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Abstract Strongly correlated polaritons in Jaynes–Cummings (JC) lattices can exhibit quantum phase transitions between the Mott-insulating and superfluid phases at integer fillings. The prerequisite to observe such phase transitions is to pump polariton excitations into a JC lattice and prepare them into appropriate ground states. Despite previous efforts, it is still challenging to generate many-body states with high accuracy. Here, we present an approach for the robust preparation of many-body ground states of polaritons in finite-sized JC lattices by optimized nonlinear ramping. We apply a Landau–Zener type of estimation to this finite-sized system and derive the optimal ramping index for selected ramping trajectories, which can greatly improve the fidelity of the prepared states. With numerical simulation, we show that by choosing an appropriate ramping trajectory, the fidelity in this approach can remain close to unity in almost the entire parameter space. This approach can shed light on high-fidelity state preparation in quantum simulators and advance the implementation of quantum simulation with practical devices.

Abstract Background The mechanism by which immune cells regulate metastasis is unclear. Understanding the role of immune cells in metastasis will guide the development of treatments improving patient survival. Methods We used syngeneic orthotopic mouse tumour models (wild-type, NOD/scid and Nude), employed knockout ( CD8 and CD4 ) models and administered CXCL4. Tumours and lungs were analysed for cancer cells by bioluminescence, and circulating tumour cells were isolated from blood. Immunohistochemistry on the mouse tumours was performed to confirm cell type, and on a tissue microarray with 180 TNBCs for human relevance. TCGA data from over 10,000 patients were analysed as well. Results We reveal that intratumoral immune infiltration differs between metastatic and non-metastatic tumours. The non-metastatic tumours harbour high levels of CD8 + T cells and low levels of platelets, which is reverse in metastatic tumours. During tumour progression, platelets and CXCL4 induce differentiation of monocytes into myeloid-derived suppressor cells (MDSCs), which inhibit CD8 + T-cell function. TCGA pan-cancer data confirmed that CD8 low Platelet high patients have a significantly lower survival probability compared to CD8 high Platelet low . Conclusions CD8 + T cells inhibit metastasis. When the balance between CD8 + T cells and platelets is disrupted,more »platelets produce CXCL4, which induces MDSCs thereby inhibiting the CD8 + T-cell function.« less

Vibrational modes in mechanical resonators provide a promising candidate to interface and manipulate classical and quantum information. The observation of coherent dynamics between distant mechanical resonators can be a key step toward scalable phonon-based applications. Here we report tunable coherent phonon dynamics with an architecture comprising three graphene mechanical resonators coupled in series, where all resonators can be manipulated by electrical signals on control gates. We demonstrate coherent Rabi oscillations between spatially separated resonators indirectly coupled via an intermediate resonator serving as a phonon cavity. The Rabi frequency fits well with the microwave burst power on the control gate. We also observe Ramsey interference, where the oscillation frequency corresponds to the indirect coupling strength between these resonators. Such coherent processes indicate that information encoded in vibrational modes can be transferred and stored between spatially separated resonators, which can open the venue of on-demand phonon-based information processing.

About one in 3,500 people have a genetic disorder called neurofibromatosis type 1, often shortened to NF1, making it one of the most common inherited diseases. People with NF1 may have benign and cancerous tumors throughout the body, learning disabilities, developmental delays, curvature of the spine and bone abnormalities. Children with NF1 often experience difficulties with attention, hyperactivity, speech and language delays and impulsivity. They may also have autism spectrum disorder, or display symptoms associated with this condition. Studies in mice with a genetic mutation that mimics NF1 suggest that abnormal development in cells in the middle of the brain may cause the cognitive symptoms. These midbrain neurons produce a chemical called dopamine and send it throughout the brain. Dopamine is essential for concentration and it is involved in how the brain processes pleasurable experiences. Now, Robinson et al. show that, at rest, the NF1 model mice release dopamine less often than typical mice. This happens because, when there are no stimuli to respond to, neighboring cells slow down the activity of dopamine-producing neurons in NF1 model mice. In the experiments, both NF1 model mice and typical mice were taught to associate environmental cues with rewards or punishments. Robinson etmore »al. then measured the release of dopamine in the mice using a sensor called dLight1, which produces different intensities of fluorescent light depending on the amount of dopamine present. This revealed that the NF1 model mice produced more dopamine in response to visual cues and had enhanced behavioral responses to these stimuli. For example, when a looming disc that mimics predators approached them from above, the NF1 model mice tried to hide in an exaggerated way compared to the typical mice. Previously, it had been shown that this type of behavior is due to the activity of the dopamine-producing neurons' neighboring cells, which Robinson et al. found is greater in NF1 model mice. Next, Robinson et al. stopped neighboring cells from interfering with the dopamine-producing neurons in NF1 model mice. This restored dopamine release to normal levels at rest, and stopped the mice from overreacting to the looming disc. The experiments help explain how the NF1 model mice process visual information. Further study of the role dopamine plays in cognitive symptoms in people with NF1 may help scientists develop treatments for the condition.« less