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Atom-interferometric quantum sensors could revolutionize navigation, civil engineering, and Earth observation. However, operation in real-world environments is challenging due to external interference, platform noise, and constraints on size, weight, and power. Here we experimentally demonstrate that tailored light pulses designed using robust control techniques mitigate significant error sources in an atom-interferometric accelerometer. To mimic the effect of unpredictable lateral platform motion, we apply laser-intensity noise that varies up to 20% from pulse-to-pulse. Our robust control solution maintains performant sensing, while the utility of conventional pulses collapses. By measuring local gravity, we show that our robust pulses preserve interferometer scale factor and improve measurement precision by 10× in the presence of this noise. We further validate these enhancements by measuring applied accelerations over a 200 μg range up to 21× more precisely at the highest applied noise level. Our demonstration provides a pathway to improved atom-interferometric inertial sensing in real-world settings., (© 2023. The Author(s).)

Quantum harmonic oscillators are central to many modern quantum technologies. We introduce a method to determine the frequency noise spectrum of oscillator modes through coupling them to a qubit with continuously driven qubit-state-dependent displacements. We reconstruct the noise spectrum using a series of different drive phase and amplitude modulation patterns in conjunction with a data-fusion routine based on convex optimization. We apply the technique to the identification of intrinsic noise in the motional frequency of a single trapped ion with sensitivity to fluctuations at the sub-Hz level in a spectral range from quasi-dc up to 50 kHz.

Modulators of epithelial-to-mesenchymal transition (EMT) have recently emerged as novel players in the field of leukemia biology. The mechanisms by which EMT modulators contribute to leukemia pathogenesis, however, remain to be elucidated. Here we show that overexpression of SNAI1, a key modulator of EMT, is a pathologically relevant event in human acute myeloid leukemia (AML) that contributes to impaired differentiation, enhanced self-renewal, and proliferation of immature myeloid cells. We demonstrate that ectopic expression of Snai1 in hematopoietic cells predisposes mice to AML development. This effect is mediated by interaction with the histone demethylase KDM1A/LSD1. Our data shed new light on the role of SNAI1 in leukemia development and identify a novel mechanism of LSD1 corruption in cancer. This is particularly pertinent given the current interest surrounding the use of LSD1 inhibitors in the treatment of multiple different malignancies, including AML., (© 2020 by The American Society of Hematology.)

Cholesteryl ester transfer protein (CETP) plays an important role in plasma lipoprotein metabolism through its ability to transfer cholesteryl ester, triglyceride, and phospholipid between lipoproteins. CETP is a member of a gene family that also includes bactericidal/permeability-increasing protein (BPI). The crystal structure of BPI shows it to be composed of two domains that share a similar structural fold that includes an apolar ligand-binding pocket. As structurally important residues are conserved between BPI and CETP, it is thought that CETP and BPI may have a similar overall conformation. We have previously proposed a model of CETP structure based on the binding characteristics of anti-CETP monoclonal antibodies (mAbs). We now present a refined epitope map of CETP that has been adapted to a structural model of CETP that uses the atomic coordinates of BPI. Four epitopes composed of CETP residues 215-219, 219-223, 223-227, and 444-450, respectively, are predicted to be situated on the external surface of the central beta-sheet and a fifth epitope (residues 225-258) on an extended linker that connects the two domains of the molecule. Three other epitopes, residues 317-331, 360-366, and 393-410, would form part of the putative carboxy-terminal beta-barrel. The ability of the corresponding mAbs to compete for binding to CETP is consistent with the proximity of the respective epitopes in the model. These results thus provide experimental evidence that is consistent with CETP and BPI having similar surface topologies.

1. Prolonged changes in the excitability of cortical neurones can be produced by altering their firing rates for brief periods. In the anaesthetized cat, increased firing of pyramidal tract cells induced by trains of antidromic conditioning shocks led to increases in cell excitability, as measured by the size of the mass response at the medullary pyramid to test shocks applied to the cortical surface. We have shown in two ways that post-synaptic mechanisms could be responsible. 2. In one experimental design, MgCl2 solution (1 mole/l.) was applied to the cortical surface in order to block synaptic activity throughout the cortical depth. Following antidromic conditioning trains, cell excitability was increased; the size of the mass response was up to 30% larger than the control values. This persisted undiminished for up to 3 hr. 3. In the second experimental design, synaptic activity was not blocked, but we compared the effects of antidromic plus synaptic activation of pyramidal tract cells with the effects of synaptic activation alone. Antidromic plus synaptic activation was obtained by applying conditioning trains to the pyramidal tract at the medulla ipsilateral to the cortical test shock; prolonged increases in the ipsilateral response to the test shock were produced. Synaptic activation alone was obtained by the same conditioning trains, but in those cells whose axons projected into the contralateral pyramidal tract; prolonged increases in the contralateral response to the cortical test shock were never seen. In many instances prolonged decreases in excitability were found. 4. We conclude that prolonged increases in excitability of pyramidal tract cells can occur in the absence of any synaptic input, demonstrating that the underlying mechanism is post-synaptic; this does not preclude the action of synaptic mechanisms when synaptic transmission is not blocked.