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Two-particle interference is a fundamental feature of quantum mechanics, and is even less intuitive than wave-particle duality for a single particle. In this duality, classical concepts--wave or particle--are still referred to, and interference happens in ordinary space-time. On the other hand, two-particle interference takes place in a mathematical space that has no classical counterpart. Entanglement lies at the heart of this interference, as it does in the fundamental tests of quantum mechanics involving the violation of Bell's inequalities (1-4). The Hong, Ou and Mandel experiment (5) is a conceptually simpler situation, in which the interference between two-photon amplitudes also leads to behaviour impossible to describe using a simple classical model. Here we report the realization of the Hong, Ou and Mandel experiment using atoms instead of photons. We create a source that emits pairs of atoms, and cause one atom of each pair to enter one of the two input channels of a beam-splitter, and the other atom to enter the other input channel. When the atoms are spatially overlapped so that the two inputs are indistinguishable, the atoms always emerge together in one of the output channels. This result opens the way to testing Bell's inequalities involving mechanical observables of massive particles, such as momentum, using methods inspired by quantum optics (6, 7), and to testing theories of the quantum-to-classical transition (8-11). Our work also demonstrates a new way to benchmark non-classical atom sources (12, 13) that may be of interest for quantum information processing (14) and quantum simulation (15)., A pair of entangled particles is described by a state vector that cannot be factored as a product of two state vectors associated with each particle. Although entanglement does not [...]

Author(s): E. R. Stofan (corresponding author) [1, 2]; C. Elachi [3]; J. I. Lunine [4]; R. D. Lorenz [5]; B. Stiles [3]; K. L. Mitchell [3]; S. Ostro [3]; L. [...]

The first two swaths collected by Cassini's Titan Radar Mapper were obtained in October of 2004 (Ta) and February of 2005 (T3). The Ta swath provides evidence for cryovolcanic processes, the possible occurrence of fluvial channels and lakes, and some tectonic activity. The T3 swath has extensive areas of dunes and two large impact craters. We interpret the brightness variations in much of the swaths to result from roughness variations caused by fracturing and erosion of Titan's icy surface, with additional contributions from a combination of volume scattering and compositional variations. Despite the small amount of Titan mapped to date, the significant differences between the terrains of the two swaths suggest that Titan is geologically complex. The overall scarcity of impact craters provides evidence that the surface imaged to date is relatively young, with resurfacing by cryovolcanism, fluvial erosion, aeolian erosion, and likely atmospheric deposition of materials. Future radar swaths will help to further define the nature of and extent to which internal and external processes have shaped Titan's surface. Keywords: Titan; Geological processes; Saturn, satellites; Satellites, surfaces

Author(s): C. Elachi [1]; S. Wall (corresponding author) [1]; M. Janssen [1]; E. Stofan [2]; R. Lopes [1]; R. Kirk [3]; R. Lorenz [4]; J. Lunine [4, 5]; F. Paganelli [...]

The Cassini Titan Radar Mapper imaged about 1% of Titan's surface at a resolution of ~0.5 kilometer, and larger areas of the globe in lower resolution modes. The images reveal a complex surface, with areas of low relief and a variety of geologic features suggestive of dome-like volcanic constructs, flows, and sinuous channels. The surface appears to be young, with few impact craters. Scattering and dielectric properties are consistent with porous ice or organics. Dark patches in the radar images show high brightness temperatures and high emissivity and are consistent with frozen hydrocarbons., Saturn's largest satellite, Titan, is the only moon and one of only four solid bodies in the solar system to host a thick atmosphere, uniquely distinguished by nitrogen and methane [...]

Author(s): C. Elachi; S. Wall; M. Janssen; E. Stofan; R. Lopes; R. Kirk; R. Lorenz; J. Lunine; F. Paganelli; L. Soderblom; C. Wood; L. Wye; H. Zebker; Y. Anderson; S. [...]

Adrenal corticosteroids have both fast and slow feedback effects on pituitary hormone release via actions in the hypothalamus. Using whole-cell patch clamp electrophysiology in hypothalamic slices, we have studied the acute effects of glucocorticoids on the electrical activity of identified neuroendocrine cells of the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the rat. The glucocorticoids dexamethasone and corticosterone caused a dose-dependent, steroid-specific suppression of the release of glutamate and an enhancement of GABA release onto identified subpopulations of PVN and SON neuroendocrine cells within 3-5 min, suggesting a non-transcriptional inhibitory effect of the steroids on presynaptic glutamate afferents and facilitatory effect on GABA afferents. These effects are not blocked by conjugating the steroid to membrane-impermeant albumin, or by prior application of the type I and II corticosteroid receptor antagonists spironolactone and RU486, implicating a non-conventional membrane corticosteroid receptor with differing actions on glutamate and GABA release mechanisms. Surprisingly, the glucocorticoid effects are abolished by blocking postsynaptic G protein activity, suggesting that the receptor is located on the postsynaptic neuroendocrine cell membrane, and that it triggers the release of one or more retrograde messengers by activating a G protein signaling cascade. Both the glucocorticoid suppression of glutamate release and facilitation d GABA release are blocked completely by type I cannabinoid receptor (CB1) antagonists, and the suppression of glutamate release is mimicked with CB1 agonists, implicating endocannabinoids as the associated retrograde messenger(s). These data indicate a novel membrane glucocorticoid receptor that is coupled to endocannabinoid synthesis and release via a G protein-dependent signaling mechanism. Supported by NIH MH066958.