An overview on waste rubber recycling by microwave devulcanization.

This review deals with waste rubber recycling by devulcanization treatment using microwave method. In fact, vulcanized rubbers have been extensively used in various fields due to their superior performances. Subsequently, the massive use of such materials, especially in the automotive industry, has generated a substantial amount of wastes which are not easily to be degraded due to the three-dimensional network formed by the vulcanization process. One of the optimal solutions for the successful recycling of rubber is devulcanization, i.e., the process in which the sulfur bonds in the vulcanized material are selectively broken. Currently, to achieve rubber devulcanization, the microwave treatment has been proposed as a promising alternative process due to its precise manipulation of process variables. Furthermore, the microwave process is easily to be coupled with effects of other elements such as chemical and swelling agents. In this work, different microwave devulcanization methods are reviewed, the utilization of the corresponding devulcanized materials has also been discussed. The reviewed contents are believed to be of great interest to academics and industries since they represent a great challenge from scientific, economic and environmental points of view.

Devulcanization of natural rubber industry waste in supercritical carbon dioxide combined with diphenyl disulfide.

The elimination of rubber wastes without affecting the environment is one of the most important challenges of the 21st century waste management. Accordingly, the present work is focused on the recycling of natural rubber (NR) industry waste by means of devulcanization in supercritical carbon dioxide (scCO2) atmosphere. With that aim, a novel device allowing to perform rubber devulcanization was developed. It consists of a triaxial compression reactor integrated into a dynamic hydraulic universal testing machine with a heating chamber. NR industry waste was devulcanized in the mentioned device at different temperatures, in scCO2 by using diphenyl disulfide (DD) as devulcanizing reagent. The devulcanization degree and quality of the treated materials were evaluated by the swelling test combined with the Horikx theory. It was appeared that a successful devulcanization, with almost no degradation, was obtained, and the devulcanization degree reached maximum value of ~90%. Thermogravimetric tests and scanning electron microscopy (SEM) images strengthened these results. Finally, it was concluded that the developed device is appropriate to perform rubber recycling, which contributes to the progress in the environmental protection.

Modeling of the Electromechanical Behavior of Barium Titanate Under Mechanical Stress and Comparison With Experimental Measurements.

Barium titanate (BaTiO3) is increasingly studied to replace lead-based piezoelectric materials, such as those which belong to the lead zirconate titanate (PZT) family, due to lead toxicity. In many applications, such as Tonpilz transducers, piezoelectric materials undergo mechanical stress simulation of which is important to control and predict electroacoustic effects. Thus, this article deals with a fully tensorial model that allows to simulate the behaviors of electrical displacements and elastic strains under mechanical stress. Simulated curves are compared with experimental ones obtained for BaTiO3 samples. It can be verified that the hysteretic curves of strains are well predicted for unpoled samples as well as for poled ones. The order of values and global behavior of the theoretical electrical displacement are also verified, even if a less precise agreement is observed. The optimized values of the physical parameters, such as d33 , are discussed, and improvements both of the model and the optimization procedure are finally proposed in order to better predict the mechanical behavior of BaTiO3.

Molecular monitoring of therapeutic milestones and clinical outcomes in patients with chronic myeloid leukemia.

BACKGROUND: In the current study, the authors determined whether adhering to molecular monitoring guidelines in patients with chronic myeloid leukemia (CML) is associated with major molecular response (MMR) and assessed barriers to adherent monitoring. METHODS: Newly treated patients with CML from the Quebec province-wide CML registry from 2005 to 2016 were included. Timely polymerase chain reaction (tPCR) was defined as the molecular assessment of BCR-ABL1 at the 3-month, 12-month, and 18-month time points from the initiation of tyrosine kinase inhibitor (TKI) therapy. The cohort was analyzed as a nested case-control study. Cases with a first-ever MMR (BCR-ABL1 ≤0.1%, assessed at any time during follow-up) were matched to up to 5 controls by duration of TKI therapy, volume of patients with CML at the treatment center, year of cohort entry, and age. Odds ratios (ORs) for the performance of tPCR and MMR were adjusted for sex, comorbidities, type of TKI, and other important covariates. RESULTS: The cohort included 496 patients. Of 392 MMR events, 67.9% occurred before 18 months. The performance of tPCR was associated with a doubling of the MMR rate (OR, 2.23; 95% confidence interval [95% CI], 1.56-3.21) and was similar with 1 to 3 tPCRs performed (P = .67). Furthermore, tPCRs at 3 months (OR, 2.77; 95% CI, 1.81-4.23) and 12 months (OR, 3.00; 95% CI, 1.64-5.49) were associated with achieving early MMR, whereas tPCRs at 18 months were not (OR, 1.23; 95% CI, 0.80-1.89). Low-volume centers were found to have lower adherence to tPCR (OR, 0.60; 95% CI, 0.40-0.89). CONCLUSIONS: Timely molecular assessment at 3 months and 12 months appears to benefit patients with CML. Adherence to timely monitoring should be encouraged, especially in low-volume treatment centers.

Recycling of waste tire rubber: Microwave devulcanization and incorporation in a thermoset resin.

This study focused on the possibility of recycling Waste Tire Rubber (WTR) to be used as polymer modifier. Thus, WTR was grinded into powder, at ambient temperature, with a disc mill PQ500 and microwave electromagnetic energy was used to devulcanize this powder with the final aim of producing a new composite by its incorporation in a thermoset resin. The influence of the treatment microwave energy on the devulcanization ratio was investigated. FTIR analysis revealed that rupture of Sulfur-Sulfur (SS) and Carbon-Sulfur (CS) bonds have occurred during the treatment. Swelling analysis showed that the microwave treatment can lead to a very significant degree of devulcanization. The Ground Tire Rubber (GTR) and the Devulcanized Ground Tire Rubber (DGTR) were then separately used to prepare epoxy based composites. It appeared that epoxy composites filled with DGTR have better mechanical properties than those filled with untreated GTR. This result agrees with scanning electron microscopy observations which highlighted a better interface coherence between DGTR and epoxy. A complementary analysis pointed out a linear relationship between the rubber modulus and the number of crosslink per chain.

Theoretical and experimental study of the electroacoustic behavior of lithium niobate under an initial mechanical stress.

Recently, a second-order formalism of piezoelectric structures under an external mechanical stress was developed. Because the yield strength of lithium niobate was unknown, this study was not able to describe and evaluate realistic benefits of a prestress load on electromechanical properties. Therefore, in this study, experimental determination of the yield strength of lithium niobate sample is performed and shows that this limit is close to 110 MPa. Then, the nonlinearities and evolutions of electroacoustic parameters of this piezoelectric material under mechanical stress are numerically studied. By varying the initial prestress, as well as azimuthal and elevation angles, the cut planes in which a prestress induces significant benefits on velocities and coupling coefficient are identified. Finally, approximate relations describing changes between electroacoustic parameters defined in the two coordinate systems of the study are determined.

The small molecule GMX1778 is a potent inhibitor of NAD+ biosynthesis: strategy for enhanced therapy in nicotinic acid phosphoribosyltransferase 1-deficient tumors.

GMX1777 is a prodrug of the small molecule GMX1778, currently in phase I clinical trials for the treatment of cancer. We describe findings indicating that GMX1778 is a potent and specific inhibitor of the NAD(+) biosynthesis enzyme nicotinamide phosphoribosyltransferase (NAMPT). Cancer cells have a very high rate of NAD(+) turnover, which makes NAD(+) modulation an attractive target for anticancer therapy. Selective inhibition by GMX1778 of NAMPT blocks the production of NAD(+) and results in tumor cell death. Furthermore, GMX1778 is phosphoribosylated by NAMPT, which increases its cellular retention. The cytotoxicity of GMX1778 can be bypassed with exogenous nicotinic acid (NA), which permits NAD(+) repletion via NA phosphoribosyltransferase 1 (NAPRT1). The cytotoxicity of GMX1778 in cells with NAPRT1 deficiency, however, cannot be rescued by NA. Analyses of NAPRT1 mRNA and protein levels in cell lines and primary tumor tissue indicate that high frequencies of glioblastomas, neuroblastomas, and sarcomas are deficient in NAPRT1 and not susceptible to rescue with NA. As a result, the therapeutic index of GMX1777 can be widended in the treatment animals bearing NAPRT1-deficient tumors by coadministration with NA. This provides the rationale for a novel therapeutic approach for the use of GMX1777 in the treatment of human cancers.

Preclinical development of the nicotinamide phosphoribosyl transferase inhibitor prodrug GMX1777.

GMX1778 was recently shown to function as a potent inhibitor of nicotinamide phosphoribosyl transferase. To translate the discovery of GMX1778 mechanism of action into optimal clinical use of its intravenously administered prodrug, GMX1777, the efficacy of GMX1777 was evaluated in xenograft models and the pharmacokinetic profile of GMX1778 and its effect on nicotinamide adenine dinucleotide cellular levels was measured by liquid chromatography/mass spectrometry. Consistent with the requirement for a prolonged exposure for cytotoxicity in vitro, a dose of 75 mg/kg of GMX1777 administered as two bolus intravenous injections in 1 day were not effective at reducing the growth of multiple myeloma (IM-9) tumors, whereas the same dose of GMX1777 administered over a 24 h intravenous infusion caused tumor regression in the IM-9 model, a small-cell lung cancer (SHP-77) model, and a colon carcinoma (HCT-116) model. A 72 h continuous intravenous infusion of GMX1777 was also effective in the IM-9 model, but was associated with a smaller therapeutic index. GMX1777 at a dose of 75 mg/kg administered over a 24 h intravenous infusion produced GMX1778 steady-state plasma levels of approximately 1 microg/ml and caused nicotinamide adenine dinucleotide levels to decrease significantly in tumors. Consistent with the GMX1778 mechanism of action, nicotinic acid protected mice treated with a lethal dose of GMX1777. These data support the design of an open-label, dose-escalation trial, in which patients with refractory solid tumors and lymphomas receive 24 h infusions of GMX1777 as a single agent in 3-week cycles. Furthermore, these results indicate that nicotinic acid is a potent antidote to treat GMX1777 overdose.

Hes6 promotes cortical neurogenesis and inhibits Hes1 transcription repression activity by multiple mechanisms.

Hes1 is a mammalian basic helix-loop-helix transcriptional repressor that inhibits neuronal differentiation together with corepressors of the Groucho (Gro)/Transducin-like Enhancer of split (TLE) family. The interaction of Hes1 with Gro/TLE is mediated by a WRPW tetrapeptide present in all Hairy/Enhancer of split (Hes) family members. In contrast to Hes1, the related protein Hes6 promotes neuronal differentiation. Little is known about the molecular mechanisms that underlie the neurogenic activity of Hes6. It is shown here that Hes6 antagonizes Hes1 function by two mechanisms. Hes6 inhibits the interaction of Hes1 with its transcriptional corepressor Gro/TLE. Moreover, it promotes proteolytic degradation of Hes1. This effect is maximal when both Hes1 and Hes6 contain the WRPW motif and is reduced when Hes6 is mutated to eliminate a conserved site (Ser183) that can be phosphorylated by protein kinase CK2. Consistent with these findings, Hes6 inhibits Hes1-mediated transcriptional repression in cortical neural progenitor cells and promotes the differentiation of cortical neurons, a process that is normally inhibited by Hes1. Mutation of Ser183 impairs the neurogenic ability of Hes6. Taken together, these findings clarify the molecular events underlying the neurogenic function of Hes6 and suggest that this factor can antagonize Hes1 activity by multiple mechanisms.