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- Brännström, Jonas, et al.
(författare)
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On the physiological location of otoacoustic emissions
- 2001
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- During recent years, much attention has been paid otoacoustic emissions in the clinical audiological practice. The received view locates their origin in the cochlea, more precisely in the outer hair cells. It is, however, still uncertain if there is an interaction between the ears regarding otoacoustic emissions. Earlier findings suggest an interaction at the level of the olivocochlear bundle. The aim of this pilot study was to find out if there is any interaction between the two cochleae in the case of otoacoustic emissions. Five subjects with normal hearing participated. Recordings were made of spontaneous otoacoustic emissions during the presentation of contralateral stimuli at three different frequencies (500, 1000 and 2000 Hz). In general, contralateral stimulation did not provoke otoacoustic emissions. It was concluded that otoacoustic emissions could be part of the fine-tuning mechanism in the cochlea. The frequency resolution, e.g. for speech, depends on very fast modulation of the incoming signal. Due to the neural distance, this modulation would lag behind, if otoacoustic emissions in one ear would effect the opposite one.
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| 5. |
- Saremi, Amin, et al.
(författare)
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Changes in Temporal and Spectral Functions of the Auditory Periphery Due to Aging and Noise-induced Cochlear Pathologies : A Comparative Clinical Study
- 2014
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Objective: This study includes a battery of psychoacoustical and electrophysiological tests to quantitatively investigate the changes in the frequency and the temporal features of the human auditory periphery caused by aging (presbyacusis) and noise-induced lesions, two common types of sensorineural hearing impairments. The scores are comparatively analyzed.Design: These clinical experiments have been implemented in MATLAB software.Study sample: 20 normal hearing adults (aged 30-54), 20 older hearing-impaired subjects (aged 65-70) with no history of Ototoxic medication or noise exposure and 7 adult men with a traceable noise-induced hearing impairment.Results: The observed temporal and spectral declines are generally consistent with the high-frequency audiometric loss depicted by the audiogram, for each group. Moreover, the test battery provides valuable information on the frequency sensitivity, temporal resolution, loudness growth, compression and otoacoustic emissions.Conclusion: These scores are compared with the predictions of a physiologicallybased cochlear model to provide evidence about specific inner-ear pathologies, beyond what the audiogram can indicate. Among these 7 clinical experiments, the results from the forward temporal masking test, the categorical loudness discrimination test and the distortion product otoacoustic emission test provide the most differential information about the underlying cellular lesions. The results indicate that the reduction in the temporal resolution is substantially age-relate since the presbyacusis listeners, unlike the other groups, obtained almost no benefit from the temporal cues provided by the gap duration at any of the experiments. Moreover, the results suggest that the DPOAEs reflect the cellular lesions associated with the acoustic overstimulation rather than the age-related strial degenerations.
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| 6. |
- Saremi, Amin, et al.
(författare)
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Effects of Acoustic Overstimulation and the Associated Cellular Lesions on the Cochlear Amplifier : Simulation Results
- 2014
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- A physiologically-based electromechanical model of the human cochlea is used in this study to explicitly simulate the effects of acoustical overstimulation, and the associated cellular deficiencies, on the gain of the cochlear amplifier. The simulations demonstrate that as the micromechanics of the stereocillia transduction channels is altered due to the traumatic acoustical overstimulation, the compressive/nonlinear behavior of the cochlear amplifier is significantly modified. When the loudness growth is estimated by the integral of the cochlear amplification with respect to the sound intensity, these modifications lead to an impaired loudness function reminiscent of the recruitment phenomenon. Furthermore, when a severe noise-induced loss of outer hair cells is assumed at basal regions of the cochlea, the model predicts a mild loss at lower frequencies followed by a steeply sloping notch-like amplification loss of approximately 80 dB around 4.5 kHz. This prediction is reasonably in line with the threshold elevations observed clinically from the noise-damaged human ears. Moreover, the results quantitatively demonstrate that the center frequency, the width and the depth of the amplification loss are directly determined by the severity and the location of the outer hair cell loss along the cochlear duct.
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| 7. |
- Anikin, Andrey, et al.
(författare)
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The role of loudness in vocal intimidation
- 2023
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Across many species, a major function of vocal communication is to convey formidability, with low voice frequencies traditionally considered the main vehicle for projecting large size and aggression. Vocal loudness is often ignored, yet it might explain some puzzling exceptions to this frequency code. Here we demonstrate, through acoustic analyses of over 3000 human vocalizations and four perceptual experiments, that vocalizers produce low frequencies when attempting to sound large, but loudness is prioritized for displays of strength and aggression. Our results show that, although being loud is effective for signaling strength and aggression, it poses a physiological tradeoff with low frequencies because a loud voice is achieved by elevating pitch and opening the mouth wide into a-like vowels. This may explain why aggressive vocalizations are often high-pitched and why open vowels are considered “large” in sound symbolism despite their high first formant. Callers often compensate by adding vocal harshness (nonlinear vocal phenomena) to undesirably high-pitched loud vocalizations, but a combination of low and loud remains an honest predictor of both perceived and actual physical formidability. The proposed notion of a loudness-frequency tradeoff thus adds a new dimension to the widely accepted frequency code and requires a fundamental rethinking of the evolutionary forces shaping the form of acoustic signals.
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| 9. |
- Lundberg, Thorbjörn, 1965-, et al.
(författare)
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What does otalgia in children represent? : A study of acute otitis media in general practice related to symptoms and tympanic membrane status over time.
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- BackgroundOtalgia is an important symptom leading children to seek health care in general practice and it can be a symptom of acute otitis media (AOM). The course of AOM can be of importance when grading severity of AOM.The aim of this study was to assess tympanic membrane TM appearance in children aged 2–16 years with otalgia in general practice and to follow their signs and symptoms over time.MethodThe children were examined at four rural health care centers in Lapland, Sweden. Symptoms such as otalgia, fever and the general condition were recorded together with endoscopic TM images and tympanometry results and stored in a central database. The same procedures were applied at follow-up visits after 3 days, 7 days and 3 months. The symptoms were given scores 0–2, the tympanograms were labeled as type A, type C and type B (scores 0–4–8) whereas TM images were graded according to the OMGRADE scale for TM´s (score 0–8). An assessment group set a diagnosis asynchronously after a consensus discussion. Diagnoses: normal, otitis media with effusion, AOM, bullous myringitis without AOM (BM), bullous myringitis with AOM (bAOM) and AOM with perforation or a wet and chagrinated appearance of the TM (pAOM). The diagnoses were scrutinized for any difference in presentation of symptoms. The course of signs and symptoms was followed up at return visits.ResultsThe children showed a normal TM and tympanogram in 19%, otitis media with effusion in 32% and AOM in 49% at first visit. The majority of children reported no symptoms after 3 days. The children with bilateral AOM reported slightly more symptoms and the BM/bAOM groups reported fewer symptoms than children with AOM. A pAOM with a chagrinated TM was found in 19% and showed a prolonged return to normal tympanograms. Forty percent of the children who presented with a chagrinated TM (pAOM) at first visit still had type-B tympanograms after 3 months.Conclusions Half of the children with otalgia were diagnosed with AOM. Symptoms resolved faster than signs. The chagrinated TM appeared to be associated with prolonged middle ear effusion.
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| 10. |
- Basic, Vladimir T., 1982-, et al.
(författare)
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Chronic cigarette smoke exposureimpairs skeletal muscle regenerative capacity in murineCOPD/emphysema model.
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Background: Cigarette smoke (CS) is a well established risk factor in the development of COPD and irreversible airflow limitation. In contrast, the extent to which CS exposure contributes to development of peripheral skeletal muscle dysfunction and wasting remains largely unknown. Decline in skeletal muscle regenerative capacity has been previously reported in COPD patients.Methods: To investigate effects of chronic CS exposure on skeletal muscle regenerative capacity, 129/SvJ mice were exposed to CS for 6 months. The expression levels of myogenin, Jarid2, Znf496, Notch1, Pax7, Fgf1 and Myh3, which are known to regulate skeletal muscle myogenesis, were studied. Additionally, number of fibers with central nuclei, myonuclei number and mean fiber cross-sectional area were assessed.Results: Compared to controls, skeletal muscles from CS-exposed mice exhibited significantly decreased expression of Jarid2, coupled with enhanced expression of Znf496, Notch1, Pax7, Fgf1 and Myh3. Expression of myogenin, a marker of terminally differentiated myofibers, was reduced. Furthermore, reduced muscle fiber crosssectional area, increased number of fibers with central nuclei and reduced myonuclei number were also observed in CS-exposed animals.Conclusions: Taken together, current results provide evidence linking chronic CS exposure and an ongoing damage/repair process as well as impaired regenerative capacity in skeletal muscles of CS-exposed mice.
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