Towards Improved Quantum Simulations and Sensing with Trapped 2D Ion Crystals via Parametric Amplification

Improving coherence is a fundamental challenge in quantum simulation and sensing experiments with trapped ions. Here we discuss, experimentally demonstrate, and estimate the potential impacts of two different protocols that enhance, through motional parametric excitation, the coherent spin-motion coupling of ions obtained with a spin-dependent force. The experiments are performed on 2D crystal arrays of approximately one hundred $^9$Be$^+$ ions confined in a Penning trap. By modulating the trapping potential at close to twice the center-of-mass mode frequency, we squeeze the motional mode and enhance the spin-motion coupling while maintaining spin coherence. With a stroboscopic protocol, we measure $5.4 \pm 0.9$ dB of motional squeezing below the ground-state motion, from which theory predicts a $10$ dB enhancement in the sensitivity for measuring small displacements using a recently demonstrated protocol [Science $\textbf{373}$, 673 (2021)]. With a continuous squeezing protocol, we measure and accurately calibrate the parametric coupling strength. Theory suggests this protocol can be used to improve quantum spin squeezing, limited in our system by off-resonant light scatter. We illustrate numerically the trade-offs between strong parametric amplification and motional dephasing in the form of center-of-mass frequency fluctuations for improving quantum spin squeezing in our set-up.Comment: 11 pages, 6 figure

Disruption of a Large Intergenic Noncoding RNA in Subjects with Neurodevelopmental Disabilities

Large intergenic noncoding (linc) RNAs represent a newly described class of ribonucleic acid whose importance in human disease remains undefined. We identified a severely developmentally delayed 16-year-old female with karyotype 46,XX,t(2;11)(p25.1;p15.1)dn in the absence of clinically significant copy number variants (CNVs). DNA capture followed by next-generation sequencing of the translocation breakpoints revealed disruption of a single noncoding gene on chromosome 2, LINC00299, whose RNA product is expressed in all tissues measured, but most abundantly in brain. Among a series of additional, unrelated subjects referred for clinical diagnostic testing who showed CNV affecting this locus, we identified four with exon-crossing deletions in association with neurodevelopmental abnormalities. No disruption of the LINC00299 coding sequence was seen in almost 14,000 control subjects. Together, these subjects with disruption of LINC00299 implicate this particular noncoding RNA in brain development and raise the possibility that, as a class, abnormalities of lincRNAs may play a significant role in human developmental disorders