Observation of the Color-Suppressed Decay B̅ 0→D0π0

journal articl

《修論報告》高等学校・平和教育における「他者」と出会うカリキュラムデザインに関する研究

departmental bulletin pape

コウゴウセイケイ ノ ブンシ コウチク キノウ ソシ オウヨウ

video/mp4講演者所属: 静岡大学工学部物質工学科助教授vide

Nanoindentation tests on diamond-machined silicon wafers

Nanoindentation tests were performed on ultraprecision diamond-turned silicon wafers and the results were compared with those of pristine silicon wafers. Remarkable differences were found between the two kinds of test results in terms of load-displacement characteristics and indent topologies. The machining-induced amorphous layer was found to have significantly higher microplasticity and lower hardness than pristine silicon. When machining silicon in the ductile mode, we are in essence always machining amorphous silicon left behind by the preceding tool pass; thus, it is the amorphous phase that dominates the machining performance. This work indicated the feasibility of detecting the presence and the mechanical properties of the machining-induced amorphous layers by nanoindentation.journal articl

Schematic representation of NF-κB inhibition by CAPE and dose response of the cells to the inhibitor.

<p>The inhibition site in the NF-κB activation pathway for CAPE is very different from that of sodium salicylate (A). CAPE effectively suppressed up-regulation of TLR1 density when stimulated with the bacterial lysate, and the degree was proportional to the concentration used (B). This compared with the results of no response to acetaminophen as the negative control. Data were expressed as mean ± SD (n = 4) and each significance was also indicated.</p

<i>In Vitro</i> Inflammation Inhibition Model Based on Semi-Continuous Toll-Like Receptor Biosensing

<div><p>A chemical inhibition model of inflammation is proposed by semi-continuous monitoring the density of toll-like receptor 1 (TLR1) expressed on mammalian cells following bacterial infection to investigate an <i>in vivo</i>-mimicked drug screening system. The inflammation was induced by adding bacterial lysate (e.g., <i>Pseudomonas aeruginosa</i>) to a mammalian cell culture (e.g., A549 cell line). The TLR1 density on the same cells was immunochemically monitored up to three cycles under optimized cyclic bacterial stimulation-and-restoration conditions. The assay was carried out by adopting a cell-compatible immunoanalytical procedure and signal generation method. Signal intensity relative to the background control obtained without stimulation was employed to plot the standard curve for inflammation. To suppress the inflammatory response, sodium salicylate, which inhibits nuclear factor-κB activity, was used to prepare the standard curve for anti-inflammation. Such measurement of differential TLR densities was used as a biosensing approach discriminating the anti-inflammatory substance from the non-effector, which was simulated by using caffeic acid phenethyl ester and acetaminophen as the two components, respectively. As the same cells exposed to repetitive bacterial stimulation were semi-continuously monitored, the efficacy and toxicity of the inhibitors may further be determined regarding persistency against time. Therefore, this semi-continuous biosensing model could be appropriate as a substitute for animal-based experimentation during drug screening prior to pre-clinical tests.</p></div

Simulation of the drug effect persistency testing using sodium salicylate.

<p>Pre-incubation with sodium salicylate during each cycle caused consistent anti-inflammatory responses to the three repeated bacterial stimulations (“1,2,3-inhibition” as a positive control) compared to that without inhibition (Non-inhibition as negative control). However, when the treatment was skipped at either the second (“1,3-inhibition”) or third cycle (“1,2-inhibition”), the inhibitory effect was not shown at the corresponding stage. This may indicate that drug efficacy persisted for 1 day. Each measurement was repeated twice under the same conditions and the significance was indicated.</p

Testing the effective dose and treatment timing, relative to bacterial stimulation, of sodium salicylate as an anti-inflammatory substance.

<p>Experimental data were obtained by measuring the signals in colorimetric mode, which represented the TLR1 density expressed on the cell surfaces (A549). When stimulated with the <i>P. aeruginosa</i> lysate, expression inhibited by sodium salicylate was most effective at a dose of 50 mM and with pre-incubation of the drug, i.e., pre-incubation in B. Data are shown in mean ± SD (n = 3) and comparisons to the control (i.e., stimulated cells without anti-inflammatory substance treatment) are marked as *** very highly significant (P<0.001), ** highly significant (P<0.01), or * significant (P<0.05). No significance (ns) was indicated otherwise.</p

Mechanism of inflammatory response via NF-κB activation against bacterial invasion.

<p>Inflammation proceeds mainly via two different routes, which are initiated by TLRs-PAMPs binding (Infection process) or bradykinin-BR interactions (Inflammation process). The former invokes inflammation by producing cytokines as a result of the response. NF-κB activation also increases the densities of other mediators such as TLRs and BRs.</p

Application of the semi-continuous analytical approach for TLR regulation to test the anti-inflammatory substance effect.

<p>Optimal conditions for the TLR regulation scheme were determined (A) and TLR expression was observed in response to two cyclic repeated bacterial stimulations (B, No treatment). Sodium salicylate was the positive inhibitor (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0105212#pone-0105212-g002" target="_blank">Figure 2</a>) and an effective dose (50 mM) was used either by co-incubation with the stimulus agent (Co-addition) or by pre-incubation (Pre-incubation). Both treatments revealed inhibition of the TLR response to serial stimulations, suggesting a model for anti-inflammatory substance screening. Each measurement was repeated twice under identical conditions and comparisons to the control (No treatment) were marked as stated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0105212#pone-0105212-g002" target="_blank">Figure 2</a> legend.</p