There are several compelling reasons for airlines to consider single pilot operations including economic savings, coping with a shortage of pilots, and automation and artificial intelligence ...technology advancement. To adequately explore this concept, differing aviation industry views of single pilot operations (SPO), challenges associated with single pilot operations, an overview of current SPO research and options, and conclusions and recommendations are presented. Ultimately, many obstacles to implementation must be overcome including convincing the general public that it safe which may be the biggest challenge of all. However, SPO will continue to move forward not only due to potential commercial aviation economic benefits, but also because one day, technology will allow it and perhaps even demand it.
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EMUNI, FZAB, GEOZS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Sensorineural hearing impairment is the most common form of hearing loss, and encompasses pathologies of the cochlea and the auditory nerve. Hearing impairment caused by abnormal neural encoding of ...sound stimuli despite preservation of sensory transduction and amplification by outer hair cells is known as 'auditory neuropathy'. This term was originally coined for a specific type of hearing impairment affecting speech comprehension beyond changes in audibility: patients with this condition report that they "can hear but cannot understand". This type of hearing impairment can be caused by damage to the sensory inner hair cells (IHCs), IHC ribbon synapses or spiral ganglion neurons. Human genetic and physiological studies, as well as research on animal models, have recently shown that disrupted IHC ribbon synapse function--resulting from genetic alterations that affect presynaptic glutamate loading of synaptic vesicles, Ca(2+) influx, or synaptic vesicle exocytosis--leads to hearing impairment termed 'auditory synaptopathy'. Moreover, animal studies have demonstrated that sound overexposure causes excitotoxic loss of IHC ribbon synapses. This mechanism probably contributes to hearing disorders caused by noise exposure or age-related hearing loss. This Review provides an update on recently elucidated sensory, synaptic and neural mechanisms of hearing impairment, their corresponding clinical findings, and discusses current rehabilitation strategies as well as future therapies.
Mutations in the OTOF gene encoding otoferlin result in a disrupted function of the ribbon synapses with impairment of the multivesicular glutamate release. Most affected subjects present with ...congenital hearing loss and abnormal auditory brainstem potentials associated with preserved cochlear hair cell activities (otoacoustic emissions, cochlear microphonics CMs). Transtympanic electrocochleography (ECochG) has recently been proposed for defining the details of potentials arising in both the cochlea and auditory nerve in this disorder, and with a view to shedding light on the pathophysiological mechanisms underlying auditory dysfunction.
We review the audiological and electrophysiological findings in children with congenital profound deafness carrying two mutant alleles of the OTOF gene. We show that cochlear microphonic (CM) amplitude and summating potential (SP) amplitude and latency are normal, consistently with a preserved outer and inner hair cell function. In the majority of OTOF children, the SP component is followed by a markedly prolonged low-amplitude negative potential replacing the compound action potential (CAP) recorded in normally-hearing children. This potential is identified at intensities as low as 90 dB below the behavioral threshold. In some ears, a synchronized CAP is superimposed on the prolonged responses at high intensity. Stimulation at high rates reduces the amplitude and duration of the prolonged potentials, consistently with their neural generation. In some children, however, the ECochG response only consists of the SP, with no prolonged potential. Cochlear implants restore hearing sensitivity, speech perception and neural CAP by electrically stimulating the auditory nerve fibers.
These findings indicate that an impaired multivesicular glutamate release in OTOF-related disorders leads to abnormal auditory nerve fiber activation and a consequent impairment of spike generation. The magnitude of these effects seems to vary, ranging from no auditory nerve fiber activation to an abnormal generation of EPSPs that occasionally trigger a synchronized electrical activity, resulting in high-threshold CAPs.
•Cochlear microphonics show a normal amplitude in OTOF patients.•The compound action potential is replaced by a prolonged negative response.•The use of hearing aids results in improvement in pure tone sensitivity.•Cochlear implants restore hearing sensitivity and speech perception.•Electrically-evoked compound action potentials are evoked through the cochlear implant.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The effects of inner ear abnormality on audibility have been explored since the early 20th century when sound detection measures were first used to define and quantify 'hearing loss'. The development ...in the 1970s of objective measures of cochlear hair cell function (cochlear microphonics, otoacoustic emissions, summating potentials) and auditory nerve/brainstem activity (auditory brainstem responses) have made it possible to distinguish both synaptic and auditory nerve disorders from sensory receptor loss. This distinction is critically important when considering aetiology and management. In this review we address the clinical and pathophysiological features of auditory neuropathy that distinguish site(s) of dysfunction. We describe the diagnostic criteria for: (i) presynaptic disorders affecting inner hair cells and ribbon synapses; (ii) postsynaptic disorders affecting unmyelinated auditory nerve dendrites; (iii) postsynaptic disorders affecting auditory ganglion cells and their myelinated axons and dendrites; and (iv) central neural pathway disorders affecting the auditory brainstem. We review data and principles to identify treatment options for affected patients and explore their benefits as a function of site of lesion.
Simulators have been integrated into flight training at various levels for decades, increasing in utility as they increased in fidelity. Today, practically all levels of qualification in ...passenger-carrying commercial airliners can be obtained entirely in the simulator, with the first experience in the aircraft on a revenue-producing flight. Flight training in the U.S. is a tightly controlled, highly regulated process overseen by the Federal Aviation Administration (FAA). It is also a very successful one; commercial aviation maintains a remarkable safety record. To that end, pilot training has been studied and analyzed extensively over the years, and as to the focus of this paper, the efficacy of simulator training has generated as much debate as consensus with regards to the utility of the devices. Much of this research, to include experiments, has focused on simulator fidelity – how well the device replicates the actual aircraft – and to what extent that training transfers to the aircraft. Very little research has focused on the role and interaction of the simulator instructor with the student(s) and what impact he/she has upon the final training result nor has elements of current instructional design methodology been considered. This paper analyzes vital simulator training concepts, examines accidents and incidents where the investigation revealed potential deficiencies in the training devices used by the crews of these airplanes, and then considers the role of the simulator instructor through the lens of modern instructional design concepts. The authors provide suggestions as to the direction of further research into the vitality of this role in maximizing the potential of training with flight simulators to further safety goals.
Fatigue remains a significant hazard in commercial aviation and has been a major concern among all stakeholders for decades. This review of the literature explores the current prescriptive structure ...of the regulatory environment (Part 117) and its effect on fatigue management. To illustrate the impact of fatigue on flight operations, this article includes a brief analysis of two National Transportation Safety Board (NTSB) accident reports where fatigue was indicated as a factor. Current research in fatigue management and efforts by the Federal Aviation Administration point to the benefits of using a Safety Management Systems (SMS) methodology to manage fatigue. Using the framework of an organization’s functioning SMS, various solutions are discussed, including using existing reporting systems to gather data and the development of potential performance indicators, with an emphasis on the need for research into commuting habits of flight crews and establishing a safety culture based upon fitness for duty.
1 Departments of Anatomy and Neurobiology, 2 Biomedical Engineering, 3 Cognitive Sciences, 4 Neurology, and 5 OtolaryngologyHead and Neck Surgery, University of California, Irvine, California
...Submitted 21 September 2004;
accepted in final form 17 December 2004
Perceptual consequences of disrupted auditory nerve activity were systematically studied in 21 subjects who had been clinically diagnosed with auditory neuropathy (AN), a recently defined disorder characterized by normal outer hair cell function but disrupted auditory nerve function. Neurological and electrophysical evidence suggests that disrupted auditory nerve activity is due to desynchronized or reduced neural activity or both. Psychophysical measures showed that the disrupted neural activity has minimal effects on intensity-related perception, such as loudness discrimination, pitch discrimination at high frequencies, and sound localization using interaural level differences. In contrast, the disrupted neural activity significantly impairs timing related perception, such as pitch discrimination at low frequencies, temporal integration, gap detection, temporal modulation detection, backward and forward masking, signal detection in noise, binaural beats, and sound localization using interaural time differences. These perceptual consequences are the opposite of what is typically observed in cochlear-impaired subjects who have impaired intensity perception but relatively normal temporal processing after taking their impaired intensity perception into account. These differences in perceptual consequences between auditory neuropathy and cochlear damage suggest the use of different neural codes in auditory perception: a suboptimal spike count code for intensity processing, a synchronized spike code for temporal processing, and a duplex code for frequency processing. We also proposed two underlying physiological models based on desynchronized and reduced discharge in the auditory nerve to successfully account for the observed neurological and behavioral data. These methods and measures cannot differentiate between these two AN models, but future studies using electric stimulation of the auditory nerve via a cochlear implant might. These results not only show the unique contribution of neural synchrony to sensory perception but also provide guidance for translational research in terms of better diagnosis and management of human communication disorders.
Address for reprint requests and other correspondence: F.-G. Zeng, 364 Med Surge II, Univ. of California, Irvine, CA 92697-1275 (E-mail: fzeng{at}uci.edu )
Abstract Objective To define brain activity corresponding to an auditory illusion of 3 and 6 Hz binaural beats in 250 Hz or 1000 Hz base frequencies, and compare it to the sound onset response. ...Methods Event-Related Potentials (ERPs) were recorded in response to unmodulated tones of 250 or 1000 Hz to one ear and 3 or 6 Hz higher to the other, creating an illusion of amplitude modulations (beats) of 3 Hz and 6 Hz, in base frequencies of 250 Hz and 1000 Hz. Tones were 2000 ms in duration and presented with approximately 1 s intervals. Latency, amplitude and source current density estimates of ERP components to tone onset and subsequent beats-evoked oscillations were determined and compared across beat frequencies with both base frequencies. Results All stimuli evoked tone-onset P50 , N100 and P200 components followed by oscillations corresponding to the beat frequency, and a subsequent tone-offset complex. Beats-evoked oscillations were higher in amplitude with the low base frequency and to the low beat frequency. Sources of the beats-evoked oscillations across all stimulus conditions located mostly to left lateral and inferior temporal lobe areas in all stimulus conditions. Onset-evoked components were not different across stimulus conditions; P50 had significantly different sources than the beats-evoked oscillations; and N100 and P200 sources located to the same temporal lobe regions as beats-evoked oscillations, but were bilateral and also included frontal and parietal contributions. Conclusions Neural activity with slightly different volley frequencies from left and right ear converges and interacts in the central auditory brainstem pathways to generate beats of neural activity to modulate activities in the left temporal lobe, giving rise to the illusion of binaural beats. Cortical potentials recorded to binaural beats are distinct from onset responses. Significance Brain activity corresponding to an auditory illusion of low frequency beats can be recorded from the scalp.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Abstract Objective The auditory Event-Related Potentials (ERP) of component P50 to sound onset and offset have been reported to be similar, but their magnetic homologue has been reported absent to ...sound offset. We compared the spatio-temporal distribution of cortical activity during P50 to sound onset and offset, without confounds of spectral change. Methods ERPs were recorded in response to onsets and offsets of silent intervals of 0.5 s (gaps) appearing randomly in otherwise continuous white noise and compared to ERPs to randomly distributed click pairs with half second separation presented in silence. Subjects were awake and distracted from the stimuli by reading a complicated text. Measures of P50 included peak latency and amplitude, as well as source current density estimates to the clicks and sound onsets and offsets. Results P50 occurred in response to noise onsets and to clicks, while to noise offset it was absent. Latency of P50 was similar to noise onset (56 ms) and to clicks (53 ms). Sources of P50 to noise onsets and clicks included bilateral superior parietal areas. In contrast, noise offsets activated left inferior temporal and occipital areas at the time of P50 . Source current density was significantly higher to noise onset than offset in the vicinity of the temporo-parietal junction. Conclusions P50 to sound offset is absent compared to the distinct P50 to sound onset and to clicks, at different intracranial sources. P50 to stimulus onset and to clicks appears to reflect preattentive arousal by a new sound in the scene. Sound offset does not involve a new sound and hence the absent P50. Significance Stimulus onset activates distinct early cortical processes that are absent to offset.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
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