分类: 物理学 >> 核物理学 提交时间: 2023-06-09
摘要: A diffraction-limited storage ring with a multi-bend achromat lattice suffers from a small dynamic aperture for conventional off-axis injection. Thus, a longitudinal on-axis injection scheme based on a new type of crab cavity is proposed in this paper. Particle tracking simulations were performed to study the disturbance of the stored beam and the motion of the injected beam during the injection process. The possibility of multi-bunch injections was discussed. In addition, the effect of the long-range wake field induced by the stored beam was analyzed. A C-band standing-wave crab cavity was designed and produced as requested, and its field distribution was measured. The corresponding results are consistent with the simulation results.
分类: 生物学 >> 生物物理学 提交时间: 2016-05-11
摘要: Inflammatory caspases (caspase-1, -4, -5 and -11) are critical for innate defences. Caspase-1 is activated by ligands of various canonical inflammasomes, and caspase-4, -5 and -11 directly recognize bacterial lipopolysaccharide, both of which trigger pyroptosis. Despite the crucial role in immunity and endotoxic shock, the mechanism for pyroptosis induction by inflammatory caspases is unknown. Here we identify gasdermin D (Gsdmd) by genome-wide clustered regularly interspaced palindromic repeat (CRISPR)-Cas9 nuclease screens of caspase-11- and caspase-1-mediated pyroptosis in mouse bone marrow macrophages. GSDMD-deficient cells resisted the induction of pyroptosis by cytosolic lipopolysaccharide and known canonical inflammasome ligands. Interleukin-1 beta release was also diminished in Gsdmd(-/-) cells, despite intact processing by caspase-1. Caspase-1 and caspase-4/5/11 specifically cleaved the linker between the amino-terminal gasdermin-N and carboxy-terminal gasdermin-C domains in GSDMD, which was required and sufficient for pyroptosis. The cleavage released the intramolecular inhibition on the gasdermin-N domain that showed intrinsic pyroptosis-inducing activity. Other gasdermin family members were not cleaved by inflammatory caspases but shared the autoinhibition; gain-of-function mutations in Gsdma3 that cause alopecia and skin defects disrupted the autoinhibition, allowing its gasdermin-N domain to trigger pyroptosis. These findings offer insight into inflammasome-mediated immunity/diseases and also change our understanding of pyroptosis and programmed necrosis.