For high-intensity curing, maximum shrinkage rates were 6-61 % higher, whereas times to achieve maximum shrinkage force rate were 15-53 % shorter compared to conventional curing. Composites specifically designed for high-intensity curing showed shrinkage parameters comparable to other investigated composites. Shrinkage behavior under conditions of high-intensity light-curing was material-dependent. Shrinkage force kinetics were more strongly affected by high-intensity curing than absolute values of linear shrinkage and shrinkage force. Despite being attractive for its convenience, high-intensity curing can lead to considerably faster development of shrinkage forces in the early stage of polymerization.Despite being attractive for its convenience, high-intensity curing can lead to considerably faster development of shrinkage forces in the early stage of polymerization. This study aims to analyze the addition of niobium silicate particles to dental adhesive resins and evaluate its physicomechanical and biological properties. The SiNb particles were produced by the sol-gel route and presented a mean particle size of 2.1 μm and a specific surface area of 616,96m2/g. An experimental adhesive resin was formulated with 66 wt% Bisphenol A-Glycidyl Methacrylate and 33 wt% Hydroxyethyl methacrylate with diphenyl(2,4,6-trimethyl benzoyl)phosphine oxide as the photoinitiator. The SiNb particles were incorporated into the adhesive resins in 1 wt% (SiNb1%) and 2 wt% (SiNb2%) concentration. A control group (SiNb0%) without the addition of particles was used. The developed adhesives were evaluated by their polymerization kinetics, refractive index, softening in solvent, cytotoxicity, mineral deposition, ultimate tensile strength, and micro shear bond strength. The refractive index range was increased by the addition of niobium silicate particles. No statistically significant differeut compromising the physico-mechanical properties on these materials.Several liposome products have been approved for the treatment of cancer. In all of them, the active agents are encapsulated in the liposome water phase passively or by transmembrane ion gradients. An alternative approach in liposomal drug delivery consists of chemically modifying drugs to form lipophilic prodrugs with strong association to the liposomal bilayer. Based on this approach, we synthesized a mitomycin c-derived lipidic prodrug (MLP) which is entrapped in the bilayer of PEGylated liposomes (PL-MLP, Promitil®), and activated by thiolytic cleavage. PL-MLP is stable in plasma with thiolytic activation of MLP occurring exclusively in tissues and is more effective and less toxic than conventional chemotherapy in various tumor models. PL-MLP has completed phase I clinical development where it has shown a favorable safety profile and a 3-fold reduction in toxicity as compared to free mitomycin c. Clinical and pharmacokinetic studies in patients with advanced colo-rectal carcinoma have indicated a significant rate of disease stabilization (39%) in this chemo-refractory population and significant prolongation of median survival in patients attaining stable disease (13.9 months) versus progressive disease patients (6.35 months). The pharmacokinetics of MLP was typically stealth with long T½ (~1 day), slow clearance and small volume of distribution. Interestingly, a longer T½, and slower clearance were both correlated with disease stabilization and longer survival. This association of pharmacokinetic parameters with patient outcome suggests that arrest of tumor growth is related to the enhanced tumor localization of long-circulating liposomes and highlights the importance of personalized pharmacokinetic evaluation in the clinical use of nanomedicines. Another important area where PL-MLP may have an added value is in chemoradiotherapy, where it has shown a strong radiosensitizing effect in animal models based on a unique mechanism of enhanced prodrug activation and encouraging results in early human testing.Cisplatin (CIS)-mediated nephrotoxicity is induced via transforming growth factor-beta (TGF-β) and TGF-β-activated kinase (TAK1). TGF-β and TAK1 are known to interact with microRNA-let-7b and microRNA-26b, respectively. Additionally, TGF-β1 is reported to down-regulate the autophagy marker microtubule-associated protein 1 light chain 3-II (LC3-II) through upregulation of microRNA-34a. Pentoxifylline (PTX) anti-inflammatory effects are mediated via suppressing TGF-β and regulating mammalian target of rapamycin (mTOR). The current study aimed to investigate the involvement of microRNAs let-7b, 26b, and 34a, and the modulating impact of PTX on CIS-induced nephrotoxicity. Moreover, we aimed at examining the ability of PTX to interact with TGF-β receptor-1 (TGFβR-1), and TAK1, and examine its ability to downgrade the previously reported toxicities. Hence, the expression of the aforementioned microRNAs, and protein levels of TGFβR-1, TGF-β1, TAK1, mTOR, LC3-II, and NF-κB were assessed. Molecular docking studies of PTX on TGFβR-1 and TAK1 were also executed. CIS induced TGF-β1, with down-regulation of microRNA-let-7b and -26b, and up-regulation of microRNA-34a. TGFβR-1, TAK1, and mTOR levels were increased, while LC3-II level was decreased. PTX significantly protected renal cells against CIS-induced changes as indicated by reverting the level of the investigated parameters, while exhibiting an antagonistic effect on TGFβR-1 and TAK1. Our results postulate a possible role of epigenetic regulation of CIS-induced nephrotoxicity through the investigated microRNAs proposing them as potential future targets for controlling this serious toxicity. PTX was able to shield CIS-induced toxicity possibly through blocking TGF-β pathway, while promoting autophagy in a TAK1 independent manner with the involvement of the examined microRNAs.Increased symptoms of asthma-like respiratory illnesses have been reported in soldiers returning from tours of duty in Afghanistan. Inhalation of desert particulate matter (PM) may contribute to this deployment-related lung disease (DRLD), but little is known about disease mechanisms. The IL-33 signaling pathway, including its receptor ST2, has been implicated in the pathogenesis of lung diseases including asthma, but its role in PM-mediated airway dysfunction has not been studied. The goal of this study was to investigate whether IL-33/ST2 signaling contributes to airway dysfunction in preclinical models of lung exposure to Afghanistan PM (APM). Wild-type (WT) and ST2 knockout (KO) mice on the BALB/C background were oropharyngeally instilled with a single dose of saline or 50 μg of APM in saline. Airway hyperresponsiveness (AHR) and inflammation were assessed after 24 h. In WT mice, a single APM exposure induced AHR and neutrophilic inflammation. WNK463 inhibitor Unlike the WT mice, ST2 KO mice that lack the receptor for IL-33 did not demonstrate AHR although airway neutrophilic inflammation was comparable to the WT mice.