CO oxidation on stepped Rh[n(1 1 1) × (1 1 1)] single crystal electrodes: a chronoamperometric study

The CO electro-oxidation reaction has been studied on Rh[n(1 1 1) × (1 1 1)]-type electrodes in 0.5 M H₂SO₄ using chronoamperometry. The transients recorded on Rh(1 1 1), Rh(5 5 4), Rh(5 5 3) and Rh(3 3 1) are characterized by a current plateau, visible directly after charging of the double layer, followed by a main oxidation feature, which consists of two peaks, a pre-peak and a main peak. The current density in the plateau region is nearly constant over time and, thus, is of (quasi) zeroth order in CO coverage. A plot of log(j_plateau) vs. E_final gives a linear relationship with a slope of ca. 45 mV dec^?1, suggesting a second electron transfer as the rate determining step. Analogously to platinum, the current density plateau was ascribed to a Langmuir–Hinshelwood type reaction between CO_ads and OH_ads with no effective freeing of sites for OH adsorption due to relaxation of the CO adlayer. The presence of two peaks, rather than one, in the main oxidation feature can be explained by assuming a low surface mobility of CO and high oxidizability of rhodium surfaces. Indeed, dual step chronoamperometry shows that the mobility of CO on rhodium surfaces in aqueous media is very low. Since rhodium surfaces are known to oxidize readily, the pre-peak and main peak can be ascribed to CO reacting with OH, which adsorbs fast at the steps and more slowly at terrace sites. Since the geometry of the steps is nearly the same on each surface, the pre-peak appears structure insensitive, while the main peak shifts considerably with the step density. Introducing randomly distributed crystalline defects by cycling the electrodes repeatedly up to the surface oxidation region prior to each potential step experiment, results in a negative shift of the main peak, while the position of the pre-peak remains fixed. From the data presented, we conclude that the reaction nucleates at the steps and grows in the direction of the terraces.     

Assessment of a gel-type chelating preparation containing 1-hydroxyethylidene-1, 1-bisphosphonate

AIM: To test an aqueous gel containing 1-hydroxyethylidene-1, 1-bisphosphonate (HEBP) regarding its interactions with sodium hypochlorite, its calcium binding capacity, and its potential in preventing the formation of a smear layer when used in conjunction with rotary root canal preparation. METHODOLOGY: The experimental aqueous gel consisted of (w/v) 2% alginate, 3% aerosil, 10% Tween 80 and 18% HEBP. Interactions of gel components with hypochlorite were assessed using iodometric titration and monochromatic ultraviolet spectrometry. Two commercial paste-type chelators containing ethylenediaminetetraacetic acid (EDTA) and peroxide (RC-Prep and Glyde) served as controls. Calcium-binding capacities were measured in mixtures with a Ca2+ standard solution buffered at pH 10 using a calcium-selective measuring chain. Finally, root canals of 16 extracted single-rooted premolars per group were instrumented using ProFile instruments dipped in the experimental gel, RC-Prep, or nothing. Additionally, canals were rinsed with 10 mL of a 1% NaOCl solution during/after preparation. Smear scores in instrumented teeth were monitored using scanning electron microscopy. RESULTS: None of the experimental gel components showed short-term interactions with hypochlorite, whilst EDTA, peroxide, RC-Prep and Glyde immediately reduced the hypochlorite in solution. The experimental gel chelated 30 mg Ca2+ g-1, compared with 16 mg Ca2+ g-1 and 11 mg Ca2+ g-1 chelated by RC-Prep and Glyde respectively. Smear scores obtained with the experimental gel were significantly (P<0.05) lower than with RC-Prep in coronal and middle root thirds, whilst no differences were observed in apical root thirds. CONCLUSIONS: Under the conditions of this study, an HEBP gel appeared advantageous over currently available products.     

IL-1α、IL-1β和TNF-α mRNA 在实验性鼠根尖周炎中的表达

目的　检测IL-1α、IL-1β和TNF-αmRNA在鼠根尖周炎组织中的表达,了解上述细胞因子与根尖周炎的关系。方法　16只SD大鼠第一、二磨牙开髓,分别于术后3d、7d、14d、28d取磨牙根尖周组织,提取总RNA,用RT-PCR方法测定IL-1α、IL-1β和TNF-αmRNA的表达,用看家基因β-Actin作内参照进行半定量分析。结果　术后7d鼠根尖周组织中即有IL-1α、TNF-α、IL-1βmRNA的表达,14d达高峰,28d有所下降,但IL-1α和TNF-α的表达量大于IL-1β表达量,相差非常显著（P＜0.01）。结论　IL-1α和TNF-α可能是导致鼠根尖周炎的主要细胞因子。     

Syndecan-1 and Wingless-type protein-1 in human ameloblastomas

BACKGROUND: Aberrant Wingless type 1 glycoprotein (Wnt) pathway in ameloblastomas and a role of syndecan-1 (SDC1) in activating Wnt signalling were perspected. SDC1 shifting from epithelium to stroma was reported in invasive non-odontogenic neoplasms. The aim of this study was to reveal the role of SDC1 and Wnt1 in intraosseous ameloblastomas (IA(s)). METHODS: SDC1 and Wnt1 expressions were investigated in 29 ameloblastoma subtypes and seven tooth buds. RESULTS: SDC1 immunostaining strongly depicted stromal cells, extracellular matrix (ECM) and basement membranes of ameloblastomas. It also showed epithelial tumour cells in the acanthomatous and plexiform subtypes, and it often occurred in stellate reticulum cells and basal ameloblasts of tooth buds. Parallel Wnt1 expression occurred in ameloblastomatous epithelial cells, but it was common in basal cells of tooth buds too. Statistically, a significant correlation was found between the percentage of IA(s)-bearing SDC1-positive stromal cells and ECM and the percentage of IA(s)-bearing Wnt1-positive epithelial cells. CONCLUSIONS: A role of SDC1 in stromal cells and ECM can be hypothesized as a critical factor for carcinogenesis and local invasiveness of IA(s).     

S1P/S1PR1通路依赖的压力对破骨前体细胞趋化效应

目的: 探究S1P/S1PR1通路轴在压力下对破骨前体细胞趋化影响的调节作用。方法: 建立体外压力模型,通过实时荧光定量聚合酶链式反应,免疫印迹实验和细胞免疫荧光检测压力下Raw264.7细胞SPHK1和S1PR1的mRNA水平和蛋白水平。采用Transwell 24孔板通过趋化实验探究S1P/S1PR1在压力下对Raw264.7细胞的迁移能力的影响。结果: 发现0.5、1.0和2.0 g/cm²压力作用下,Raw264.7细胞的SPHK1和S1PR1的表达及Raw264.7细胞的趋化显著降低。在S1PR1受体功能性激动剂FTY720作用下,压力作用下趋化能力被抑制的Raw264.7细胞趋化水平显著增加。结论: S1P/S1PR1信号轴在正畸治疗中调节破骨前体细胞迁移与功能发挥重要作用。[关键词] S1P/S1PR1通路 压力 破骨前体细胞 趋化     

Cytoplasmic HMGB1 and HMGB1-Beclin1 complex are increased in radioresistant oral squamous cell carcinoma

Cytoplasmic high mobility group box 1 (HMGB1) is an autophagy regulator, and autophagy is important in the radioresistance of various solid cancers. We evaluated the degree of autophagy and cytoplasmic HMGB1 in radioresistant oral squamous cell carcinoma (SCC) by culturing the SCC15 and quasiliquid layer 1 (QLL1) SCC cell lines that originate from cancer of the oral tongue and a metastatic lymph node, respectively, and then delivered radiation to induce radioresistance to cells. We then compared the degree of autophagy between non-irradiated control and radioresistant cancer cells using a western blot assay. We also compared the total and cytoplasmic concentrations of HMGB1 between the non-irradiated control and radioresistant cancer cells by western blot assay, and extracellular concentrations of HMGB1 with an enzyme-linked immunosorbent assay (ELISA). Formation of an HMGB1-Beclin1 complex was evaluated by immunofluorescence and co-immunoprecipitation assays. Autophagy increased in the radioresistant SCC15 cells (compared with non-irradiated control SCC15 cells) but not in the radioresistant QLL1 cells. The total amount of HMGB1 expression within cells did not differ; however, the degree of cytoplasmic HMGB1 expression was higher in radioresistant SCC15 cells than in non-irradiated control SCC15 cells. The HMGB1-Beclin1 complex, which is a main regulator of autophagy, was also increased in radioresistant SCC15 cells compared with non-irradiated control SCC15 cells. Autophagy flux and cytoplasmic HMGB1-Beclin1 increased after the acquisition of radioresistance in oral SCC.