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To maintain a robust catalog of resident space objects (RSOs), space situational awareness (SSA) mission operators depend on ground- and space-based sensors to repeatedly detect, characterize, and track objects in orbit. Although some space sensors are capable of monitoring large swaths of the sky with wide fields of view (FOVs), others—such as maneuverable optical telescopes, narrow-band imaging radars, or satellite laser-ranging systems—are restricted to relatively narrow FOVs and must slew at a finite rate from object to object during observation. Since there are many objects that a narrow FOV sensor could choose to observe within its field of regard (FOR), it must schedule its pointing direction and duration using some algorithm. This combinatorial optimization problem is known as the sensor-tasking problem. In this paper, we developed a deep reinforcement learning agent to task a space-based narrow-FOV sensor in low Earth orbit (LEO) using the proximal policy optimization algorithm. The sensor’s performance—both as a singular sensor acting alone, but also as a complement to a network of taskable, narrow-FOV ground-based sensors—is compared to the greedy scheduler across several figures of merit, including the cumulative number of RSOs observed and the mean trace of the covariance matrix of all of the observable objects in the scenario. The results of several simulations are presented and discussed. Additionally, the results from an LEO SSA sensor in different orbits are evaluated and discussed, as well as various combinations of space-based sensors.

Exposures to cocaine and morphine produce similar adaptations in nucleus accumbens (NAc)-based behaviors, yet produce very different adaptations at NAc excitatory synapses. In an effort to explain this paradox, we found that both drugs induced NMDA receptor-containing, AMPA receptor-silent excitatory synapses, albeit in distinct cell types through opposing cellular mechanisms. Cocaine selectively induced silent synapses in D1-type neurons, likely via a synaptogenesis process, whereas morphine induced silent synapses in D2-type neurons via internalization of AMPA receptors from pre-existing synapses. After drug withdrawal, cocaine-generated silent synapses became 'unsilenced' by recruiting AMPA receptors to strengthen excitatory inputs to D1-type neurons, whereas morphine-generated silent synapses were likely eliminated to weaken excitatory inputs to D2-type neurons. Thus, these cell type-specific, opposing mechanisms produced the same net shift of the balance between excitatory inputs to D1- and D2-type NAc neurons, which may underlie certain common alterations in NAc-based behaviors induced by both classes of drugs.

Objective. To determine if Staphylococcus aureus stimulates the L-arginine‐nitric oxide (NO) synthase pathway in articular cartilage. Methods. A heat-killed and sonicated (denatured) S aureus preparation was added to cultures of bovine articular cartilage. NO production was measured as accumulated nitrite in the culture medium and by the NO synthase‐dependent conversion of 3 H‐L-arginine to 3 H‐L-citrulline in cartilage homogenates. Inducible NO synthase (iNOS) messenger RNA (mRNA) expression was analyzed by Northern blot. Proteoglycan synthesis was measured by 35 SO4 incorporation into glycosaminoglycan. Results. Nitrite accumulation and 3 H‐L-citrulline formation in cartilage were elevated by denatured S aureus (compared with unstimulated control cartilage) and inhibited by the NO synthase inhibitor N G monomethyl-L-arginine. Northern blot analysis revealed increased iNOS mRNA expression in bovine chondrocytes in response to denatured S aureus stimulation. Denatured S aureus suppressed the accumulation of 35 SO4-labeled macromolecules representing newly synthesized proteoglycans in bovine articular cartilage. The suppressed proteoglycan synthesis was due to the presence of NO. Conclusion. These findings support the hypothesis that a component of S aureus can stimulate iNOS in articular cartilage, and that NO generated from this enzyme down-regulates cartilage matrix proteoglycan synthesis.