12 research outputs found
Transmission electron microscopic observation of nanoindentations made on ductile-machined silicon wafers
Nanoindentation tests were performed on a ductile-machined silicon wafer with a Berkovich diamond indenter, and the resulting indents were examined with a transmission electron microscope. It was found that the machining-induced subsurface amorphous layer undergoes significant plastic flow, and the microstructure of the indent depends on the indentation load. At a small load (~20 mN),most of the indented region remains to be amorphous with minor crystalline nuclei; while under a large load (~50 mN),the amorphous phase undergoes intensive recrystallization. The understanding and utilization of this phenomenon might be useful for improving the microscopic surface properties of silicon parts produced by a ductile machining process.journal articl
CYLD acts as a negative regulator for NTHi-induced NF-κB activation via negative cross-talk with TRAF6/7.
<p>A. CYLD knockdown by siRNA-CYLD markedly reduced expression of CYLD and enhanced NTHi-induced NF-κB-dependent promoter activity in HMEEC cells. B, overexpression of WT-CYLD inhibited NTHi-induced NF-κB-dependent promoter activity in HMEEC cells. C, NTHi-induced DNA binding activity of NF-κB was enhanced by CYLD knockdown, as assessed by EMSA. D, CYLD knockdown by siRNA-CYLD enhanced NTHi-induced IL-1β and IL-8 expression at mRNA level in HMEEC-1 cells. E, TRAF7 synergistically enhanced TRAF6-induced NF-κB-dependent promoter activity. Overexpression of WT-CYLD inhibited TRAF6- and TRAF7-induced NF-κB-dependent promoter activity, whereas CYLD knockdown by siRNA-CYLD enhanced TRAF6- and TRAF7-induced NF-κB-dependent promoter activity in lung epithelial A549 cells. *<i>p<0.05</i>, compared with NTHi-inoculated in Mock in A, B and D. Values are means ± S.D. (n = 3).</p
Schematic representation of the negative regulation of NTHi-induced inflammatory response by CYLD.
<p>Schematic representation of the negative regulation of NTHi-induced inflammatory response by CYLD.</p
NTHi-induced CYLD is responsible for down-regulation of inflammatory response.
<p>A & B, NTHi induced CYLD expression at both mRNA (A) and protein levels (B) in HMEEC-1 cells. C, NTHi induced CYLD expression at the mRNA level in the middle ear of WT mice. D & E, NTHi induced expression of CYLD and IL-1β (D) or MIP-2 (E) at the mRNA level in the lung of WT mice. *<i>p<0.05</i> compared with CON. Values are means ± S.D. (n = 3). <i>CON</i>, control.</p
CYLD inhibits TRAF6 and TRAF7 in a deubiquitination-dependent manner.
<p>A, NTHi induced ubiquitination of TRAF6. B, co-expressing WT-CYLD inhibited, whereas CYLD knockdown by siRNA-CYLD enhanced the ubiquitination of TRAF6 in HeLa cells. C, NTHi induced ubiquitination of TRAF7. D, co-expressing WT-CYLD inhibited, whereas CYLD knockdown by siRNA-CYLD enhanced the ubiquitination of TRAF7 in HeLa cells.</p
