Integrating planar circuits with superconducting 3D microwave cavities using tunable low-loss couplers

We design and test a low-loss interface between superconducting 3-dimensional microwave cavities and 2-dimensional circuits, where the coupling rate is highly tunable. This interface seamlessly integrates a magnetic antenna and a Josephson junction based coupling element with a cavity, and we demonstrate that the introduced loss from this integration only limits the quality factor to 4.5 million. The cavity external coupling rate can then be tuned from negligibly small to over 3 orders of magnitude larger than the internal loss rate with a characteristic time of 3.2 ns. This switching speed does not impose additional limits on the coupling rate because it is much faster than the coupling rate. Moreover, the coupler can be controlled by baseband signals to avoid interference with microwave signals near the cavity or qubit frequencies. Finally, the coupling element introduces a 0.04 Hz/photon self-Kerr nonlinearity to the cavity, remaining linear in high photon number operations

Tissue-resident, extravascular Ly6c- monocytes are critical for inflammation in the synovium

Monocytes are abundant immune cells that infiltrate inflamed organs. However, the majority of monocyte studies focus on circulating cells, rather than those in tissue. Here, we identify and characterize an intravascular synovial monocyte population resembling circulating non-classical monocytes and an extravascular tissue-resident monocyte-lineage cell (TR-MC) population distinct in surface marker and transcriptional profile from circulating monocytes, dendritic cells, and tissue macrophages that are conserved in rheumatoid arthritis (RA) patients. TR-MCs are independent of NR4A1 and CCR2, long lived, and embryonically derived. TR-MCs undergo increased proliferation and reverse diapedesis dependent on LFA1 in response to arthrogenic stimuli and are required for the development of RA-like disease. Moreover, pathways that are activated in TR-MCs at the peak of arthritis overlap with those that are downregulated in LFA1-/- TR-MCs. These findings show a facet of mononuclear cell biology that could be imperative to understanding tissue-resident myeloid cell function in RA.</p