Yuqi Yan

Orbital angular momentum (OAM), which describes the “phase twist” (helical phase pattern) of light beams, has recently gained interest due to its potential applications in many diverse areas. Particularly promising is the use of OAM for optical communications since: (i) coaxially propagating OAM beams with different azimuthal OAM states are mutually orthogonal, (ii) inter-beam crosstalk can be minimized, and (iii) the beams can be efficiently multiplexed and demultiplexed. As a result, multiple OAM states could be used as different carriers for multiplexing and transmitting multiple data streams, thereby potentially increasing the system capacity. In this paper, we review recent progress in OAM beam generation/detection, multiplexing/demultiplexing, and its potential applications in different scenarios including free-space optical communications, fiber-optic communications, and RF communications. Technical challenges and perspectives of OAM beams are also discussed.

Excitatory amino acid transporters (EAATs) are responsible for excitatory amino acid transportation and are associated with auto-immune diseases in the central nervous system and peripheral tissues. However, the subcellular location and function of EAAT2 in macrophages are still obscure. In this study, we demonstrated that LPS stimulation increases expression of EAAT2 (coded by Slc1a2) via NF-κB signaling. EAAT2 is necessary for inflammatory macrophage polarization through sustaining mTORC1 activation. Mechanistically, lysosomal EAAT2 mediates lysosomal glutamate and aspartate efflux to maintain V-ATPase activation, which sustains macropinocytosis and mTORC1. We also found that mice with myeloid depletion of Slc1a2 show alleviated inflammatory responses in LPS-induced systemic inflammation and high-fat diet induced obesity. Notably, patients with type II diabetes (T2D) have a higher level of expression of lysosomal EAAT2 and activation of mTORC1 in blood macrophages. Taken together, our study links the subcellular location of amino acid transporters with the fate decision of immune cells, which provides potential therapeutic targets for the treatment of inflammatory diseases.

activated the TLR2/4/MyD88/NF-κB signaling pathway to promote expression of arylalkylamine N-acetyltransferase (AANAT, a rate-limiting enzyme for melatonin production), and MyD88 deficiency in colonic epithelial cells abolished the influence of intestinal microbiota on colonic melatonin production. Collectively, we revealed a specific underlying mechanism of gut microbiota to modulate host melatonin production, which might provide novel therapeutic ideas for melatonin-related diseases.