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Anthony J. Ricci
Researcher at Stanford University
Publications - 131
Citations - 6246
Anthony J. Ricci is an academic researcher from Stanford University. The author has contributed to research in topics: Hair cell & Mechanotransduction. The author has an hindex of 38, co-authored 120 publications receiving 5586 citations. Previous affiliations of Anthony J. Ricci include Case Western Reserve University & University of Texas Medical Branch.
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Localization of inner hair cell mechanotransducer channels using high-speed calcium imaging
TL;DR: The observations, supported by theoretical simulations, suggest there are no functional mechanically sensitive transducer channels in first row stereocilia and imply the channels are present only at the bottom of the tip links.
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Mechanisms of Aminoglycoside Ototoxicity and Targets of Hair Cell Protection
TL;DR: These mechanisms of aminoglycosides' antimicrobial as well as ototoxic mechanisms are reviewed in regard to established and potential future targets of hair cell protection.
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Mechanosensitive Hair Cell-Like Cells from Embryonic and Induced Pluripotent Stem Cells
TL;DR: A stepwise guidance protocol starting with mouse embryonic stem and induced pluripotent stem cells, which were directed toward becoming ectoderm capable of responding to otic-inducing growth factors, resulted in otic progenitor cells being subjected to varying differentiation conditions.
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Functional auditory hair cells produced in the mammalian cochlea by in utero gene transfer
TL;DR: It is demonstrated that manipulation of cell fate by transcription factor misexpression produces functional sensory cells in the postnatal mammalian cochlea and it is expected that the in utero gene transfer paradigm will enable the design and validation of gene therapies to ameliorate hearing loss in mouse models of human deafness.
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Functional hair cell mechanotransducer channels are required for aminoglycoside ototoxicity
Abdelrahman M. Alharazneh,Abdelrahman M. Alharazneh,Lauren Luk,Markus E. Huth,Ashkan Monfared,Peter S. Steyger,Alan G. Cheng,Anthony J. Ricci +7 more
TL;DR: Data indicate that the patency of MET channels mediated AG entry into hair cells and its toxicity, and suggest that limiting permeation of AGs through MET channel or preventing their entry into endolymph are potential therapeutic targets for preventing hair cell death and hearing loss.