A millimeter wave propagation experiment from the ATS-E spacecraft

Millimeter wave propagation experiment from Applications Technology Satellite-

Usability of Nomadic User Interfaces

Abstract. During the last decade, a number of research activities have been performed to enable user interfaces and the underlying user activities to be migrated from one device to another. We call this “Nomadic User Interfaces”. The primary goal of these research activities has been to develop the technologies to enable this. However, not much is known about the usability aspects of Nomadic User Interfaces. In this paper we present the results of three different user tests that we conducted to investigate the usefulness and the usability issues of several prototype Nomadic User Interface systems that we developed

Lipopolysaccharide-induced leptin release is neurally controlled

Our hypothesis is that leptin release is controlled neurohormonally. Conscious, male rats bearing indwelling, external, jugular catheters were injected with the test drug or 0.9% NaCl (saline), and blood samples were drawn thereafter to measure plasma leptin. Anesthesia decreased plasma leptin concentrations within 10 min to a minimum at 120 min, followed by a rebound at 360 min. Administration (i.v.) of lipopolysaccharide (LPS) increased plasma leptin to almost twice baseline by 120 min, and it remained on a plateau for 360 min, accompanied by increased adipocyte leptin mRNA. Anesthesia largely blunted the LPS-induced leptin release at 120 min. Isoproterenol (β-adrenergic agonist) failed to alter plasma leptin but reduced LPS-induced leptin release significantly. Propranolol (β-receptor antagonist) produced a significant increase in plasma leptin but had no effect on the response to LPS. Phentolamine (α-adrenergic receptor blocker) not only increased plasma leptin (P < 0.001), but also augmented the LPS-induced increase (P < 0.001). α-Bromoergocryptine (dopaminergic-2 receptor agonist) decreased plasma leptin (P < 0.01) and blunted the LPS-induced rise in plasma leptin release (P < 0.001). We conclude that leptin is at least in part controlled neurally because anesthesia decreased plasma leptin and blocked its response to LPS. The findings that phentolamine and propranolol increased plasma leptin concentrations suggest that leptin release is inhibited by the sympathetic nervous system mediated principally by α-adrenergic receptors because phentolamine, but not propranolol, augmented the response to LPS. Because α-bromoergocryptine decreased basal and LPS-induced leptin release, dopaminergic neurons may inhibit basal and LPS-induced leptin release by suppression of release of prolactin from the adenohypophysis

Measurement of the neutron lifetime using an asymmetric magneto- gravitational trap and in situ detection

The precise value of the mean neutron lifetime, $\tau_n$, plays an important role in nuclear and particle physics and cosmology. It is a key input for predicting the ratio of protons to helium atoms in the primordial universe and is used to search for new physics beyond the Standard Model of particle physics. There is a 3.9 standard deviation discrepancy between $\tau_n$ measured by counting the decay rate of free neutrons in a beam (887.7 $\pm$ 2.2 s) and by counting surviving ultracold neutrons stored for different storage times in a material trap (878.5$\pm$0.8 s). The experiment described here eliminates loss mechanisms present in previous trap experiments by levitating polarized ultracold neutrons above the surface of an asymmetric storage trap using a repulsive magnetic field gradient so that the stored neutrons do not interact with material trap walls and neutrons in quasi-stable orbits rapidly exit the trap. As a result of this approach and the use of a new in situ neutron detector, the lifetime reported here (877.7 $\pm$ 0.7 (stat) +0.4/-0.2 (sys) s) is the first modern measurement of $\tau_n$ that does not require corrections larger than the quoted uncertainties.Comment: 9 pages, 3 figures, 2 table

PU.1 controls fibroblast polarization and tissue fibrosis

Fibroblasts are polymorphic cells with pleiotropic roles in organ morphogenesis, tissue homeostasis and immune responses. In fibrotic diseases, fibroblasts synthesize abundant amounts of extracellular matrix, which induces scarring and organ failure. By contrast, a hallmark feature of fibroblasts in arthritis is degradation of the extracellular matrix because of the release of metalloproteinases and degrading enzymes, and subsequent tissue destruction. The mechanisms that drive these functionally opposing pro-fibrotic and pro-inflammatory phenotypes of fibroblasts remain unknown. Here we identify the transcription factor PU.1 as an essential regulator of the pro-fibrotic gene expression program. The interplay between transcriptional and post-transcriptional mechanisms that normally control the expression of PU.1 expression is perturbed in various fibrotic diseases, resulting in the upregulation of PU.1, induction of fibrosis-associated gene sets and a phenotypic switch in extracellular matrix-producing pro-fibrotic fibroblasts. By contrast, pharmacological and genetic inactivation of PU.1 disrupts the fibrotic network and enables reprogramming of fibrotic fibroblasts into resting fibroblasts, leading to regression of fibrosis in several organs

Status of the UCNτ experiment

The neutron is the simplest nuclear system that can be used to probe the structure of the weak interaction and search for physics beyond the standard model. Measurements of neutron lifetime and β-decay correlation coefficients with precisions of 0.02% and 0.1%, respectively, would allow for stringent constraints on new physics. The UCNτ experiment uses an asymmetric magneto-gravitational UCN trap with in situ counting of surviving neutrons to measure the neutron lifetime, τ_n = 877.7s (0.7s)_(stat) (+0.4/−0.2s)_(sys). We discuss the recent result from UCNτ, the status of ongoing data collection and analysis, and the path toward a 0.25 s measurement of the neutron lifetime with UCNτ

Position-sensitive detection of ultracold neutrons with an imaging camera and its implications to spectroscopy

Position-sensitive detection of ultracold neutrons (UCNs) is demonstrated using an imaging charge-coupled device (CCD) camera. A spatial resolution less than 15 $\mu$m has been achieved, which is equivalent to an UCN energy resolution below 2 pico-electron-volts through the relation $\delta E = m_0g \delta x$. Here, the symbols $\delta E$, $\delta x$, $m_0$ and $g$ are the energy resolution, the spatial resolution, the neutron rest mass and the gravitational acceleration, respectively. A multilayer surface convertor described previously is used to capture UCNs and then emits visible light for CCD imaging. Particle identification and noise rejection are discussed through the use of light intensity profile analysis. This method allows different types of UCN spectroscopy and other applications.Comment: 12 figures, 28 pages, accepted for publication in NIM

Search for neutron dark decay: n → χ + e⁺e⁻

In January, 2018, Fornal and Grinstein proposed that a previously unobserved neutron decay branch to a dark matter particle (χ) could account for the discrepancy in the neutron lifetime observed in two different types of experiments. One of the possible final states discussed includes a single χ along with an e⁺e⁻ pair. We use data from the UCNA (Ultracold Neutron Asymmetry) experiment to set limits on this decay channel. Coincident electron-like events are detected with ∼ 4π acceptance using a pair of detectors that observe a volume of stored Ultracold Neutrons (UCNs). We use the timing information of coincidence events to select candidate dark sector particle decays by applying a timing calibration and selecting events within a physically-forbidden timing region for conventional n → p + e⁻ + ν̅_e decays. The summed kinetic energy (E_(e⁺e⁻)) from such events is reconstructed and used to set limits, as a function of the χ mass, on the branching fraction for this decay channel