长波红外差分干涉仪在低温工况下会因光学元件受到非均匀应力作用产生干涉条纹的畸变,从而降低干涉仪系统性能。本文为解决低温工况干涉条纹弯曲畸变问题,基于长波红外差分干涉仪光机系统进行了干涉条纹畸变影响因素分析,结合光-机-热...长波红外差分干涉仪在低温工况下会因光学元件受到非均匀应力作用产生干涉条纹的畸变,从而降低干涉仪系统性能。本文为解决低温工况干涉条纹弯曲畸变问题,基于长波红外差分干涉仪光机系统进行了干涉条纹畸变影响因素分析,结合光-机-热耦合分析方法,对干涉仪系统低温工作状态进行仿真。随后设计了针对影响条纹畸变的关键元件——光栅元件的低温微应力动态稳定支撑安装结构,结构优化后的光栅表面面形均方根(Root Mean Square,RMS)值为3.89×10^(-2) nm,面形峰谷值(Peak to Valley,PV)值为2.21×10^(-1) nm,分别较优化前初始系统的分析结果减小了5个数量级,系统仿真干涉条纹畸变小于1个探测器像元。全系统低温验证试验表明,优化结构可有效抑制干涉条纹畸变,畸变量小于2个探测器像元,试验与仿真计算结果一致性较好,验证了优化分析方法的有效性。该优化方案对提升反射式光学系统结构低温稳定性,提高系统工作能力有较大意义和价值。展开更多
The management of colorectal cancer(CRC)poses a significant challenge,necessitating the development of innovative and effective therapeutics.Our research has shown that notoginsenoside Ft1(Ng-Ft1),a small molecule,mar...The management of colorectal cancer(CRC)poses a significant challenge,necessitating the development of innovative and effective therapeutics.Our research has shown that notoginsenoside Ft1(Ng-Ft1),a small molecule,markedly inhibits subcutaneous tumor formation in CRC and enhances the proportion of CD8^(+)T cells in tumor-bearing mice,thus restraining tumor growth.Investigation into the mechanism revealed that Ng-Ft1 selectively targets the deubiquitination enzyme USP9X,undermining its role in shieldingβ-catenin.This leads to a reduction in the expression of downstream effectors in the Wnt signaling pathway.These findings indicate that Ng-Ft1 could be a promising small-molecule treatment for CRC,working by blocking tumor progression via the Wnt signaling pathway and augmenting CD8^(+)T cell prevalence within the tumor environment.展开更多
文摘长波红外差分干涉仪在低温工况下会因光学元件受到非均匀应力作用产生干涉条纹的畸变,从而降低干涉仪系统性能。本文为解决低温工况干涉条纹弯曲畸变问题,基于长波红外差分干涉仪光机系统进行了干涉条纹畸变影响因素分析,结合光-机-热耦合分析方法,对干涉仪系统低温工作状态进行仿真。随后设计了针对影响条纹畸变的关键元件——光栅元件的低温微应力动态稳定支撑安装结构,结构优化后的光栅表面面形均方根(Root Mean Square,RMS)值为3.89×10^(-2) nm,面形峰谷值(Peak to Valley,PV)值为2.21×10^(-1) nm,分别较优化前初始系统的分析结果减小了5个数量级,系统仿真干涉条纹畸变小于1个探测器像元。全系统低温验证试验表明,优化结构可有效抑制干涉条纹畸变,畸变量小于2个探测器像元,试验与仿真计算结果一致性较好,验证了优化分析方法的有效性。该优化方案对提升反射式光学系统结构低温稳定性,提高系统工作能力有较大意义和价值。
基金supported by Shanghai Pujiang Program(No.20PJ1413000)the National Natural Science Foundation of China(No.82173106,82130115,81290108033,82004004,and 82074011)。
文摘The management of colorectal cancer(CRC)poses a significant challenge,necessitating the development of innovative and effective therapeutics.Our research has shown that notoginsenoside Ft1(Ng-Ft1),a small molecule,markedly inhibits subcutaneous tumor formation in CRC and enhances the proportion of CD8^(+)T cells in tumor-bearing mice,thus restraining tumor growth.Investigation into the mechanism revealed that Ng-Ft1 selectively targets the deubiquitination enzyme USP9X,undermining its role in shieldingβ-catenin.This leads to a reduction in the expression of downstream effectors in the Wnt signaling pathway.These findings indicate that Ng-Ft1 could be a promising small-molecule treatment for CRC,working by blocking tumor progression via the Wnt signaling pathway and augmenting CD8^(+)T cell prevalence within the tumor environment.
