxic and hypoxic conditions to simulate mild and severe COVID-19, respectively. Remdesivir induced mitochondrial fragmentation, reduced redox potential, and suppressed mitochondrial respiration at levels below the estimated plasma concentration under both normoxic and hypoxic conditions. Non-mitochondrial damage such as electrophysiological alterations and sarcomere disarray were also observed. Importantly, some of these changes persisted after the cessation of treatment, culminating in increased cell death. Mechanistically, we found that inhibition of DRP1, a regulator of mitochondrial fission, ameliorated the cardiotoxic effects of remdesivir, showing that remdesivir-induced cardiotoxicity was preventable and excessive mitochondrial fission might contribute to this phenotype. Conclusions Using an in vitro model, we demonstrated that remdesivir can induce cardiotoxicity in hiPSC-CMs at clinically relevant concentrations. These results reveal previously unknown potential side-effects of remdesivir and highlight the importance of further investigations with in vivo animal models and active clinical monitoring to prevent lasting cardiac damage to patients. [ABSTRACT FROM AUTHOR]

Published
2022
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9. Genetic variation in CFH predicts phenytoin-induced maculopapular exanthema in European-descent patients

Author

McCormack, Mark, Gui, Hongsheng, Ingason, Andrés, Speed, Doug, Wright, Galen E B, Zhang, Eunice J., Secolin, Rodrigo, Yasuda, Clarissa, Kwok, Maxwell, Wolking, Stefan, Becker, Felicitas, Rau, Sarah, Avbersek, Andreja, Heggeli, Kristin, Leu, Costin, Depondt, Chantal, Sills, Graeme J., Marson, Anthony G., Auce, Pauls, Brodie, Martin J., Francis, Ben, Johnson, Michael R., Koeleman, Bobby P C, Striano, Pasquale, Coppola, Antonietta, Zara, Federico, Kunz, Wolfram S., Sander, Josemir W., Lerche, Holger, Klein, Karl Martin, Weckhuysen, Sarah, Krenn, Martin, Gudmundsson, Lárus J, Stefánsson, Kári, Krause, Roland, Shear, Neil, Ross, Colin J D, Delanty, Norman, Pirmohamed, Munir, Carleton, Bruce C., Cendes, Fernando, Lopes-Cendes, Iscia, Liao, Wei-Ping, O'Brien, Terence J., Sisodiya, Sanjay M., Cherny, Stacey, Kwan, Patrick, Baum, Larry, Cavalleri, Gianpiero L., International League Against Epilepsy Consortium on Complex Epilepsies, Bisulli, Francesca, Mccormack, Mark, Gui, Hongsheng, Ingason, André, Speed, Doug, Wright, Galen E B, Zhang, Eunice J, Secolin, Rodrigo, Yasuda, Clarissa, Kwok, Maxwell, Wolking, Stefan, Becker, Felicita, Rau, Sarah, Avbersek, Andreja, Heggeli, Kristin, Leu, Costin, Depondt, Chantal, Sills, Graeme J, Marson, Anthony G, Auce, Paul, Brodie, Martin J, Francis, Ben, Johnson, Michael R, Koeleman, Bobby P C, Striano, Pasquale, Coppola, Antonietta, Zara, Federico, Kunz, Wolfram S, Sander, Josemir W, Lerche, Holger, Klein, Karl Martin, Weckhuysen, Sarah, Krenn, Martin, Gudmundsson, Lárus J, Stefánsson, Kári, Krause, Roland, Shear, Neil, Ross, Colin J D, Delanty, Norman, Pirmohamed, Munir, Carleton, Bruce C, Cendes, Fernando, Lopes-Cendes, Iscia, Liao, Wei-Ping, O'Brien, Terence J, Sisodiya, Sanjay M, Cherny, Stacey, Kwan, Patrick, Baum, Larry, Cavalleri, Gianpiero L, EPIGEN Consortium, Canadian Pharmacogenomics Network, for the EpiPGX Consortium, Int League Epilepsy Consortium, Læknadeild (HÍ), Faculty of Medicine (UI), Heilbrigðisvísindasvið (HÍ), School of Health Sciences (UI), Háskóli Íslands, University of Iceland, Wellcome Trust, Imperial College Healthcare NHS Trust- BRC Funding, Commission of the European Communities, McCormack, Mark, Zhang, Eunice J., Sills, Graeme J., Marson, Anthony G., Brodie, Martin J., Johnson, Michael R., Kunz, Wolfram S., Sander, Josemir W., Carleton, Bruce C., O'Brien, Terence J., Sisodiya, Sanjay M., Cavalleri, Gianpiero L., International League Against Epilepsy Consortium on Complex Epilepsie, and Bisulli, Francesca

Subjects
0301 basic medicine, Linkage disequilibrium, Pharmacogenomic Variants, Neurology [D14] [Human health sciences], Genome-wide association study, HLA-A-ASTERISK-3101, Linkage Disequilibrium, 0302 clinical medicine, Flogaveiki, INDUCED HYPERSENSITIVITY REACTIONS, Medicine, genetics, POPULATION, education.field_of_study, Public health, Taugavísindi, 3. Good health, Carbamazepine, Neurology, Factor H, Complement Factor H, Association studies in genetics, Lýðheilsa, Anticonvulsants, Drug Eruptions, Erfðarannsóknir, Life Sciences & Biomedicine, STEVENS-JOHNSON-SYNDROME, Population, Antiepileptic drugs, adverse drug reaction, Clinical Neurology, Mutation, Missense, Human leukocyte antigen, Complement factor I, Case control studies, White People, Article, 03 medical and health sciences, Asian People, RISK-FACTOR, Seizures, Genetic variation, Humans, GENOME-WIDE ASSOCIATION, education, METAANALYSIS, Retrospective Studies, Science & Technology, Neurology & Neurosurgery, Neurologie [D14] [Sciences de la santé humaine], Epilepsy, HLA-A Antigens, business.industry, Genetic Variation, Correction, CUTANEOUS ADVERSE-REACTIONS, 1103 Clinical Sciences, Généralités, 1702 Cognitive Science, GENOTYPES, 030104 developmental biology, Apolipoproteins, Case-Control Studies, Phenytoin, LAMOTRIGINE, Immunology, Alternative complement pathway, epilepsy, Neurosciences & Neurology, Neurology (clinical), Human medicine, 1109 Neurosciences, business, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract

Publisher's version (útgefin grein), Objective To characterize, among European and Han Chinese populations, the genetic predictors of maculopapular exanthema (MPE), a cutaneous adverse drug reaction common to antiepileptic drugs. Methods We conducted a case-control genome-wide association study of autosomal genotypes, including Class I and II human leukocyte antigen (HLA) alleles, in 323 cases and 1,321 drug-tolerant controls from epilepsy cohorts of northern European and Han Chinese descent. Results from each cohort were meta-analyzed. Results We report an association between a rare variant in the complement factor H–related 4 (CFHR4) gene and phenytoin-induced MPE in Europeans (p = 4.5 × 10–11; odds ratio [95% confidence interval] 7 [3.2–16]). This variant is in complete linkage disequilibrium with a missense variant (N1050Y) in the complement factor H (CFH) gene. In addition, our results reinforce the association between HLA-A*31:01 and carbamazepine hypersensitivity. We did not identify significant genetic associations with MPE among Han Chinese patients. Conclusions The identification of genetic predictors of MPE in CFHR4 and CFH, members of the complement factor H–related protein family, suggest a new link between regulation of the complement system alternative pathway and phenytoin-induced hypersensitivity in European-ancestral patients., This study was not industry-sponsored. The work was supported by a grant from the European Commission (7th Framework Programme Grant 279062, EpiPGX). M.M.C. and G.L.C. are supported by Science Foundation Ireland, grant 13/CDA/2223, and an RCSI seed funding grant GA 14-1899. This project was supported by the General Research Funds (HKU7623/08M and HKU7747/07M to S.C., CUHK4466/06M to P.K.) and Health and Medical Research Fund (HMRF 01120086 to P.K.) from Hong Kong. Some results presented in this article were prepared using the HPC facilities of the University of Luxembourg. This work was partly undertaken at UCLH/UCL, which received a proportion of funding from the Department of Health's NIHR Biomedical Research Centres funding scheme (J.W.S., S.M.S.). The work was also supported by the Epilepsy Society, UK (J.W.S., S.M.S.), by the foundation “no epilep,” the German Chapter of the ILAE (DGfE) (both to H.L.). F.C. and I.L.-C. are supported by Fundação de Amparo à Pesquisa do Estado de São Paulo, Brazil, through grant 2013/07559-3. J.E.Z. and M.P. thank the NHS Chair of Pharmacogenetics programme and MRC Centre for Drug Safety Science for support in Liverpool. B.C.C. and C.J.D.R. are supported by the Canadian Institutes of Health Research (CIHR) Drug Safety and Effectiveness Network (FRN-117588), the Canada Foundation for Innovation and the Canadian Dermatology Foundation. G.E.B.W. is supported by a CIHR Fellowship. The funders of the study had no role in the study design, data collection, data analysis, data interpretation, or writing of the report. M.M.C., H.G., and G.L.C. had full access to all the data in the study and the corresponding authors had final responsibility for the decision to submit for publication. The Article Processing Charge was funded by the European Commission OpenAIRE2020 project.

Published
2017
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10. Development of rapid detection systems for enrofloxacin, tylosin, malachite green residues in animal food products

Author

Kwok, Maxwell Ka Shing and Kwok, Maxwell Ka Shing

Abstract

In recent years, food safety has become a very important issue in Hong Kong and Mainland China, especially after the discovery of contamination of milk products by melamine and the contamination of seafood by malachite green. The Hong Kong government regulates the presence of harmful substances in food through Ordinance Cap.132AF HARMFUL SUBSTANCES IN FOOD REGULATIONS and Cap.139N PUBLIC HEALTH (ANIMALS AND BIRDS) (CHEMICAL RESIDUES) REGULATION. Approximately 50 chemicals are listed, including antibiotics, synthetic hormones and some harmful chemicals. The Hong Kong government has instituted a system of monitoring the residue levels of these banned substances in food products using liquid chromatography–mass spectrometry and gas chromatography–mass spectrometry. These techniques are highly sensitive, but are time-consuming and only capable of testing limited quantities of food samples. There is an urgent need for a rapid and reliable detection system that can detect such banned substances in larger quantities. This project will develop an immunoassay-based detection system for the rapid detection of residues in food animal products. The chemicals, enrofloxacin, tylosin and malachite green are the chosen targets for detection. Conjugation of these chemicals to protein carriers was conducted and the resultant conjugates were injected into animals for antibody production. Specific antibodies were purified and finally incorporated into the detection systems.

Published
2011

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