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Larry M.C. Chow

Researcher at Hong Kong Polytechnic University

Publications -  77
Citations -  2448

Larry M.C. Chow is an academic researcher from Hong Kong Polytechnic University. The author has contributed to research in topics: Multiple drug resistance & P-glycoprotein. The author has an hindex of 26, co-authored 72 publications receiving 2202 citations. Previous affiliations of Larry M.C. Chow include Harvard University & Wayne State University.

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Sensitive and Inexpensive Molecular Test for Falciparum Malaria: Detecting Plasmodium falciparum DNA Directly from Heat-Treated Blood by Loop-Mediated Isothermal Amplification,

TL;DR: The LAMP assay does not require purified DNA for efficient DNA amplification, thereby reducing the cost and turnaround time for P. falciparum diagnosis, and requires only basic instruments, and assay positivity can be verified by visual inspection.
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Pseudolaric acid B, a novel microtubule-destabilizing agent that circumvents multidrug resistance phenotype and exhibits antitumor activity in vivo.

TL;DR: PAB circumvents P-glycoprotein overexpression-induced drug resistance and is effective in inhibiting tumor growth in vivo, which will facilitate the future development of PAB as a cancer therapeutic.
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Flavonoid dimers as bivalent modulators for P-glycoprotein-based multidrug resistance: synthetic apigenin homodimers linked with defined-length poly(ethylene glycol) spacers increase drug retention and enhance chemosensitivity in resistant cancer cells.

TL;DR: A series of apigenin-based flavonoid dimers, linked by poly(ethylene glycol) chains of various lengths, have been synthesized, which modulate drug chemosensitivity and retention in breast and leukemic MDR cells with the optimal number of ethylene glycol units equal to 2-4.
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Modulation of multidrug resistance protein 1 (MRP1/ABCC1)-mediated multidrug resistance by bivalent apigenin homodimers and their derivatives.

TL;DR: It is demonstrated that flavonoid dimers can be employed as an effective modulator of MRP1-mediated drug resistance in cancer cells by inhibiting DOX transport, increasing intracellular DOX retention, and finally resensitizing 2008/MRP1 to DOX.