Ignition of Deflagration and Detonation Ahead of the Flame due to Radiative Preheating of Suspended Micro Particles

We study a flame propagating in the gaseous combustible mixture with suspended inert particles. The gas is assumed to be transparent for the radiation emitted by the combustion products, while particles absorb and re-emit the radiation. Thermal radiation heats the particles, which in turn transfer the heat to the surrounding gaseous mixture by means of heat conduction, so that the gas temperature lags that of the particles. We consider different scenarios depending on the spatial distribution of the particles, their size and the number density. In the case of uniform distribution of the particles the radiation causes a modest increase of the temperature ahead of the flame and the corresponding increase of the flame velocity. The effects of radiation preheating is stronger for a flame with smaller normal velocity. In the case of non-uniform distribution of the particles, such that the particles number density is smaller just ahead of the flame and increases in the distant region ahead of the flame, the preheating caused by the thermal radiation may trigger additional independent source of ignition. This scenario requires the formation of a temperature gradient with the maximum temperature sufficient for ignition in the region of denser particles cloud ahead of the advancing flame. Depending on the steepness of the temperature gradient formed in the unburned mixture, either deflagration or detonation can be initiated via the Zeldovich's gradient mechanism. The ignition and the resulting combustion regimes depend on the temperature profile which is formed in effect of radiation absorption and gas-dynamic expansion. In the case of coal dust flames propagating through a layered dust cloud the effect of radiation heat transfer can result in the propagation of combustion wave with velocity up to 1000m/s and can be a plausible explanation of the origin of dust explosion in coal mines.Comment: 45 pages, 14 figures. Accepted for publication Combustion and Flame 29 June 201

Anatocismo

El anatocismo, la capitalización de intereses, no es una entidad de la responsabilidad civil y, por lo tanto, las limitaciones del art. 623 del Código Civil y art. 770 del Código Civil y Comercial no son aplicables a la indemnización por deuda derivada de la responsabilidad civil, contractual o extracontractual.Facultad de Ciencias Jurídicas y Sociales (JURSOC

Anatocismo

El anatocismo, la capitalización de intereses, no es una entidad de la responsabilidad civil y, por lo tanto, las limitaciones del art. 623 del Código Civil y art. 770 del Código Civil y Comercial no son aplicables a la indemnización por deuda derivada de la responsabilidad civil, contractual o extracontractual.Facultad de Ciencias Jurídicas y Sociales (JURSOC

SK2 channels are required for function and long-term survival of efferent synapses on mammalian outer hair cells

Cochlear hair cells use SK2 currents to shape responses to cholinergic efferent feedback from the brain. Using SK2-/- mice, we demonstrate that, in addition to their previously defined role in modulating hair cell membrane potentials, SK2 channels are necessary for long-term survival of olivocochlear fibers and synapses. Loss of the SK2 gene also results in loss of electrically driven olivocochlear effects in vivo, and down regulation of ryanodine receptors involved in calcium-induced calcium release, the main inducer of nAChR evoked SK2 activity. Generation of double-null mice lacking both the α10 nAChR gene, loss of which results in hypertrophied olivocochlear terminals, and the SK2 gene, recapitulates the SK2-/- synaptic phenotype and gene expression, and also leads to down regulation of α9 nAChR gene expression. The data suggest a hierarchy of activity necessary to maintain early olivocochlear synapses at their targets, with SK2 serving an epistatic, upstream, role to the nAChRs.Fil: Murthy, Vidya. Tufts University; Estados UnidosFil: Maison, Stéphane F.. Massachusetts Eye and Ear Infirmary; Estados Unidos. Harvard Medical School; Estados UnidosFil: Taranda, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Tufts University; Estados UnidosFil: Haque, Nadeem. University of Notre Dame; Estados UnidosFil: Bond, Chris T.. Oregon Health Sciences University; Estados UnidosFil: Elgoyhen, Ana Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Adelman, John P.. Oregon Health Sciences University; Estados UnidosFil: Liberman, M. Charles. Massachusetts Eye and Ear Infirmary; Estados Unidos. Harvard Medical School; Estados UnidosFil: Vetter, Douglas E.. Tufts University; Estados Unido

Chronic Conductive Hearing Loss Leads to Cochlear Degeneration

Synapses between cochlear nerve terminals and hair cells are the most vulnerable elements in the inner ear in both noise-induced and age-related hearing loss, and this neuropathy is exacerbated in the absence of efferent feedback from the olivocochlear bundle. If age-related loss is dominated by a lifetime of exposure to environmental sounds, reduction of acoustic drive to the inner ear might improve cochlear preservation throughout life. To test this, we removed the tympanic membrane unilaterally in one group of young adult mice, removed the olivocochlear bundle in another group and compared their cochlear function and innervation to age-matched controls one year later. Results showed that tympanic membrane removal, and the associated threshold elevation, was counterproductive: cochlear efferent innervation was dramatically reduced, especially the lateral olivocochlear terminals to the inner hair cell area, and there was a corresponding reduction in the number of cochlear nerve synapses. This loss led to a decrease in the amplitude of the suprathreshold cochlear neural responses. Similar results were seen in two cases with conductive hearing loss due to chronic otitis media. Outer hair cell death was increased only in ears lacking medial olivocochlear innervation following olivocochlear bundle cuts. Results suggest the novel ideas that 1) the olivocochlear efferent pathway has a dramatic use-dependent plasticity even in the adult ear and 2) a component of the lingering auditory processing disorder seen in humans after persistent middle-ear infections is cochlear in origin

A point mutation in the hair cell nicotinic cholinergic receptor prolongs cochlear inhibition and enhances noise protection

The transduction of sound in the auditory periphery, the cochlea, is inhibited by efferent cholinergic neurons projecting from the brainstem and synapsing directly on mechanosensory hair cells. One fundamental question in auditory neuroscience is what role(s) this feedback plays in our ability to hear. In the present study, we have engineered a genetically modified mouse model in which the magnitude and duration of efferent cholinergic effects are increased, and we assess the consequences of this manipulation on cochlear function. We generated the Chrna9L9′T of knockin mice with a threonine for leucine change (L9′T) at position 9′ of the second transmembrane domain of the α9 nicotinic cholinergic subunit, rendering α9-containing receptors that were hypersensitive to acetylcholine and had slower desensitization kinetics. The Chrna9L9′T allele produced a 3-fold prolongation of efferent synaptic currents in vitro. In vivo, Chrna9L9′T mice had baseline elevation of cochlear thresholds and efferent-mediated inhibition of cochlear responses was dramatically enhanced and lengthened: both effects were reversed by strychnine blockade of the α9α10 hair cell nicotinic receptor. Importantly, relative to their wild-type littermates, Chrna9L9′T/L9′T mice showed less permanent hearing loss following exposure to intense noise. Thus, a point mutation designed to alter α9α10 receptor gating has provided an animal model in which not only is efferent inhibition more powerful, but also one in which sound-induced hearing loss can be restrained, indicating the ability of efferent feedback to ameliorate sound trauma.Fil: Taranda, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Tufts University School of Medicine; Estados UnidosFil: Maison, Stéphane F.. Massachusetts Eye and Ear Infirmary; Estados UnidosFil: Ballestero, Jimena Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Katz, Eleonora. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Savino, Jessica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Vetter, Douglas E.. Tufts University School of Medicine; Estados UnidosFil: Boulter, Jim. University of California at Los Angeles; Estados UnidosFil: Liberman, M. Charles. Massachusetts Eye and Ear Infirmary; Estados UnidosFil: Fuchs, Paul A.. The Johns Hopkins University School of Medicine; Estados UnidosFil: Elgoyhen, Ana Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Farmacología; Argentin