A scalable architecture for quantum computation with molecular nanomagnets

A proposal for a magnetic quantum processor that consists of individual molecular spins coupled to superconducting coplanar resonators and transmission lines is carefully examined. We derive a simple magnetic quantum electrodynamics Hamiltonian to describe the underlying physics. It is shown that these hybrid devices can perform arbitrary operations on each spin qubit and induce tunable interactions between any pair of them. The combination of these two operations ensures that the processor can perform universal quantum computations. The feasibility of this proposal is critically discussed using the results of realistic calculations, based on parameters of existing devices and molecular qubits. These results show that the proposal is feasible, provided that molecules with sufficiently long coherence times can be developed and accurately integrated into specific areas of the device. This architecture has an enormous potential for scaling up quantum computation thanks to the microscopic nature of the individual constituents, the molecules, and the possibility of using their internal spin degrees of freedom.Comment: 27 pages, 6 figure

Transcription Factor Efg1 Shows a Haploinsufficiency Phenotype in Modulating the Cell Wall Architecture and Immunogenicity of Candida albicans

The Candida albicans transcription factor Efg1 is known to be involved in many different cellular processes, including morphogenesis, general metabolism, and virulence. Here we show that besides its manifold roles, Efg1 also has a prominent effect on cell wall structure and composition, strongly affecting the structural glucan part. Deletion of only one allele of EFG1 already results in severe phenotypes for cell wall biogenesis, comparable to those with deletion of both alleles, indicative of a severe haploinsufficiency for EFG1. The observed defects in structural setup of the cell wall, together with previously reported alterations in expression of cell surface proteins, result in altered immunogenic properties of strains with compromised Efg1 function. This is shown by interaction studies with macrophages and primary dendritic cells. The structural changes in the cell wall carbohydrate meshwork presented here, together with the manifold changes in cell wall protein composition and metabolism reported in other studies, contribute to the altered immune response mounted by innate immune cells and to the altered virulence phenotypes observed for strains lacking EFG1

Multi-band quantum ratchets

We investigate directed motion in non-adiabatically rocked ratchet systems sustaining few bands below the barrier. Upon restricting the dynamics to the lowest M bands, the total system-plus-bath Hamiltonian is mapped onto a discrete tight-binding model containing all the information both on the intra- and inter-well tunneling motion. A closed form for the current in the incoherent tunneling regime is obtained. In effective single-band ratchets, no current rectification occurs. We apply our theory to describe rectification effects in vortex quantum ratchets devices. Current reversals upon variation of the ac-field amplitude or frequency are predicted.Comment: Accepted for publication in Physical Review Letter

Release from UNC93B1 reinforces the compartmentalized activation of select TLRs

Nucleic acid-sensing Toll-like receptors (TLRs) are subject to complex regulation to facilitate the recognition of microbial DNA and RNA while limiting the recognition of an organism's own nucleic acids1. Failure to properly regulate these TLRs can lead to autoimmune and autoinflammatory diseases2-6. Intracellular localization of these receptors is thought to be crucial for the discrimination between self and non-self7, but the molecular mechanisms that reinforce compartmentalized activation of intracellular TLRs remain poorly understood. Here we describe a mechanism that prevents the activation of TLR9 from locations other than endosomes. This control is achieved through the regulated release of the receptor from its trafficking chaperone UNC93B1, which occurs only within endosomes and is required for ligand binding and signal transduction. Preventing release of TLR9 from UNC93B1, either by mutations in UNC93B1 that increase affinity for TLR9 or through an artificial tether that impairs release, results in defective signalling. Whereas TLR9 and TLR3 are released from UNC93B1, TLR7 does not dissociate from UNC93B1 in endosomes and is regulated by distinct mechanisms. This work defines a checkpoint that reinforces the compartmentalized activation of TLR9, and provides a mechanism by which activation of individual endosomal TLRs may be distinctly regulated