Hall-conductivity sign change and fluctuations in amorphous Nbx_{x}Ge1−x_{1-x} films

The sign change in the Hall conductivity has been studied in thin amorphous Nb$_{1-x}$Ge$_x (x\approx$0.3) films. By changing the film thickness it is shown that the field at which the sign reversal occurs shifts to lower values (from above to below the mean-field transition field $H_{c2}$) with increasing film thickness. This effect can be understood in terms of a competition between a positive normal and a negative fluctuation contribution to the Hall conductivity.Comment: 5 pages, 4 figures, to appear in Phys. Rev.

Biocompatibility of a High-Plasticity, Calcium Silicate-Based, Ready-to-Use Material

The Bio-C Sealer is a recently developed high-plasticity, calcium-silicate-based, ready-to-use material. In the present study, chemical elements of the materials were characterized using scanning electron microscopy (SEM), X-ray diffraction (XRD), and Fourier transform infrared spectroscopy (FTIR). The biocompatibility of the Bio-C Sealer was investigated using cytotoxicity tests and histological responses in the roots of dogs’ teeth. XRD, SEM, and FTIR produced hydrated calcium silicate in the presence of water molecules. In addition, FTIR showed the formation of calcium hydroxide and polyethylene glycol, a dispersing agent. The 1:4 dilutions of Bio-C Sealer presented weaker cytotoxicity than the Calcipex II in an in vitro system using the V-79 cell line. After 90 d, the periradicular tissue response of beagle dog roots was histologically evaluated. Absence of periradicular inflammation was reported in 17 of the 18 roots assessed with the Bio-C Sealer, whereas mature vertical periodontal ligament fibers were observed in the apical root ends filled with the Bio-C Sealer. Based on these results and previous investigations, the Bio-C Sealer is recommended as an effective root-end filling material. These results are relevant for clinicians considering the use of Bio-C Sealer for treating their patients

Plasma Pentraxin 3 is a More Potent Predictor of Endothelial Dysfunction than High-Sensitive C-Reactive Protein

An infl ammatory response is a key event for endothelial dysfunction. Pentraxin 3 (PTX3) is an infl ammatory protein produced at infl ammation sites such as leukocytes and vascular endothelial cells. Here, we compared the relationships between endothelial function assessed by flow-mediated dilation (FMD), and the levels of plasma PTX3 and highsensitive C-reactive protein (hsCRP), another infl ammatory protein of the pentraxin family. Levels of FMD, PTX3 and hsCRP were measured twice within 6 to 8 months and retrospectively analyzed in 36 patients with coronary artery disease. We examined the associations between the values of FMD and the levels of PTX3 and hsCRP at the fi rst measurement, and between the change ratios (second value/fi rst value) of these parameters. Univariate linear regression analysis showed significantly negative correlations between FMD values and PTX3 and hsCRP levels at the fi rst measurement, and significant associations with taking statins or calcium antagonists. Multivariate linear stepwise regression analysis identifi ed PTX3 levels and taking statins and calcium antagonists as independent factors for endothelial function. The change ratio of FMD correlated more closely with that of PTX3 than of hsCRP (r =-0.446, P = 0.006 versus r =-0.330, P = 0.050). Significantly more patients with decreased FMD values had increased levels of PTX3 than those of hsCRP at the second measurement compared with the fi rst measurement. Furthermore, the ratio of patients with increased PTX3, but not increased hsCRP, was significantly reduced among those with increased, rather than decreased, FMD values. Endothelial dysfunction might be more accurately predicted by plasma PTX3 levels than by serum hsCRP levels

Plasma Pentraxin 3 is a More Potent Predictor of Endothelial Dysfunction than High-Sensitive C-Reactive Protein

An infl ammatory response is a key event for endothelial dysfunction. Pentraxin 3 (PTX3) is an infl ammatory protein produced at infl ammation sites such as leukocytes and vascular endothelial cells. Here, we compared the relationships between endothelial function assessed by flow-mediated dilation (FMD), and the levels of plasma PTX3 and highsensitive C-reactive protein (hsCRP), another infl ammatory protein of the pentraxin family. Levels of FMD, PTX3 and hsCRP were measured twice within 6 to 8 months and retrospectively analyzed in 36 patients with coronary artery disease. We examined the associations between the values of FMD and the levels of PTX3 and hsCRP at the fi rst measurement, and between the change ratios (second value/fi rst value) of these parameters. Univariate linear regression analysis showed significantly negative correlations between FMD values and PTX3 and hsCRP levels at the fi rst measurement, and significant associations with taking statins or calcium antagonists. Multivariate linear stepwise regression analysis identifi ed PTX3 levels and taking statins and calcium antagonists as independent factors for endothelial function. The change ratio of FMD correlated more closely with that of PTX3 than of hsCRP (r =-0.446, P = 0.006 versus r =-0.330, P = 0.050). Significantly more patients with decreased FMD values had increased levels of PTX3 than those of hsCRP at the second measurement compared with the fi rst measurement. Furthermore, the ratio of patients with increased PTX3, but not increased hsCRP, was significantly reduced among those with increased, rather than decreased, FMD values. Endothelial dysfunction might be more accurately predicted by plasma PTX3 levels than by serum hsCRP levels