Exploring the Potential of Integrated Optical Sensing and Communication (IOSAC) Systems with Si Waveguides for Future Networks

Advanced silicon photonic technologies enable integrated optical sensing and communication (IOSAC) in real time for the emerging application requirements of simultaneous sensing and communication for next-generation networks. Here, we propose and demonstrate the IOSAC system on the silicon nitride (SiN) photonics platform. The IOSAC devices based on microring resonators are capable of monitoring the variation of analytes, transmitting the information to the terminal along with the modulated optical signal in real-time, and replacing bulk optics in high-precision and high-speed applications. By directly integrating SiN ring resonators with optical communication networks, simultaneous sensing and optical communication are demonstrated by an optical signal transmission experimental system using especially filtering amplified spontaneous emission spectra. The refractive index (RI) sensing ring with a sensitivity of 172 nm/RIU, a figure of merit (FOM) of 1220, and a detection limit (DL) of 8.2*10-6 RIU is demonstrated. Simultaneously, the 1.25 Gbps optical on-off-keying (OOK) signal is transmitted at the concentration of different NaCl solutions, which indicates the bit-error-ratio (BER) decreases with the increase in concentration. The novel IOSAC technology shows the potential to realize high-performance simultaneous biosensing and communication in real time and further accelerate the development of IoT and 6G networks.Comment: 11pages, 5 figutre

Exciton emission of quasi-2D InGaN in GaN matrix grown by molecular beam epitaxy

We investigate the emission from confined excitons in the structure of a single-monolayer-thick quasi-two-dimensional (quasi-2D) Inx Ga1-x N layer inserted in GaN matrix. This quasi-2D InGaN layer was successfully achieved by molecular beam epitaxy (MBE), and an excellent in-plane uniformity in this layer was confirmed by cathodoluminescence mapping study. The carrier dynamics have also been investigated by time-resolved and excitation-power-dependent photoluminescence, proving that the recombination occurs via confined excitons within the ultrathin quasi-2D InGaN layer even at high temperature up to ∼220 K due to the enhanced exciton binding energy. This work indicates that such structure affords an interesting opportunity for developing high-performance photonic devices

The Gut-Microglia Connection: Implications for Central Nervous System Diseases

The importance of the gut microbiome in central nervous system (CNS) diseases has long been recognized; however, research into this connection is limited, in part, owing to a lack of convincing mechanisms because the brain is a distant target of the gut. Previous studies on the brain revealed that most of the CNS diseases affected by the gut microbiome are closely associated with microglial dysfunction. Microglia, the major CNS-resident macrophages, are crucial for the immune response of the CNS against infection and injury, as well as for brain development and function. However, the current understanding of the mechanisms controlling the maturation and function of microglia is obscure, especially regarding the extrinsic factors affecting microglial function during the developmental process. The gut microflora has been shown to significantly influence microglia from before birth until adulthood, and the metabolites generated by the microbiota regulate the inflammation response mediated by microglia in the CNS; this inspired our hypothesis that microglia act as a critical mediator between the gut microbiome and CNS diseases. Herein, we highlight and discuss current findings that show the influence of host microbiome, as a crucial extrinsic factor, on microglia within the CNS. In addition, we summarize the CNS diseases associated with both the host microbiome and microglia and explore the potential pathways by which the gut bacteria influence the pathogenesis of CNS diseases. Our work is thus a comprehensive theoretical foundation for studies on the gut-microglia connection in the development of CNS diseases; and provides great potential for researchers to target pathways associated with the gut-microglia connection and overcome CNS diseases

A novel lncRNA linc-AhRA negatively regulates innate antiviral response in murine microglia upon neurotropic herpesvirus infection

Microglia are the primary cellular source of type I interferons (I-IFNs) in the brain upon neurotropic virus infection. Although the I-IFN-based antiviral innate immune response is crucial for eliminating viruses, overproduction led to immune disorders. Therefore, the relatively long-lasting I-IFNs must be precisely controlled, but the regulatory mechanism for the innate antiviral response in microglia remains largely unknown. Long non-coding RNAs (lncRNAs) are being recognized as crucial factors in numerous diseases, but their regulatory roles in the innate antiviral response in microglia are undefined.Methods: The high-throughput RNA sequencing was performed to obtain differentially expressed lncRNAs (DELs) in primary microglia infected with or without the neurotropic herpes simplex virus type 1 (HSV-1). We selected four DELs ranked in the top 15 in basic level and their fold change induced by HSV-1, i.e., FPKMHSV-1/FPKMCells.We subsequently found a key lncRNA affecting the innate antiviral response of microglia significantly. We next used dual-luciferase reporter assays, bioinformatical tools, and truncation mutants of both lncRNA and targeted proteins to elucidate the downstream and upstream mechanism of action of lncRNA. Further, we established microglia-specific knock-in (KI) mice to investigate the role of lncRNA in vivo.Results: We identified a long intergenic non-coding RNA, linc-AhRA, involved in regulating the innate antiviral response in murine microglia. linc-AhRA is activated by aryl hydrocarbon receptor (AhR) and restricts I-IFN production in microglia upon neurotropic herpesvirus infection and innate immune stimulation. Mechanistically, linc-AhRA binds to both tripartite motif-containing 27 (TRIM27) and TANK-binding kinase 1 (TBK1) through its conserved 117nt fragment as a molecular scaffold to enhance TRIM27-TBK1 interaction. This interaction facilitates the TRIM27-mediated ubiquitination of TBK1 and results in ubiquitin-proteasome-dependent degradation of TBK1. Consequently, linc-AhRA suppresses I-IFN production through facilitating TBK1 degradation and limits the microglial innate immune response against neurotropic herpesvirus infection. Microglia-specific KI of linc-AhRA mice shows a weakened antiviral immune response upon neurotropic herpesvirus challenge due to a reduction of TBK1 in microglia.Conclusion: Our findings indicate that linc-AhRA is a negative regulator of I-IFN production in microglia to avoid excessive autoimmune responses. These findings uncover a previously unappreciated role for lncRNA conserved fragments in the innate antiviral response, providing a strong foundation for developing nucleotide drugs based on conserved functional fragments within lncRNAs

Heat-Shock Protein 90 Promotes Nuclear Transport of Herpes Simplex Virus 1 Capsid Protein by Interacting with Acetylated Tubulin

Although it is known that inhibitors of heat shock protein 90 (Hsp90) can inhibit herpes simplex virus type 1 (HSV-1) infection, the role of Hsp90 in HSV-1 entry and the antiviral mechanisms of Hsp90 inhibitors remain unclear. In this study, we found that Hsp90 inhibitors have potent antiviral activity against standard or drug-resistant HSV-1 strains and viral gene and protein synthesis are inhibited in an early phase. More detailed studies demonstrated that Hsp90 is upregulated by virus entry and it interacts with virus. Hsp90 knockdown by siRNA or treatment with Hsp90 inhibitors significantly inhibited the nuclear transport of viral capsid protein (ICP5) at the early stage of HSV-1 infection. In contrast, overexpression of Hsp90 restored the nuclear transport that was prevented by the Hsp90 inhibitors, suggesting that Hsp90 is required for nuclear transport of viral capsid protein. Furthermore, HSV-1 infection enhanced acetylation of α-tubulin and Hsp90 interacted with the acetylated α-tubulin, which is suppressed by Hsp90 inhibition. These results demonstrate that Hsp90, by interacting with acetylated α-tubulin, plays a crucial role in viral capsid protein nuclear transport and may provide novel insight into the role of Hsp90 in HSV-1 infection and offer a promising strategy to overcome drug-resistance

Research on knocking characteristics of kerosene spark-ignition engine for unmanned aerial vehicle (UAV) by numerical simulation

The favorable physicochemical properties of kerosene have contributed to its widely application in aviation. However, knocking is more prone to take place in kerosene than in gasoline under the same conditions. This paper presents a study on the knock characteristics of a ROTAX914 engine that is fueled by kerosene. The knocking combustion process was simulated under various engine operating conditions. The effect of engine ignition timing, exhaust gas recirculation (EGR), and mixture concentration on the engine knocking combustion were studied based on a three-dimensional simulation. The results showed that engine knock could be effectively suppressed by delayed ignition timing. With increased EGR rates, knocking intensity was greatly suppressed.This study received financial support from the Shenzhen Science and Technology Innovation Committee (JCYJ20170817114345260 and JCYJ20170811161008128). The authors also thank technicians and students from Beijing Institute of Technology for their support on engine bench tests and data analyse