Quantum control of complex objects in the regime of large size and mass provides opportunities for sensing applications and tests of fundamental physics. The realization of such extreme quantum states of matter remains a major challenge. We demonstrate a quantum interface that combines optical trapping of solids with cavity-mediated light-matter interaction. Precise control over the frequency and position of the trap laser with respect to the optical cavity allowed us to laser-cool an optically trapped nanoparticle into its quantum ground state of motion from room temperature. The particle comprises 108 atoms, similar to current Bose-Einstein condensates, with the density of a solid object. Our cooling technique, in combination with optical trap manipulation, may enable otherwise unachievable superposition states involving large masses.

The coupling of a levitated submicron particle and an optical cavity field promises access to a unique parameter regime both for macroscopic quantum experiments and for high-precision force sensing. We report a demonstration of such controlled interactions by cavity cooling the center-of-mass motion of an optically trapped submicron particle. This paves the way for a light-matter interface that can enable room-temperature quantum experiments with mesoscopic mechanical systems.optical trapping | quantum optics | cavity optomechanics | nanoparticles | nanomechanics T he ability to trap and to manipulate individual atoms is at the heart of current implementations of quantum simulations (1, 2), quantum computing (3), and long-distance quantum communication (4,5). Controlling the motion of larger particles opens up avenues for quantum science, both for the study of fundamental quantum phenomena in the context of matter wave interference (6), and for unique sensing and transduction applications in the context of quantum optomechanics (7,8). Specifically, it has been suggested that cavity cooling of a single submicron particle in high vacuum allows for the generation of quantum states of motion in a room-temperature environment (9-11), as well as for unprecedented force sensitivity (12, 13). Here, we take steps into this regime. We demonstrate cavity cooling of an optically levitated submicron particle consisting of ∼10 9 atoms (estimated diameter of 340 nm). The particle is trapped at modest vacuum levels of a few millibars in the standingwave field of an optical cavity and is cooled through coherent scattering into the modes of the same cavity (14, 15). We estimate that our cooling rates are sufficient for ground-state cooling, provided that optical trapping at a vacuum level of 10 −7 mbar can be realized in the future, e.g., by using additional active-feedback schemes to stabilize the optical trap in three dimensions (16)(17)(18)(19).Cooling and coherent control of single atoms inside an optical cavity are well-established techniques within atomic quantum optics (20)(21)(22)(23)(24). The main idea of cavity cooling relies on the fact that the presence of an optical cavity can resonantly enhance scattering processes of laser light that deplete the kinetic energy of the atom, specifically those processes where a photon that is scattered from the atom is Doppler shifted to a higher frequency. It was realized early on that such cavity-enhanced scattering processes can be used to achieve laser cooling even of objects without exploitable internal level structure such as molecules and submicron particles (14,15,25,26). For nanoscale objects, cavity cooling has been demonstrated in a series of recent experiments with nanobeams (27-29) and membranes of nanometerscale thickness (e.g., refs. 30 and 31). To guarantee long interaction times with the cavity field, these objects were mechanically clamped, which however introduces additional dissipation and heating through the mechanical support structure. As a consequence, quantum...

Mandates for mask use in public during the recent coronavirus disease 2019 (COVID-19) pandemic, worsened by global shortage of commercial supplies, have led to widespread use of homemade masks and mask alternatives. It is assumed that wearing such masks reduces the likelihood for an infected person to spread the disease, but many of these mask designs have not been tested in practice. We have demonstrated a simple optical measurement method to evaluate the efficacy of masks to reduce the transmission of respiratory droplets during regular speech. In proof-of-principle studies, we compared a variety of commonly available mask types and observed that some mask types approach the performance of standard surgical masks, while some mask alternatives, such as neck gaiters or bandanas, offer very little protection. Our measurement setup is inexpensive and can be built and operated by nonexperts, allowing for rapid evaluation of mask performance during speech, sneezing, or coughing.

The B apolipoproteins, apo-B48 and apo-B100, are key structural proteins in those classes of lipoproteins considered to be atherogenic [e.g., chylomicron remnants, ,f-VLDL, LDL, oxidized LDL, and Lp(a)J. Here we describe the development of transgenic mice expressing high levels of human apo-B48 and apo-B100. A 79.5-kb human genomic DNA fragment containing the entire human apo-B gene was isolated from a P1 bacteriophage library and microinjected into fertilized mouse eggs. 16 transgenic founders expressing human apo-B were generated, and the animals with the highest expression had plasma apo-B100 levels nearly as high as those of normolipidemic humans (-50 mg/dl). The human apo-B100 in transgenic mouse plasma was present largely in lipoproteins of the LDL class as shown by agarose gel electrophoresis, chromatography on a Superose 6 column, and density gradient ultracentrifugation. When the human apo-B transgenic founders were crossed with transgenic mice expressing human apo(a), the offspring that expressed both transgenes had high plasma levels of human Lp(a). Both the human apo-B and Lp(a) transgenic mice will be valuable resources for studying apo-B metabolism and the role of apo-B and Lp(a) in atherosclerosis. (J. Clin. Invest. 1993. 92:3029-3037.) Key words: P1 bacteriophage -low density lipoproteins * cholesterol

We report three-dimensional cooling of a levitated nanoparticle inside an optical cavity. The cooling mechanism is provided by cavity-enhanced coherent scattering off an optical tweezer. The observed 3D dynamics and cooling rates are as theoretically expected from the presence of both linear and quadratic terms in the interaction between the particle motion and the cavity field. By achieving nanometer-level control over the particle location we optimize the position-dependent coupling and demonstrate axial cooling by two orders of magnitude at background pressures of 6 × 10 −2 mbar. We also estimate a significant (> 40 dB) suppression of laser phase noise heating, which is a specific feature of the coherent scattering scheme. The observed performance implies that quantum ground state cavity cooling of levitated nanoparticles can be achieved for background pressures below 1 × 10 −7 mbar. arXiv:1812.09358v2 [quant-ph]

Group II PLA 2 has been implicated in inflammatory processes in both man and other animals and has been shown to be involved in inflammatory conditions, such as arthritis and sepsis. Transgenic mice expressing the human group II PLA 2 gene have been generated using a 6.2-kb genomic fragment. These mice express the group II PLA 2 gene abundantly in liver, lung, kidney, and skin, and have serum PLA 2 activity levels approximately eightfold higher than nontransgenic littermates. The group II PLA 2 transgenic mice reported here exhibit epidermal and adnexal hyperplasia, hyperkeratosis, and almost total alopecia. The chronic epidermal hyperplasia and hyperkeratosis seen in these mice is similar to that seen in a variety of dermatopathies, including psoriasis. However, unlike what is seen with these dermatopathies, no significant inflammatory-cell influx was observed in the skin of these animals, or in any other tissue examined.

Plasma levels of high density lipoprotein (HDL) cholesterol and its major protein component apolipoprotein (apo) A-I are significantly reduced in both acute and chronic inflammatory conditions, but the basis for this phenomenon is not well understood. We hypothesized that secretory phospholipase A 2 (sPLA 2 ), an acute phase protein that has been found in association with HDL, promotes HDL catabolism. A series of HDL metabolic studies were performed in transgenic mice that specifically overexpress human sPLA 2 but have no evidence of local or systemic inflammation. We found that HDL isolated from these mice have a significantly lower phospholipid and cholesteryl ester and significantly greater triglyceride content. transgenic mice was significantly enhanced compared with control mice. In summary, these data demonstrate that overexpression of sPLA 2 alone in the absence of inflammation causes profound alterations of HDL metabolism in vivo and are consistent with the hypothesis that sPLA 2 may promote HDL catabolism in acute and chronic inflammatory conditions. Plasma concentrations of high density lipoprotein (HDL) 1 cholesterol and its major apoprotein apoA-I are inversely associated with atherosclerotic cardiovascular disease (1, 2). The factors responsible for the substantial variation in HDL cholesterol and apoA-I levels in humans remain incompletely understood. Metabolic studies of HDL and apoA-I in humans have established that variation in their levels is due in substantial part to variation in the rate of apoA-I catabolism (3-7). Although the determinants of apoA-I catabolism have not been fully elucidated, the size and lipid composition of HDL have been recognized to substantially influence the catabolic rate of apoA-I (8, 9).One clinical setting that is invariably associated with reduced HDL cholesterol and apoA-I levels is systemic inflammation. Acute inflammatory states such as sepsis are associated with profoundly reduced HDL cholesterol levels (10). Furthermore, chronic inflammatory states such as rheumatoid arthritis and systemic lupus are also associated with reduced levels of HDL cholesterol (11-18), as well as with increased risk of cardiovascular disease (19,20). One of the major factors thought to be implicated in the reduced levels of HDL cholesterol during inflammation is the serum amyloid A (SAA) protein, which increases markedly during acute infection and inflammation and is also elevated in chronic inflammatory states (10,21,22). However, expression of SAA has never been directly demonstrated to alter HDL metabolism in vivo in the absence of systemic inflammation. We recently demonstrated that marked overexpression of human SAA alone in the absence of a generalized acute phase response had no effect on HDL cholesterol and apoA-I levels in human apoA-I transgenic mice (23). This observation raised the question as to whether other factors associated with systemic inflammation may modulate HDL metabolism.Group IIA secretory phospholipase A 2 (sPLA 2 ) is an acute phase protein and plasma leve...

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