Radiation effect on silicon photonics chips for space quantum key distribution.

Quantum communication satellites have potential for applications in future quantum networks. Photonics integrated chips, due to their compact and lightweight nature, are well-suited for satellite deployment. However, the harsh radiation environment of space can cause permanent damage to these chips, resulting in degraded performance or complete loss of functionality. In this work, we conducted a series of radiation experiments to evaluate the effects of γ rays and high energy protons on quantum key distribution transmitter chips. The results suggest that the insertion loss of the chip is slightly reduced by about 1.5 dB after 100 krad (Si) γ ray irradiation, and further reduced by about 0.5 to 1 dB after 2.39 × 1011/cm2 proton radiation. The half-wave voltages, extinction ratios, and polarization angles are not changed significantly within the measurement error range. Our work proves the feasibility of deploying quantum constellations utilizing terminals based on photonics chips.

A 1.25-GHz multi-amplitude modulator driver in 0.18 µm SiGe BiCOMOS technology for high speed quantum key distribution.

Quantum key distribution (QKD) research has yielded highly fruitful results and is currently undergoing an industrialization transformation. In QKD systems, electro-optic modulators are typically employed to prepare the required quantum states. While various QKD systems operating at GHz repetition frequency have demonstrated exceptional performance, they predominantly rely on instruments or printed circuit boards to fulfill the driving circuit function of the electro-optic modulator. Consequently, these systems tend to be complex with low integration levels. To address this challenge, we have introduced a modulator driver integrated circuit in 0.18 µm SiGe BiCMOS technology. The circuit can generate multiple-level driving signals with a clock frequency of 1.25 GHz and a rising edge of ∼50 ps. Each voltage amplitude can be independently adjusted, ensuring the precise preparation of quantum states. The measured signal-to-noise ratio was more than 17 dB, resulting in a low quantum bit error rate of 0.24% in our polarization-encoding system. This work will contribute to the advancement of QKD system integration and promote the industrialization process in this field.

NecroX-5 alleviate lipopolysaccharide-induced acute respiratory distress syndrome by inhibiting TXNIP/NLRP3 and NF-κB.

The activation of NLRP3 inflammasome and NF-κB pathway, associating with oxidativestress, have been implicated in the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). NecroX-5 has been reported to exhibit theeffectsofanti-oxidation and anti-stress in various diseases. However, the role of NecroX-5 in ALI has not been explicitly demonstrated. The aim of this study was to explore the therapeutic effects and potential mechanism action of NecroX-5 on ALI. Here, we found that NecroX-5 pretreatment dramatically diminished the levels of IL-1ß, IL-18 and ROS in in RAW264.7 cells challenged with LPS and ATP. Furthermore, NecroX-5 suppressed the activation of NLRP3 inflammasome and NF-κB signalpathway. In addition, NecroX-5 also inhibited the thioredoxin-interacting protein (TXNIP) expression. In vivo, NecroX-5 reduced the LPS-induced lung histopathological injury, the number of TUNEL-positive cells, lung wet/dry (W/D) ratio, levels of total protein and inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) in mice. Additionally, LPS-induced upregulation of myeloperoxidase (MPO), ROS production and malondialdehyde (MDA) were inhibited by NecroX-5 administration. Thus, our results demonstrate that NecroX-5 protects against LPS-induced ALI by inhibiting TXNIP/NLRP3 and NF-κB.

Trichostatin A modulates the macrophage phenotype by enhancing autophagy to reduce inflammation during polymicrobial sepsis.

Sepsis is a syndrome of life-threatening organ dysfunction caused by dysregulated host responses to infection. Macrophage polarization is a key process involved in the pathogenesis of sepsis. Recent evidence has demonstrated that autophagy participates in the regulation of macrophage polarization in different phases of inflammation. Here, we investigated whether trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, promotes the macrophage M2 phenotype by enhancing autophagy to counteract excessive inflammation in a cecal ligation and puncture (CLP) mouse model. TSA stimulation increased the proportions of M2 marker (CD206, CD124 and CD23)-labeled RAW264.7 macrophages. Furthermore, with increasing TSA doses, autophagy was enhanced gradually. Interestingly, the autophagy activator rapamycin (Rap), also known as an mTOR inhibitor, unexpectedly decreased the proportions of M2 marker-labeled macrophages. However, TSA treatment reversed the Rap-induced decreases in CD206-labeled macrophages. Next, we stimulated different groups of RAW264.7 cells with the autophagy inhibitors MHY1485 or 3-methyladenine (3-MA). Inhibition of autophagy at any stage in the process suppressed TSA-induced macrophage M2 polarization, but the effect was not associated with mTOR activity. In vivo, TSA administration promoted peritoneal macrophage M2 polarization, increased LC3 II expression, attenuated sepsis-induced organ (lung, liver and kidney) injury, and altered systemic inflammatory cytokine secretion. However, 3-MA abolished the protective effects of TSA in CLP mice and decreased the number of M2 peritoneal macrophages. Therefore, TSA promotes the macrophage M2 phenotype by enhancing autophagy to reduce systemic inflammation and ultimately improves the survival of mice with polymicrobial sepsis.

Construction of leaky strains and extracellular production of exogenous proteins in recombinant Escherichia coli.

In this study, a strategy of the construction of leaky strains for the extracellular production of target proteins was exploited, in which the genes mrcA, mrcB, pal and lpp (as a control) from Escherichia coli were knocked out by using single- and/or double-gene deletion methods. Then the recombinant strains for the expression of exogenous target proteins including Trx-hPTH (human parathyroid hormone 1-84 coupled with thioredoxin as a fusion partner) and reteplase were reconstructed to test the secretory efficiency of the leaky strains. Finally, the fermentation experiments of the target proteins from these recombinant leaky strains were carried out in basic media (Modified R media) and complex media (Terrific Broth media) in flasks or fermenters. The results demonstrated that the resultant leaky strains were genetically stable and had a similar growth profile in the complex media as compared with the original strain, and the secretory levels of target proteins into Modified R media from the strains with double-gene deletion (up to 88.9%/mrcA lpp-pth) are higher than the excretory levels from the strains with single-gene deletion (up to 71.1%/lpp-pth) and the host E. coli JM109 (DE3) (near zero). The highest level of extracellular production of Trx-hPTH in fermenters is up to 680 mg l(-1).