High-Q Magnetic Levitation and Control of Superconducting Microspheres at Millikelvin Temperatures.

We report the levitation of a superconducting lead-tin sphere with 100 µm diameter (corresponding to a mass of 5.6 µg) in a static magnetic trap formed by two coils in an anti-Helmholtz configuration, with adjustable resonance frequencies up to 240 Hz. The center-of-mass motion of the sphere is monitored magnetically using a dc superconducting quantum interference device as well as optically and exhibits quality factors of up to 2.6×10^{7}. We also demonstrate 3D magnetic feedback control of the motion of the sphere. The setup is housed in a dilution refrigerator operating at 15 mK. By implementing a cryogenic vibration isolation system, we can attenuate environmental vibrations at 200 Hz by approximately 7 orders of magnitude. The combination of low temperature, large mass, and high quality factor provides a promising platform for testing quantum physics in previously unexplored regimes with high mass and long coherence times.

Efficient Bell state analyzer for time-bin qubits with fast-recovery WSi superconducting single photon detectors.

We experimentally demonstrate a high-efficiency Bell state measurement for time-bin qubits that employs two superconducting nanowire single-photon detectors with short dead-times, allowing projections onto two Bell states, |ψ⁻〉 and |ψ⁺〉. Compared to previous implementations for time-bin qubits, this yields an increase in the efficiency of Bell state analysis by a factor of thirty.

Modeling a measurement-device-independent quantum key distribution system.

We present a detailed description of a widely applicable mathematical model for quantum key distribution (QKD) systems implementing the measurement-device-independent (MDI) protocol. The model is tested by comparing its predictions with data taken using a proof-of-principle, time-bin qubit-based QKD system in a secure laboratory environment (i.e. in a setting in which eavesdropping can be excluded). The good agreement between the predictions and the experimental data allows the model to be used to optimize mean photon numbers per attenuated laser pulse, which are used to encode quantum bits. This in turn allows optimization of secret key rates of existing MDI-QKD systems, identification of rate-limiting components, and projection of future performance. In addition, we also performed measurements over deployed fiber, showing that our system's performance is not affected by environment-induced perturbations.

Real-world two-photon interference and proof-of-principle quantum key distribution immune to detector attacks.

Several vulnerabilities of single-photon detectors have recently been exploited to compromise the security of quantum-key-distribution (QKD) systems. In this Letter, we report the first proof-of-principle implementation of a new quantum-key-distribution protocol that is immune to any such attack. More precisely, we demonstrated this new approach to QKD in the laboratory over more than 80 km of spooled fiber, as well as across different locations within the city of Calgary. The robustness of our fiber-based implementation, together with the enhanced level of security offered by the protocol, confirms QKD as a realistic technology for safeguarding secrets in transmission. Furthermore, our demonstration establishes the feasibility of controlled two-photon interference in a real-world environment and thereby removes a remaining obstacle to realizing future applications of quantum communication, such as quantum repeaters and, more generally, quantum networks.

Eomesodermin, HAND1, and CSH1 proteins are induced by cellular stress in a stress-activated protein kinase-dependent manner.

Eomesodermin (Eomes) is a transcription factor essential for trophoblast development. Stress stimuli activate stress-activated protein kinase (MAPK8/9) and modulate transcription factors in trophoblast stem cells (TSC). In this study, we test the hypothesis that stress-induced Eomes upregulation and downstream trophoblast development are MAPK8/9-dependent. Immunocytochemical and immunoblot assays suggest that Eomes is induced by hyperosmolar stress in a dose- and time-dependent manner. Two MAPK8/9 inhibitors that work by different mechanisms, LJNKl1 and SP600125, block induction of Eomes protein by stress. During normal TSC differentiation, the transcription factor heart and neural crest derivatives expressed 1 (HAND1) is dependent on Eomes, and chorionic somatomammotropin hormone 1 (CSH1) expression is dependent on HAND1. Similar to Eomes, HAND1 and CSH1 induction by stress are MAPK8/9-dependent, and CSH1 is induced in nearly all stressed TSC. CSH1 induction normally requires downregulation of the transcription factor inhibitor of differentiation 2 (ID2) as well as HAND1 upregulation. It was shown previously that hyperosmolar stress induces AMP-activated protein kinase (PRKAA1/2)-dependent ID2 loss in a MAPK8/9-independent manner. Inhibition of PRKAA1/2 with compound C and LJNKl1, more than MAPK8/9 inhibitors alone, inhibits the induction of CSH1 by stress. Taken together these data suggest that stress-induced MAPK8/9 and PRKAA1/2 regulate transcription factors Eomes/HAND1 and ID2, respectively. Together this network mediates induction of CSH1 by stress. Therefore, stress triggers a proportional increase in a normal early TSC differentiation event that could be adaptive in inducing CSH1. But the flexibility of TSC to undergo stress-induced differentiation could lead to pathophysiological consequences if stress endured and TSC differentiation became unbalanced.

Cellular stress causes reversible, PRKAA1/2-, and proteasome-dependent ID2 protein loss in trophoblast stem cells.

Stress reduces fertility, but the mechanisms mediating this are not understood. For a successful pregnancy, placental trophoblast stem cells (TSCs) in the implanting embryo proliferate and then a subpopulation differentiates to produce hormones. Normally, differentiation occurs when inhibitor of differentiation 2 (ID2) protein is lost in human and mouse placental stem cells. We hypothesize that stress enzyme-dependent differentiation occurs in association with insufficient TSC accumulation. We studied a well-defined model where TSC differentiation requires ID2 loss. The loss of ID2 derepresses the promoter of chorionic somatomammotropin hormone 1 (CSH1), the first hormone after implantation. Csh1 mRNA is known to be induced in stressed TSCs. In this study, we demonstrate that AMP-activated protein kinase (PRKAA1/2, aka AMPK) mediates the stress-induced proteasome-dependent loss of ID2 at high stress levels. At very low stress levels, PRKAA1/2 mediates metabolic adaptation exemplified by the inactivation of acetyl coA carboxylase by phosphorylation without ID2 loss. At the highest stress levels, irreversible TSC differentiation as defined by ID2 loss and slower cell accumulation occurs. However, lower stress levels lead to reversible differentiation accompanied by metabolic adaptation. These data support the hypothesis that PRKAA1/2 mediates preparation for differentiation that is induced by stress at levels where a significant decrease in cell accumulation occurs. This supports the interpretation that enzyme-mediated increases in differentiation may compensate when insufficient numbers of stem cells accumulate.

Fast and simple characterization of a photon pair source.

We present an exact model of the detection statistics of a probabilistic source of photon pairs from which a fast, simple and precise method to measure the source's brightness and photon channel transmissions is demonstrated. We measure such properties for a source based on spontaneous parametric downconversion in a periodically poled LiNbO(3) crystal producing pairs at 810 and 1550 nm wavelengths. We further validate the model by comparing the predicted and measured values for the g((2))(0) of a heralded single photon source over a wide range of the brightness. Our model is of particular use for monitoring and tuning the brightness on demand as required for various quantum communication applications. We comment on its applicability to sources involving spectral and/or spatial filtering.

Propranolol treatment of chronically hospitalized aggressive patients.

Violent behavior in psychiatric patients may result in long-term hospitalization. There is no FDA-approved psychopharmacologic treatment for aggression. In this study, 20 chronically aggressive hospitalized patients were administered 1 week of placebo followed by an open trial of increasing doses of propranolol. Patients who had an equivocal or definite clinical response were entered into an open add-on double-blind discontinuation study phase. Aggressive behavior was objectively documented throughout the study. After the open phase of the study, 7 patients had a greater than 50% decrease in aggressive behavior. Four patients entered the double-blind discontinuation phase. The clinical course of 3 of those patients was consistent with the positive response to propranolol. The results of this study are consistent with a therapeutic effect of propranolol in some patients with aggressive behavior. Further studies are indicated.

Patella alta and the adolescent growth spurt.

The presence of patella alta has been linked to recurrent dislocation of the patella and the patello-femoral stress syndrome. It is not known whether patella alta is an inherited or acquired trait. To investigate the relationship of patella during the adolescent growth spurt, serial orthoroentgenograms (growth study films) were retrospectively analyzed in 19 patients. Two were found in whom proximal patella migration could be correlated (r = 0.85) with femoral growth rate. This was significant at the p = 0.01 level. Girls had a higher correlation of patella height to growth rate than boys. In certain cases, patella alta is an acquired rather than inherited condition; this supports the theory that overgrowth during the growth spurt can lead to patella alta in some individuals.