Stanford University
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Kate Reidy
Affiliate, Materials Science and Engineering
BioKate Reidy will begin as an Assistant Professor of Materials Science and Engineering at Stanford in September 2026. Her research takes a ‘bottom up' approach to nanoscale design, tailoring material properties by understanding and manipulating their atomic structure. She combines advanced characterization with in situ microscopy to elucidate growth mechanisms, chemical composition, and response to stimuli at the atomic scale.
Her research group aims to push the limits of nanoscale engineering by observing and controlling atomic-scale kinetic and thermodynamic phenomena such as adsorption, diffusion, nucleation, defect and interface formation - mapping such structural dynamics to quantum, energy, and opto-electronic properties. She is broadly interested in the functional utilization of quantum properties of nanomaterials in our classical world.
Prior to joining Stanford, Kate was a Miller Postdoctoral Fellow at UC Berkeley and Lawrence Berkeley National Lab. She completed her PhD in Materials Science & Engineering at MIT as a MIT Energy initiative and William Asbjornsen Albert Memorial Fellow, entitled 'Atomic-Scale Design at the 2D/3D Interface using Electron Microscopy'. She received her B.Sc in Nanoscience, Physics, and Chemistry of Advanced Materials from Trinity College Dublin, Ireland. Her work has been recognized by the MIT School of Engineering, Microscopy Society of America, Materials Research Society Gold Award, 'Best Doctoral Thesis' Award at MIT DMSE, and the Lemelson-Vest Award for Innovation. -
Leon Reilly
Undergraduate, Mathematics
Undergraduate, PhilosophyBiohttps://leonreilly.io/
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Richard J. Reimer, MD
Professor of Neurology and Neurological Sciences (Adult Neurology)
Current Research and Scholarly InterestsReimer Lab interests
A primary interest of our lab is to understand how nerve cells make and recycle neurotransmitters, the small molecules that they use to communicate with each other. In better defining these processes we hope to achieve our long-term goal of identifying novel sites for treatment of diseases such as epilepsy and Parkinson Disease. In our studies on neurotransmitter metabolism we have focused our efforts on transporters, a functional class of proteins that move neurotransmitters and other small molecules across membranes in cells. Transporters have many characteristics that make them excellent pharmacological targets, and not surprisingly some of the most effective treatments for neuropsychiatric disorders are directed at transporters. We are specifically focusing on two groups of transporters vesicular neurotransmitter transporters that package neurotransmitters into vesicles for release, and glutamine transporters that shuttle glutamine, a precursor for two major neurotransmitters glutamate and GABA, to neurons from glia, the supporting cells that surround them. We are pursuing these goals through molecular and biochemical studies, and, in collaboration with the Huguenard and Prince labs, through physiological and biosensor based imaging studies to better understand how pharmacological targeting of these molecules will influence neurological disorders.
A second interest of our lab is to define mechanism underlying the pathology of lysosomal storage disorders. Lysosomes are membrane bound acidic intracellular organelles filled with hydrolytic enzymes that normally function as recycling centers within cells by breaking down damaged cellular macromolecules. Several degenerative diseases designated as lysosomal storage disorders (LSDs) are associated with the accumulation of material within lysosomes. Tay-Sachs disease, Neimann-Pick disease and Gaucher disease are some of the more common LSDs. For reasons that remain incompletely understood, these diseases often affect the nervous system out of proportion to other organs. As a model for LSDs we are studying the lysosomal free sialic acid storage disorders. These diseases are the result of a defect in transport of sialic acid across lysosomal membranes and are associated with mutations in the gene encoding the sialic acid transporter sialin. We are using molecular, genetic and biochemical approaches to better define the normal function of sialin and to determine how loss of sialin function leads to neurodevelopmental defects and neurodegeneration associated with the lysosomal free sialic acid storage disorders.
