Investigation of the Evolution of Stratum Fracture during the Cavity Expansion of Underground Coal Gasification

The evolution of fracture zone controls the safety of underground coal gasification (UCG) in terms of gas emission and water leakage. In order to understand the fracture propagation in the confining rock of a UCG cavity with various influence factors, this paper implemented a set of numerical models based on different geological and operating conditions. Analysis was implemented on the mechanism of fracture propagation and its evolution characteristics, suggesting that (a) continuum expansion of the cavity leads a near-field fracture circle in confining rock initially, followed by the roof caving and successive propagation of shear band. (b) The key observed influence factors of fracture propagation are the grade of confining rock, overburden pressure, dimension of the cavity and gasifying pressure, the linear relationships between them, and the fracture height. Additionally, the fracture depth in the base board was mainly caused by tensile fracture. (c) A model was proposed based on the evolution of fracture height and depth in roof and base board, respectively. Validation of this model associated with orthogonal tests suggests a good capacity for predicting fracture distribution. This paper has significance in guiding the design of the gasifying operation and safety assessment of UCG cavities

Investigation of the Evolution of Stratum Fracture during the Cavity Expansion of Underground Coal Gasification

The evolution of fracture zone controls the safety of underground coal gasification (UCG) in terms of gas emission and water leakage. In order to understand the fracture propagation in the confining rock of a UCG cavity with various influence factors, this paper implemented a set of numerical models based on different geological and operating conditions. Analysis was implemented on the mechanism of fracture propagation and its evolution characteristics, suggesting that (a) continuum expansion of the cavity leads a near-field fracture circle in confining rock initially, followed by the roof caving and successive propagation of shear band. (b) The key observed influence factors of fracture propagation are the grade of confining rock, overburden pressure, dimension of the cavity and gasifying pressure, the linear relationships between them, and the fracture height. Additionally, the fracture depth in the base board was mainly caused by tensile fracture. (c) A model was proposed based on the evolution of fracture height and depth in roof and base board, respectively. Validation of this model associated with orthogonal tests suggests a good capacity for predicting fracture distribution. This paper has significance in guiding the design of the gasifying operation and safety assessment of UCG cavities

Null Mutation of α1D Ca2+ Channel Gene Results in Deafness but No Vestibular Defect in Mice

Multiple Ca2+ channels confer diverse functions to hair cells of the auditory and vestibular organs in the mammalian inner ear. We used gene-targeting technology to generate α1D Ca2+ channel-deficient mice to determine the physiological role of these Ca2+ channels in hearing and balance. Analyses of auditory-evoked brainstem recordings confirmed that α1D−/− mice were deaf and revealed that heterozygous (α1D+/−) mice have increased hearing thresholds. However, hearing deficits in α1D+/− mice were manifested mainly by the increase in threshold of low-frequency sounds. In contrast to impaired hearing, α1D−/− mice have balance performances equivalent to their wild-type littermates. Light and electron microscope analyses of the inner ear revealed outer hair cell loss at the apical cochlea, but no apparent abnormality at the basal cochlea and the vestibule. We determined the mechanisms underlying the auditory function defects and the normal vestibular functions by examining the Ba2+ currents in cochlear inner and outer hair cells versus utricular hair cells in α1D+/− mice. Whereas the whole-cell Ba2+ currents in inner hair cells consist mainly of the nimodipine-sensitive current (~85%), the utricular hair cells express only ~50% of this channel subtype. Thus, differential expression of α1D channels in the cochlear and utricular hair cells confers the phenotype of the α1D null mutant mice. Because vestibular and cochlear hair cells share common features and null deletion of several genes have yielded both deafness and imbalance in mice, α1D null mutant mice may serve as a model to disentangle vestibular from auditory-specific functions

Cochlear NMDA Receptors as a Therapeutic Target of Noise-Induced Tinnitus

Background: Accumulating evidence suggests that tinnitus may occur despite normal auditory sensitivity, probably linked to partial degeneration of the cochlear nerve and damage of the inner hair cell (IHC) synapse. Damage to the IHC synapses and deafferentation may occur even after moderate noise exposure. For both salicylate- and noise-induced tinnitus, aberrant N-methyl-d-aspartate (NMDA) receptor activation and related auditory nerve excitation have been suggested as origin of cochlear tinnitus. Accordingly, NMDA receptor inhibition has been proposed as a pharmacologic approach for treatment of synaptopathic tinnitus. Methods: Round-window application of the NMDA receptor antagonist AM-101 (Esketamine hydrochloride gel; Auris Medical AG, Basel, Switzerland) was tested in an animal model of tinnitus induced by acute traumatic noise. The study included the quantification of IHC ribbon synapses as a correlate for deafferentation as well as the measurement of the auditory brainstem response (ABR) to close-threshold sensation level stimuli as an indication of sound-induced auditory nerve activity. Results: We have shown that AM-101 reduced the trauma-induced loss of IHC ribbons and counteracted the decline of ABR wave I amplitude generated in the cochlea/auditory nerve. Conclusion: Local round-window application of AM-101 may be a promising therapeutic intervention for the treatment of synaptopathic tinnitus