Bias Stability Investigation of a Triaxial Navigation-Compatible Accelerometer with an Electrostatic Spring

The bias stability performance of accelerometers is essential for an inertial navigation system. The traditional pendulous accelerometer usually has a flexible connection structure, which could limit the long-term bias stability. Here, based on the main technologies employed in previous space missions of our group, we developed a terrestrial triaxial navigation-compatible accelerometer. Because there is no mechanical connection between the inertial test mass and the frame, the bias performance relies on the stability of the equivalent electrostatic spring, where further sources are analyzed to get the optimal electrostatic force scheme. To investigate the bias stability under different ranges, the vertical and horizontal measurement ranges are designed at 5 g and ±10 mg, respectively. A low-noise high-voltage levitation scheme is adopted to extend the vertical measurement range from sub-mg to more than earth’s 1-g gravity. Finally, the experimental validation results show that the 24-h bias stability of vertical and two horizontal directions come to 13.8 μg, 0.84 μg, and 0.77 μg, respectively

1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion via Targeting the NF-E2-Related Factor 2–Hemeoxygenase-1–HMGB1 Pathway in Macrophages

1,25-Dihydroxyvitamin D [1,25(OH)2D3] is recognized as a key mediator of inflammatory diseases, including sepsis. Clinical studies demonstrate that 1,25 (OH)2D3 protects patients from sepsis, but clinical treatment with 1,25(OH)2D3 is rare. In this study, we report that 1,25(OH)2D3 treatment has beneficial effects and improves the survival rate in LPS-induced mouse sepsis model by blocking the secretion of high-mobility group box 1 (HMGB1), a key late regulator of sepsis. LPS-induced HMGB1 secretion is attenuated by 1,25(OH)2D3via blocking HMGB1 translocation from the nucleus to the cytoplasm in macrophages. 1,25(OH)2D3 can induce the expression of hemeoxygenase-1 (HO-1), which is essential for blocking HMBG1 nuclear translocation and its secretion. When siHO-1 or an HO-1 inhibitor are used, the effect of 1,25(OH)2D3 on inhibition of HMGB1 secretion is suppressed. Considering that HO-1 is a downstream gene of NF-E2-related factor 2 (Nrf2), we further confirm that Nrf2 activation can be activated by 1,25(OH)2D3 upon LPS exposure. Together, we provide evidence that 1,25(OH)2D3 attenuates LPS-induced HMGB1 secretion via the Nrf2/HO-1 pathway in macrophages

Stair-Like Narrow Nanographene with Diradicaloid Character at the Topological Interface

π-magnetism of finite-sized nanoribbon occurring on the topological molecular interfaces remains largely unexplored due to limited experimental examples. Herein, we report rational design, solution synthesis and systematical characterization of a novel type of stair-like aza-nanographene (ANG) ANG-a~b with precise N-doping on the interfacial cove-edges. Within the same molecular π-backbone, ANG-a had a closed-shell structure due to the electronic perturbation of cove-edge substitution; while ANG-b hosted a spin-polarized interface state, and impressively its open-shell singlet diradicaloid structure produced a combined optoelectronic, magnetic and physicochemical characteristics. Besides, dicationic ANG-b was also synthesized and characterized as a ground-state diradicaloid, again closely associated with the interfacial spin-polarization in the charged π-system. Our studies might provide insights into future structural engineering of topological open-shell materials with robust yet exotic spin-polarized interface states

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<p>1,25-Dihydroxyvitamin D [1,25(OH)₂D₃] is recognized as a key mediator of inflammatory diseases, including sepsis. Clinical studies demonstrate that 1,25 (OH)₂D₃ protects patients from sepsis, but clinical treatment with 1,25(OH)₂D₃ is rare. In this study, we report that 1,25(OH)₂D₃ treatment has beneficial effects and improves the survival rate in LPS-induced mouse sepsis model by blocking the secretion of high-mobility group box 1 (HMGB1), a key late regulator of sepsis. LPS-induced HMGB1 secretion is attenuated by 1,25(OH)₂D₃via blocking HMGB1 translocation from the nucleus to the cytoplasm in macrophages. 1,25(OH)₂D₃ can induce the expression of hemeoxygenase-1 (HO-1), which is essential for blocking HMBG1 nuclear translocation and its secretion. When siHO-1 or an HO-1 inhibitor are used, the effect of 1,25(OH)₂D₃ on inhibition of HMGB1 secretion is suppressed. Considering that HO-1 is a downstream gene of NF-E2-related factor 2 (Nrf2), we further confirm that Nrf2 activation can be activated by 1,25(OH)₂D₃ upon LPS exposure. Together, we provide evidence that 1,25(OH)₂D₃ attenuates LPS-induced HMGB1 secretion via the Nrf2/HO-1 pathway in macrophages.</p

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<p>1,25-Dihydroxyvitamin D [1,25(OH)₂D₃] is recognized as a key mediator of inflammatory diseases, including sepsis. Clinical studies demonstrate that 1,25 (OH)₂D₃ protects patients from sepsis, but clinical treatment with 1,25(OH)₂D₃ is rare. In this study, we report that 1,25(OH)₂D₃ treatment has beneficial effects and improves the survival rate in LPS-induced mouse sepsis model by blocking the secretion of high-mobility group box 1 (HMGB1), a key late regulator of sepsis. LPS-induced HMGB1 secretion is attenuated by 1,25(OH)₂D₃via blocking HMGB1 translocation from the nucleus to the cytoplasm in macrophages. 1,25(OH)₂D₃ can induce the expression of hemeoxygenase-1 (HO-1), which is essential for blocking HMBG1 nuclear translocation and its secretion. When siHO-1 or an HO-1 inhibitor are used, the effect of 1,25(OH)₂D₃ on inhibition of HMGB1 secretion is suppressed. Considering that HO-1 is a downstream gene of NF-E2-related factor 2 (Nrf2), we further confirm that Nrf2 activation can be activated by 1,25(OH)₂D₃ upon LPS exposure. Together, we provide evidence that 1,25(OH)₂D₃ attenuates LPS-induced HMGB1 secretion via the Nrf2/HO-1 pathway in macrophages.</p