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Articles by R Si
Total Records ( 2 ) for R Si
  L. F Allard , A Borisevich , W Deng , R Si , M Flytzani Stephanopoulos and S. H. Overbury

High-resolution aberration-corrected electron microscopy was performed on a series of catalysts derived from a parent material, 2 at.% Au/Fe2O3 (WGC ref. no. 60C), prepared by co-precipitation and calcined in air at 400°C, and a catalyst prepared by leaching surface gold from the parent catalyst and exposed to various treatments, including use in the water–gas shift reaction at 250°C. Aberration-corrected JEOL 2200FS (JEOL USA, Peabody, MA) and Vacuum Generators HB-603U STEM instruments were used to image fresh, reduced, leached, used and re-oxidized catalyst samples. A new in situ heating technology (Protochips Inc., Raleigh, NC, USA), which permits full sub-Ångström imaging resolution in the JEOL 2200FS was used to study the effects of temperature on the behavior of gold species. A remarkable stability of gold to redox treatments up to 400°C, with atomic gold decorating step surfaces of iron oxide was identified. On heating the samples in vacuum to 700°C, it was found that monodispersed gold began to sinter to form nanoparticles above 500°C. Gold species internal to the iron oxide support material was shown to diffuse to the surface at elevated temperature, coalescing into discrete nanocrystals. The results demonstrate the value of in situ heating for understanding morphological changes in the catalyst with elevated temperature treatments.

  Y Feng , L Zou , R Si , Y Nagasaka and W. Chao

Myeloid differentiation factor 88 (MyD88), an adaptor critical for innate immune function, plays a role in neutrophil recruitment and myocardial injury after transient ischemia. However, how MyD88 signaling modulates neutrophil function and myocardial injury remains unclear. In an in vivo model of neutrophil migration and a chimeric model of MyD88 deletion, we demonstrated that Gr-1-positive (Gr-1+) neutrophil migration was significantly decreased by 68% in MyD88-deficient (Myd88–/–) mice and by 33% in knockout->wild-type (KO->WT; donor->recipient) chimeric mice, which lacked MyD88 in bone marrow cells but maintained normal MyD88 expression in the heart. This marked attenuation in neutrophil migration was associated with decreased peritoneal neutrophil CXCR2 expression and lower peritoneal KC, a neutrophil chemoattractant, in MyD88–/– mice. Moreover, in vitro, KC induces significantly more downregulation of CXCR2 expression in MyD88–/– than WT neutrophils. In an in vivo model of myocardial ischemia-reperfusion (I/R) injury, KO->WT chimeric mice had significantly smaller infarct sizes compared with the WT->WT mice. While there was a marked increase in proinflammatory cytokine/chemokine expression in the myocardium following I/R, there was no significant difference between WT->WT and KO->WT mice. In contrast, Gr-1+ neutrophil recruitment in the myocardium was markedly attenuated in MyD88–/– mice. Deletion of Toll-interleukin-1 receptor (TIR)-domain-containing adaptor protein-inducing interferon-β-mediated transcription factor (Trif), another innate immune adaptor, had no effect on the KC-mediated CXCR2 downregulation or on myocardial neutrophil recruitment after I/R. Taken together, these findings suggest that MyD88 signaling is essential for maintaining neutrophil migratory function and chemokine receptor expression. MyD88 signaling in bone marrow-derived circulating cells may play a specific and critical role in the development of myocardial I/R-induced injury.

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