S
Sai Kiang Lim
Researcher at Agency for Science, Technology and Research
Publications - 167
Citations - 24991
Sai Kiang Lim is an academic researcher from Agency for Science, Technology and Research. The author has contributed to research in topics: Mesenchymal stem cell & Microvesicles. The author has an hindex of 52, co-authored 152 publications receiving 18269 citations. Previous affiliations of Sai Kiang Lim include Genome Institute of Singapore & National University of Singapore.
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Journal ArticleDOI
Weiss Response to Sengupta et al. (DOI: 10.1089/scd.2020.0095).
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Mesenchymal Stem Cell Exosomes Promote Growth Plate Repair and Reduce Limb-Length Discrepancy in Young Rats
Keng Lin Wong,Shipin Zhang,Sharon Si Heng Tan,Yi Ann Cheow,Ruenn Chai Lai,Sai Kiang Lim,James Hoi Po Hui,Wei Seong Toh +7 more
TL;DR: This proof-of-concept study demonstrates for the first time the potential use of MSC exosomes as a minimally invasive cell-free therapeutic to promote physeal repair and reduce limb-length discrepancy following growth plate injuries.
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Membrane lipid binding molecules for the isolation of bona fide extracellular vesicle types and associated biomarkers in liquid biopsy
TL;DR: It is proposed that isolating EV subtypes is a technically viable and robust strategy to overcome the current bottleneck of isolating EVs for liquid biopsy and its potential for accelerated biomarker discovery and validation through examples of pre-clinical studies.
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Deriving clinically compliant mescenchymal stem cells (MSC) from differentiated human ESCs and elucidating MSC paracrine proteome
Qizhou Lian,Siu Kwan Sze,Dominique P.V. de Kleijn,Elia Lye,Eileen Khia Way Tan,Teck Yew Low,Chuen Neng Lee,Eng Hin Lee,Bing Lim,Sai Kiang Lim,Sai Kiang Lim +10 more
TL;DR: Deriving clinically compliant mescenchymal stem cells (MSC) from differentiated human ESCs and elucidating MSC paracrine proteome is described.
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An anemic patient with phenotypical beta-thalassemic trait has elevated level of structurally normal beta-globin mRNA in reticulocytes.
TL;DR: Detailed structural analysis of the β‐globin mRNA and gene by sequencing of RT‐PCR and PCR products, respectively, did not detect any mutations and indicated that a relative insufficiency of structurally normal β‐ globin mRNA was not a cause of this β‐thalassemic phenotype.