Ignition mechanism in nanocomposites thermites

Nanocomposite thermites (n-thermites) have been actively investigated for a wide range of potential applications including propellants, explosives, and pyrotechnics. There have been several recent efforts aimed at understanding ignition mechanisms of nanocomposite reactive materials. Although significant progress has been made, ignition mechanisms remain elusive. At the same time, a robust ignition model is required to incorporate these materials in practical energetic formulations. A challenge of this effort is to describe the mechanisms of ignition of n-thermites prepared by Arrested Reactive Milling (ARM) with different stimuli, including heat, spark and impact and also develop a multi-step kinetic model describing different processes affecting ignition. The role of thermally initiated heterogeneous exothermic reactions is evaluated and the effect of decomposition of oxidizer and respective oxygen gas release on ignition is described. N-thermite powders are prepared by ARM and evaluated using thermal analysis, electron microscopy and other analytical techniques. Experimental studies of ignition of n-thermites stimulated by heating, electric spark and impact are conducted with the goal of developing a reaction model capable of describing different experimental data sets. State of the art thermo-analytical equipment and advanced isoconversion methods are used to describe stability and redox reaction mechanisms in the prepared samples. Multiple reaction steps are identified and described quantitatively. Thin layers of the prepared powders coated onto an electrically heated Ni-Cr filament are ignited at heating rates between 200-17000 K/s in a miniature vacuum chamber. Ignition is monitored based on both photodiode and pressure transducer signals recorded simultaneously. For spark-induced ignition, powder layers of different thickness are placed in a grounded brass holder. A needle-like electrode is placed above the powder and sparks with different energies are produced. Real time measurements of current and optical signatures produced by the ignited sample at different wavelengths are taken. The results are processed to determine the spark energy, minimum ignition energy, ignition delay, and other parameters. Shock ignition of nanocomposite 8Al-MoO3 thermite particles are independently carried out at the University of Illinois Urbana Champaign. An individual particle is targeted by a miniature, laser-driven flyer plate accelerated to a speed in the range of 0.5-2 km/s. Ignition delays observed in both shock and spark ignition experiments for the same material are close to each other and vary in the range of 120 - 200 ns. A reaction mechanism including multiple oxidation steps starting with the Cabrera-Mott (CM) reaction followed by direct oxidative growth of and phase changes in different alumina polymorphs is validated for a stoichiometric 2Al-3CuO nanocomposite powder prepared by ARM. The reaction kinetics describing these reaction steps are shown to remain credible for the ARM-prepared reactive composites with different scales of mixing, interface morphologies, and component ratios, as long as the components remained Al and CuO. This work presents a further validation and development of this multistep model to describe reaction in another ARM-prepared thermite system, 8Al-MoO3

Allergen Exposure in Lymphopenic Fas-Deficient Mice Results in Persistent Eosinophilia Due to Defects in Resolution of Inflammation

Asthma is characterized by chronic airway type-2 inflammation and eosinophilia, yet the mechanisms involved in chronic, non-resolving inflammation remain poorly defined. Previously, our group has found that when Rag-deficient mice were reconstituted with Fas-deficient B6 LPR T cells and sensitized and challenged, the mice developed a prolonged type-2-mediated airway inflammation that continued for more than 6 weeks after the last antigen exposure. Surprisingly, no defect in resolution was found when intact B6 LPR mice or T cell specific Fas-conditional knockout mice were sensitized and challenged. We hypothesize that the homeostatic proliferation induced by adoptive transfer of T cells into Rag-deficient mice may be an important mechanism involved in the lack of resolution. To investigate the role of homeostatic proliferation, we induced lymphopenia in the T cell-specific Fas-conditional knockout mice by non-lethal irradiation and sensitized them when T cells began to repopulate. Interestingly, we found that defective Fas signaling on T cells plus antigen exposure during homeostatic proliferation was sufficient to induce prolonged eosinophilic airway inflammation. In conclusion, our data show that the combination of transient lymphopenia, abnormal Fas-signaling, and antigen exposure leads to the development of a prolonged airway eosinophilic inflammatory phase in our mouse model of experimental asthma

Non-apoptotic Fas (CD95) Signaling on T Cells Regulates the Resolution of Th2-Mediated Inflammation

Fas (CD95/APO-1) and its ligand (FasL/CD95L) promote the resolution of type 2 lung inflammation and eosinophilia. We previously found that Fas-deficiency on T cells, but not eosinophils, delayed resolution of inflammation. However, Fas can signal both cell death and have a positive signaling function that can actually activate cells. In this study, we investigated whether Fas-induced death or Fas-activated signaling pathways promote resolution of allergic lung inflammation. By increasing T cell survival through two Fas-independent pathways, using Bim-deficient T cells or Bcl-xL overexpressing T cells, no differences in resolution of Th2-mediated inflammation was observed. Furthermore, Th2 cells were inherently resistant to Fas-mediated apoptosis and preferentially signaled through non-apoptotic pathways following FasL treatment. Utilizing Fas-mutant mice deficient in apoptotic but sufficient for non-apoptotic Fas signaling pathways, we demonstrate that non-apoptotic Fas signaling in T cells drives resolution of Th2-mediated airway inflammation. Our findings reveal a previously unknown role for non-apoptotic Fas signaling on Th2 cells in the induction of resolution of type 2 inflammation

Active DNA demethylation at enhancers during the vertebrate phylotypic period

Contains fulltext : 157230.pdf (publisher's version ) (Closed access