Critical change in the Fermi surface of iron arsenic superconductors at the onset of superconductivity

The phase diagram of a correlated material is the result of a complex interplay between several degrees of freedom, providing a map of the material's behavior. One can understand (and ultimately control) the material's ground state by associating features and regions of the phase diagram, with specific physical events or underlying quantum mechanical properties. The phase diagram of the newly discovered iron arsenic high temperature superconductors is particularly rich and interesting. In the AE(Fe1-xTx)2As2 class (AE being Ca, Sr, Ba, T being transition metals), the simultaneous structural/magnetic phase transition that occurs at elevated temperature in the undoped material, splits and is suppressed by carrier doping, the suppression being complete around optimal doping. A dome of superconductivity exists with apparent equal ease in the orthorhombic / antiferromagnetic (AFM) state as well as in the tetragonal state with no long range magnetic order. The question then is what determines the critical doping at which superconductivity emerges, if the AFM order is fully suppressed only at higher doping values. Here we report evidence from angle resolved photoemission spectroscopy (ARPES) that critical changes in the Fermi surface (FS) occur at the doping level that marks the onset of superconductivity. The presence of the AFM order leads to a reconstruction of the electronic structure, most significantly the appearance of the small hole pockets at the Fermi level. These hole pockets vanish, i. e. undergo a Lifshitz transition, at the onset of superconductivity. Superconductivity and magnetism are competing states in the iron arsenic superconductors. In the presence of the hole pockets superconductivity is fully suppressed, while in their absence the two states can coexist.Comment: Updated version accepted in Nature Physic

The neurotechnology patent landscape in a time of neuroethics : 2016-2020

Over the past decades, invasive and non-invasive neuromodulation approaches have emerged to manage neurologic and psychiatric conditions, along with powerful functional neuroimaging methods that provide insights to the physiologic bases for cognition and behavior. However, new capabilities realized by neurotechnology also introduce new concerns. Neurotechnology has proliferated into industries such as defense, advertising, and retail, evolving in ways that may impinge on the privacy of thought and create injustices in human performance. In these contexts, newfound access to the brain raises broad concerns for human rights. In this thesis, I examine 779 patents granted by the USPTO between 2016 and 2020 as a publicly accessible record of inventions early in commercial development to understand the characteristics of neurotechnology innovation and assess their ethical and social implications. By applying qualitative methods to existing patent infrastructure, I develop a perspective of an innovation landscape rooted strongly in healthcare. Neuromodulation is most prominent, with conditions affecting the injured or aging brain a substantial focus. Neurotechnology across other industries such as entertainment and finance raise concerns about consent and coercion. I further consider how these inventions may support or impede the mental protections proposed by neurorights advocates. With some concerns identified in past work and in this thesis, anticipating that more ethically fraught innovation may come down the commercial pipeline is a critical exercise. Such a practice is also fundamental to the anticipatory tenet of neuroethics. To this end, I conclude by welcoming patent experts into the neuroethics circle, and at the same time urge ongoing attention to the patent landscape as a means of informing outreach and ensuring long term societal benefits.Medicine, Faculty ofMedicine, Department ofGraduat

Hemizygous variants in protein phosphatase 1 regulatory subunit 3F (<i>PPP1R3F</i>) are associated with a neurodevelopmental disorder characterized by developmental delay, intellectual disability, and autistic features

Abstract PPP1R3F (R3F) is a member of the glycogen targeting subunits (GTSs), which belong to the large group of regulatory subunits of protein phosphatase 1 (PP1), a major eukaryotic serine/threonine protein phosphatase that regulates diverse cellular processes. Here, we describe the identification of hemizygous variants in PPP1R3F associated with a novel X-linked recessive neurodevelopmental disorder in 13 unrelated individuals. This disorder is characterized by developmental delay, mild intellectual disability, neurobehavioral issues such as autism spectrum disorder, seizures, and other neurological findings including tone, gait, and cerebellar abnormalities. PPP1R3F variants segregated with disease in affected hemizygous males that inherited the variants from their heterozygous carrier mothers. We show that R3F is predominantly expressed in brain astrocytes and localizes to the endoplasmic reticulum in cells. Glycogen content in PPP1R3F knockout astrocytoma cells appears to be more sensitive to fluxes in extracellular glucose levels than in wild-type cells, suggesting that R3F functions in maintaining steady brain glycogen levels under changing glucose conditions. We performed functional studies on nine of the identified variants and observed defects in PP1 binding, protein stability, subcellular localization, and regulation of glycogen metabolism in most of them. Collectively, the genetic and molecular data indicate that deleterious variants in PPP1R3F are associated with a new X-linked disorder of glycogen metabolism, highlighting the critical role of GTSs in neurological development. This research expands our understanding of neurodevelopmental disorders and the role of PP1 in brain development and proper function.</jats:p