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BackgroundSynchrotron radiation experimental methods have unique advantages in studying the structure and physical properties of materials, but it is a challenge for many experimental methods to achieve synchrotron radiation in situ high temperature conditions, especially above 2 000 K. Laser heating methods can achieve rapid, micro-region extreme high temperature conditions, and have become an important tool for the study of high temperature physical properties.PurposeThis study aims to develop a portable laser heating device for Shanghai Synchrotron Radiation Facility (SSRF) in situ experiments in the field of extreme high temperature research, such as high entropy alloys, turbine blades, aviation materials, etc.MethodsA 100 W continuously tunable near-infrared fiber laser was used as the heating souce, the sample was heated up by laser through the focusing lens and generated thermal radiation. The radiation spectrum was collected through the spectral collection focusing lens and measured by spectrometers. The temperature gradient and temperature stability of the sample were fitted by the blackbody radiation method. Finally, the melting experiment of pure tungsten sheets in vacuum was conducted to verify its maximum heating temperature, and the temperature gradient and stability measurement of the device were calibrated with platinum samples.ResultsWe Experimental results show that melting point of about 3 695 K for tungsten sheets in vacuum is achieved using this device, and X-ray diffraction patterns of MoS2 and CTAB-MoS2 materials under 1 608 K in situ are obtained at the surface diffraction beamline station of SSRF.ConclusionsThe laser heating method developed expands the extreme experimental conditions in SSRF, and provides an important means to study high temperature physics for materials.

Sialic acid (SIA) has been reported to be a risk factor for atherosclerosis (AS) due to its high plasma levels in such patients. However, the effect of increasing SIA in circulation on endothelial function during AS progression remains unclear. In the present study, ApoE−/− mice and endothelial cells line (HUVEC cells) were applied to investigate the effect of SIA on AS progression and its potential molecular mechanism. In vivo, mice were injected intraperitoneally with Neu5Ac (main form of SIA) to keep high‐level SIA in circulation. ORO, H&E, and Masson staining were applied to detect the plaque progression. In vitro, HUVECs were treated with Neu5Ac at different times, CCK‐8, RT‐PCR, western blot, and immunoprecipitation methods were used to analyze its effects on endothelial function and the potential involved mechanism. Results from the present study showed that high plasma levels of Neu5Ac in ApoE−/− mice could aggravate the plaque areas as well as increase necrotic core areas and collagen fiber contents. Remarkably, Neu5Ac levels in circulation displayed a positive correlation with AS plaque areas. Furthermore, results from HUVECs showed that Neu5Ac inhibited cells viability in a time/dose‐dependent manner, by then induced the activation of inflammation makers such as ICAM‐1 and IL‐1β. Mechanism study showed that the activation of excessive autophagy medicated by SQSTM1/p62 displayed an important role in endothelium inflammatory injury. Neu5Ac could modify SQSTM1/p62 as a sialylation protein, and then increase its level with ubiquitin binding, further inducing ubiquitination degradation and being involved in the excessive autophagy pathway. Inhibition of sialylation by P‐3Fax‐Neu5Ac, a sialyltransferase inhibitor, reduced the binding of SQSTM1/p62 to ubiquitin. Together, these findings indicated that Neu5Ac increased SQSTM1/p62‐ubiquitin binding through sialylation modification, thereby inducing excessive autophagy and subsequent endothelial injury. Inhibition of SQSTM1/p62 sialylation might be a potential strategy for preventing such disease with high levels of Neu5Ac in circulation. [ABSTRACT FROM AUTHOR]