1,033 research outputs found
Modelling of the carburizing and nitriding processes
The thermo-chemical diffusion process of carburizing and nitriding was modeled in the present study. The analyses led to the prediction of surface hardened layers dimensions and hardness in commercial steels. A diffusion model based on Fick’s laws was applied to such steels in order to describe the growth kinetics of layers, then the analytical model was employed to perform finite element calculations. In such a way it was possible to calculate the carbon and nitrogen concentration in the cross sections of cylindrical samples and the consequent hardness profiles coupled with those of the residual stresses. The results from analytical model and FE calculations were compared with experimental data
Effect of layered double hydroxide intercalated with fluoride ions on the physical, biological and release properties of a dental composite resin
OBJECTIVES:
The aim of this work was the preparation of a new fluoride-releasing dental material characterized by a release of fluoride relatively constant over time without any initial toxic burst effect. This type of delivery is obtained by a matrix controlled elution and elicits the beneficial effect of a low amount of fluoride on human dental pulp stem cells (hDPSCs) towards mature phenotype.
METHODS:
The modified hydrotalcite intercalated with fluoride ions (LDH-F), used as filler, was prepared via ion exchange procedure and characterized by X-ray diffraction and FT-IR spectroscopy. The LDH-F inorganic particles (0.7, 5, 10, 20wt.%) were mixed with a photo-activated Bis-GMA/TEGDMA (45/55wt/wt) matrix and novel visible-light cured composites were prepared. The dynamic thermo-mechanical properties were determined by dynamic mechanical analyzer. The release of fluoride ions in physiological solution was determined using a ionometer. Total DNA content was measured by a PicoGreen dsDNA quantification kit to assess the proliferation rate of hDPSCs. Alkaline phosphatase activity (ALP) was measured in presence of fluoride resins.
RESULTS:
Incorporation of even small mass fractions (e.g. 0.7 and 5wt.%) of the fluoride LDH in Bis-GMA/TEGDMA dental resin significantly improved the mechanical properties of the pristine resin, in particular at 37°C. The observed reinforcement increases on increasing the filler concentration. The release of fluoride ions resulted very slow, lasting months. ALP activity gradually increased for 28 days in hDPSCs cell grown, demonstrating that low concentrations of fluoride contributed to the cell differentiation.
CONCLUSIONS:
The prepared composites containing different amount of hydrotalcite filler showed improved mechanical properties, slow fluoride release and promoted hDPSCs cell proliferation and cell differentiation
Galectin-1, an Endogenous Lectin Produced by Thymic Epithelial Cells, Induces Apoptosis of Human Thymocytes
Galectin-1, a β-galactoside binding protein, is produced by thymic epithelial cells and binds to human thymocytes. We have previously reported that galectin-1 induces the apoptosis of activated T lymphocytes. Because the majority of thymocytes die via apoptosis while still within the thymus, we tested whether galectin-1 could induce the apoptosis of these cells. We now report that in vitro exposure to galectin-1 induced apoptosis of two subsets of CD4lo CD8lo thymocytes. The phenotypes of susceptible thymocytes were consistent with that of both negatively selected and nonselected cells. Galectin-1–induced apoptosis was enhanced by preexposure of thymocytes to antibody to CD3, suggesting that galectin-1 may be a participant in T-cell– receptor mediated apoptosis. In contrast, pretreatment of thymocytes with dexamethasone had no effect on galectin-1 susceptibility. We noted that 71% of the cells undergoing apoptosis after galectin-1 treatment had a DNA content greater than 2N, indicating that proliferating thymocytes were most sensitive to galectin-1. We propose that galectin-1 plays a role in the apoptosis of both negatively selected and nonselected thymocytes, and that the susceptibility of thymocytes to galectin-1 is regulated, in part, by entry or exit from the cell cycle
NOSTROMO - D1.2 - Final Project Results Report
The main objective of the NOSTROMO project has been to develop, demonstrate and evaluate an innovative modelling approach for the rigorous and comprehensive assessment of the performance impact of future ATM concepts and solutions at ECAC network level. This approach brings together the ability of bottom-up microscopic models to capture emergent behaviour and interdependencies between different solutions with the level of tractability and interpretability required to effectively support decision-making.
This report provides a summary of NOSTROMO accomplishments and contributions to the SESAR Programme. It gathers technical lessons learned and concludes proposing further developments to facilitate the use of the NOSTROMO methodology in the future SESAR 3 Programme
Productive performance and histological features of intestinal mucosa of broiler chickens fed different dietary protein levels
ABSTRACT To evaluate the effect of decreasing dietary protein on growth performance, carcass traits, and intestinal mucosal morphometry, 180 female Hubbard strain broiler chickens were divided into 3 groups and fed 3 isoenergetic diets ad libitum from 14 d of age until slaughter age (49 d). The treatments varied according to 3 protein levels: high-protein diet (HiP, 22.5% CP, DM basis), medium-protein diet (MedP, 20.5% CP), and low-protein diet (LowP, 18.5%). Diets were obtained by replacing wheat middlings with soybean meal and were formulated to meet or exceed broiler amino acid requirements of the NRC. Morphometric indices of duodenum, jejunum, and ileum were measured at the end of the feeding period and included villus height, crypt depth, villus-to-crypt ratio, and apparent villus surface area. The dietary protein level had a significant effect on final BW of birds, whereas ADG, ADFI, and feed efficiency remained unaffected by dietary treatment. The muscle (breast and drumstick) yields were significantly higher in birds fed the HiP diet compared with those of the MedP and LowP diets. Meat quality traits were not affected by the protein level. The villus surface area of all intestinal segments did not change among groups. Instead, reducing the dietary protein level to 20.5% resulted in a higher villus height and villus height to crypt depth ratio in the duodenum and ileum. On the basis of our findings, even if the high-protein diet promoted meat yield, a medium-protein diet could positively support broiler growth performance, as confirmed by favorable morphometric features of the intestine
In vitro effect of amifostine on haematopoietic progenitors exposed to carboplatin and non-alkylating antineoplastic drugs: haematoprotection acts as a drug-specific progenitor rescue.
We evaluated the protective ability of amifostine on peripheral blood mononuclear cell (PBMC)-derived colony-forming unit (CFU) and PB CD34+ cells which were previously exposed in vitro to etoposide, carboplatin, doxorubicin and taxotere. Amifostine pretreatment protected PBMC-derived CFU from the toxic effect of etoposide, carboplatin and taxotere. A significant detrimental effect was exerted by amifostine on the growth of doxorubicin-treated PBMC-derived CFU. Liquid cultures of PB CD34+ cells reproduced faithfully the effects observed on growth of PBMC-derived CFU and confirmed amifostine chemoprotection against etoposide and carboplatin with its detrimental effect on doxorubicin-treated progenitors. Combining the data of viable cell count, cytometric estimation of apoptosis, cell cycle and viable cell replication rate, we found that amifostine protects from etoposide and carboplatin toxicity mainly through a mechanism of cell rescue. Conversely, the detrimental effect of amifostine on the growth of doxorubicin-treated PB CD34+ cells is apparently due to an increased G2/M arrest. In conclusion, amifostine protects haematopoietic progenitors from etoposide, carboplatin and taxotere. Progenitor rescue is the mechanism through which amifostine reduced etoposide and carboplatin toxicity
ROS in cancer therapy: the bright side of the moon.
Reactive oxygen species (ROS) constitute a group of highly reactive molecules that have evolved as regulators of important signaling pathways. It is now well accepted that moderate levels of ROS are required for several cellular functions, including gene expression. The production of ROS is elevated in tumor cells as a consequence of increased metabolic rate, gene mutation and relative hypoxia, and excess ROS are quenched by increased antioxidant enzymatic and nonenzymatic pathways in the same cells. Moderate increases of ROS contribute to several pathologic conditions, among which are tumor promotion and progression, as they are involved in different signaling pathways and induce DNA mutation. However, ROS are also able to trigger programmed cell death (PCD). Our review will emphasize the molecular mechanisms useful for the development of therapeutic strategies that are based on modulating ROS levels to treat cancer. Specifically, we will report on the growing data that highlight the role of ROS generated by different metabolic pathways as Trojan horses to eliminate cancer cells
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