Assessment of pH Value and Release of Calcium Ions in Calcium Silicate Cements: An In Vitro Comparative Study.

The goal of this study was to evaluate the pH and the release of calcium from four calcium-silicate-based cements. METHODS: Four materials were tested (ProClinic MTA; Angelus MTA; ProRoot MTA; Biodentine). The palatal canal root of acrylic upper molars was filled with each cement. Afterwards, they were set in phosphate-buffered saline. Measurements were taken by atomic adsorption spectroscopy (AAS) at 3, 24, 72, 168, 336, 672, and 1008 h. The pH was measured at the same timepoints. Kruskal-Wallis tests were carried out in each period, as the Kolmogorov-Smirnov and Shapiro-Wilk tests showed no parametric results. RESULTS: Significant differences (p < 0.05) in calcium release were found at the 3-, 24-, and 72-hour evaluations. All of the analyzed groups presented a release of calcium ions up to 168 h, and the general tendency was to increase up to 672 h, with a maximum release of 25.45 mg/g in the ProRoot group. We could only observe significant differences (p < 0.05) in pH value over 168 h between the Biodentine (7.93) and Angelus MTA (7.31) groups. CONCLUSIONS: There were significant differences (p < 0.05) in calcium release. Nevertheless, no significant differences (p > 0.05) in the pH values were found at the studied timepoints, except for the values at 168 h.

Chaotic parameters from fluorescence spectra to resolve fraudulent mixtures of fresh and expired protected designation of origin extra virgin olive oils.

One of the most profitable products from the Mediterranean basin is extra virgin olive oil (EVOO), and, therefore, some of them have protected designation of origin (PDO) labels. In order to prevent fraudulent practices, a method to quantify adulterants has been developed. 459 binary blends composed of PDO EVOO in date (Saqura, Oleoestepa, and Duque de Baena) mixed with expired PDO EVOO (Quinta do Vallouto, Señorío de Segura, and Planeta) to serve as adulterants (<17%) have been analyzed. Using a laser diode as a source light, the fluorescence emission has been measured and 20 chaotic parameters from the resulting spectra have been calculated. Using these as independent variables of multi-parameter regression models, the concentration of adulterant has been estimated. Every model was evaluated through the mean square error, adjusted correlation coefficient, Mallows' Cp, Akaike information criterion, Hannan-Quinn criterion, and Bayesian information criterion. This approach was validated by the leave-one-out cross-validation method and the results were promising (lower than 10% quantification error). Additionally, the structure of the sensor has been designed and developed by a 3D printer and has the potential of being applied in situ for real-time and cost-effective analysis at oil mills or for quality control.

2-Deoxy-D-glucose cooperates with arsenic trioxide to induce apoptosis in leukemia cells: involvement of IGF-1R-regulated Akt/mTOR, MEK/ERK and LKB-1/AMPK signaling pathways.

While the anti-tumor efficacy of 2-deoxy-D-glucose (2-DG) is normally low in monotherapy, it may represent a valuable radio- and chemo-sensitizing agent. We here demonstrate that 2-10 mM 2-DG cooperates with arsenic trioxide (ATO) and other antitumor drugs to induce apoptosis in human myeloid leukemia cell lines. Using ATO and HL60 as drug and cell models, respectively, we observed that 2-DG/ATO combination activates the mitochondrial apoptotic pathway, as indicated by Bid-, and Bax-regulated cytochrome c and Omi/HtrA2 release, XIAP down-regulation, and caspase-9/-3 pathway activation. 2-DG neither causes oxidative stress nor increases ATO uptake, but causes inner mitochondria membrane permeabilization as well as moderate ATP depletion, which nevertheless do not satisfactorily explain the pro-apoptotic response. Surprisingly 2-DG causes cell line-specific decrease in LKB-1/AMPK phosphorylation/activation, and also causes Akt/mTOR/p70S6K and MEK/ERK activation, which is prevented by co-treatment with ATO. The use of kinase-specific pharmacologic inhibitors and/or siRNAs reveals that apoptosis is facilitated by AMPK inactivation and restrained by Akt and ERK activation, and that Akt and ERK activation mediates AMPK inhibition. Finally, 2-DG stimulates IGF-1R phosphorylation/activation, and co-treatment with IGF-1R inhibitor prevents 2-DG effects on Akt, ERK and AMPK, and facilitates 2-DG-provoked apoptosis. In summary 2-DG elicits IGF-1R-mediated AMPK inactivation and Akt and ERK activation, which facilitates or restrain apoptosis, respectively. 2-DG-provoked AMPK inactivation increases the apoptotic efficacy of ATO, while in turn ATO-provoked Akt and ERK inactivation may increase the efficacy of 2-DG as anti-tumor drug.