30 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
One-Dimensional Strain Solitons Manipulated Superlubricity on Graphene Interface
The frictional properties of a uniaxial tensile strained
graphene
interface are studied using molecular dynamics simulations. A misfit
interval statistical method (MISM) is applied to characterize the
atomistic misfits at the interface and strain soliton pattern. During
sliding along both armchair and zigzag directions, the lateral force
depends on the ratio of graphene flake length (L)
to strain soliton spacing (Ls) and becomes
nearly zero when L is an integer multiple of 3Ls. Furthermore, the strain solitons propagate
along the armchair sliding direction dynamically, while fission and
fusion are repeatedly evidenced along the zigzag sliding direction.
The underlying superlubric mechanism is revealed by a single-atom
quasi-static model. The cancellation of lateral force for the contacting
atoms exhibits a dynamic balance when sliding along the armchair direction
but a quasi-static balance along the zigzag direction. A diagram of
flake length with respect to tensile strain (L–ε)
is proposed to predict the critical condition for the transition
from nonsuperlubricity to superlubricity. Our results provide insights
on the design of superlubric devices
Some Considerations of an Approximate Analysis on Unstable Vibrations of an Asymmetrical Shaft Supported by Asymmetrical Pedestals
application/pdfThe approximation previously proposed by the authors is applied to an analysis of unstable vibrations of a rotating asymmetrical shaft supported by asymmetrically flexible bearing pedestals. A frequency equation is represented by the determinant of the 4th order, 8th order, or 12th order, according as a directional inequality of bearing pedestal stiffness is negligibly small, small but considerable, or not small. Instability regions are obtained by solving each frequency equation. No matter what the directional inequality of stiffness of bearing pedestal may be, the position, width and number of instability regions can be sufficiently determined by use of the determinant of the 8th order. Instability regions derived from approximation are found to agree well with those obtained by an analog computer.departmental bulletin pape
IL-13 Induces YY1 through the AKT Pathway in Lung Fibroblasts
<div><p>A key feature of lung fibrosis is the accumulation of myofibroblasts. Interleukin 13 (IL-13) is a pro-fibrotic mediator that directly and indirectly influences the activation of myofibroblasts. Transforming growth factor beta (TGF-β) promotes the differentiation of fibroblasts into myofibroblasts, and can be regulated by IL-13. However, IL-13’s downstream signaling pathways are not completely understood. We previously reported that the transcription factor Yin Yang 1 (YY1) is upregulated in fibroblasts treated with TGF-β and in the lungs of mice and patients with pulmonary fibrosis. Moreover, YY1 directly regulates collagen and alpha smooth muscle actin (α-SMA) expression in fibroblasts. However, it is not known if IL-13 regulates fibroblast activation through YY1 expression. We hypothesize that IL-13 up-regulates YY1 expression through regulation of AKT activation, leading to fibroblast activation. In this study we found that YY1 was upregulated by IL-13 in lung fibroblasts in a dose- and time-dependent manner, resulting in increased α-SMA. Conversely, knockdown of YY1 blocked IL-13-induced α-SMA expression in fibroblasts. Furthermore, AKT phosphorylation was increased in fibroblasts treated with IL-13, and AKT overexpression upregulated YY1, whereas blockade of AKT phosphorylation suppressed the induction of YY1 by IL-13 <i>in vitro</i>. <i>In vivo</i> YY1 was upregulated in fibrotic lungs from CC10-IL-13 transgenic mice compared to that from wild-type littermates, which was associated with increased AKT phosphorylation. Taken together, these findings demonstrate that IL-13 is a potent stimulator and activator of fibroblasts, at least in part, through AKT-mediated YY1 activation.</p></div
Silencing expression of Foxo1 increases Na<sub>V</sub>1.5 expression.
<p>Western blots showed decrease of Foxo1 protein by 50 MOI (n = 4) and 100 MOI Adv-Foxo1 RNAi (n = 4) increased Na<sub>V</sub>1.5 protein in HL-1 cells in comparison with 100 MOI Adv-scramble RNAi (n = 4) (A) and this inhibition reached the significant difference (*p<0.05) at 100 MOI Adv-Foxo1-RNAi (C). RT-PCR showed that Na<sub>V</sub>1.5 mRNA was increased by 50 MOI Foxo1-RNAi (n = 4) in comparison with that in cells expression scramble RNAi (n = 4) (B). The values of Na<sub>V</sub>1.5 mRNA relative ß-actin between Foxo1-RANi and scramble RNAi groups were significant different (**p<0.05) (D).</p
Foxo1 decreases <i>SCN5a</i> promoter activity.
<p>A. Luciferase constructs contain proximal region of <i>SCN5a</i> promoter which has Foxo1 binding insulin response elements and mutations. B. Foxo1 significantly suppressed <i>SCN5a</i> promoter activity with dose dependence (**p<0.01, n = 3). C. Individual or double mutations of Foxo1 binding sites in <i>SCN5a</i> promoter region prevented Foxo1 inhibition (**p<0.01) compared with wild type <i>SCN5a</i>; Double mutation of Foxo1 binding sites had significantly more effective (<sup>#</sup>p<0.05) than mutation 1 (n = 6 in all individual groups).</p
H<sub>2</sub>O<sub>2</sub> -mediated downregulation of Na<sub>V</sub>1.5 requires Foxo1.
<p>Western blot analysis showed that Na<sub>V</sub>1.5 protein was significantly increased (*p<0.05) in HL-1 cells cultured in the medium with 25 µM H<sub>2</sub>O<sub>2</sub> treatment for 48 hours after the cells expressed Foxo1-RNAi for 24 hours (n = 4) compared with scramble RNAi group (n = 4) (A, C). RT-PCR analysis showed that Na<sub>V</sub>1.5 significantly increased (**p<0.01) in HL-1 cells in the medium with 25 µM H<sub>2</sub>O<sub>2</sub> treatment for 48 hours after the cells expressed Foxo1-RNAi for 24 hours (n = 4) compared with scramble RNAi group (n = 4) (B, D).</p
