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The High Energy Photon Source (HEPS), a 6â GeV green-field diffraction-limited storage ring light source, will be built in Beijing, China. The HEPS design has been evolving for about ten years, and is now mostly finished and ready for construction. The storage ring is based on a modified hybrid seven-bend achromat (7BA) design, where bending magnets with reverse bending angles and longitudinal gradients are adopted to reach an ultralow natural emittance of 34.2â pm with a circumference of 1360.4â m. The central slice of the dipole in the middle of the modified hybrid 7BA, with flexible magnetic field, is used as the source of the bending-magnet beamline. Moreover, alternating high- and low-beta sections are specially designed to generate and deliver X-ray synchrotron radiation with high brightness of 5â ×â 1022â photons s-1 mm-2 mrad-2 (0.1% bandwidth)-1. Here, the HEPS storage ring design and solutions to the challenges inherent in this ultralow-emittance design are presented.
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[This retracts the article DOI: 10.3892/etm.2020.8760.].
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Alzheimer's disease (AD), is a severe neurodegenerative disease that currently lacks an optimally effective therapeutic agent for its management. Saikosaponin D (SSD) is a component extracted from the herb Bupleurum falcatum that is commonly used in Chinese medicine. Although SSD has been reported to exert neuroprotective effects, its pharmacological role in AD has not been previously elucidated. Therefore, the aim of the present study was to investigate whether SSD treatment improves the cognitive function and pathological features of 3xTg mice, a triple-transgenic mouse model of AD that displays classical pathological features of AD. The effects of SSD treatment on the behavioral, histological and physiological features of the animal were quantified. Results from the behavioral experiments on the SSD-treated 3xTg mice identified a significant reduction in memory impairment. In addition, histological staining results indicated that SSD application could preserve the morphology of neurons, reduce apoptosis and significantly inhibit amyloid-ß deposition in the hippocampus of 3xTg mice. SSD treatment also decelerated the activation of microglia and astrocytes in the hippocampus of 3xTg mice, possibly via the inhibition of the NF-κB signal transduction pathway. Therefore, the present study demonstrated the protective effects of SSD against progressive neurodegeneration and identified the potential underlying pharmacological mechanism. It was speculated that SSD may serve as a possible therapeutic agent in AD treatment in the future.