It is well-established that excessive noise exposure can systematically shift audiometric thresholds (i.e., noise-induced hearing loss, NIHL) making sounds at the lower end of the dynamic range difficult to detect. An often overlooked symptom of NIHL is the degraded ability to resolve temporal fluctuations in supra-threshold signals. Given that the temporal properties of speech are highly dynamic, it is not surprising that NIHL greatly reduces one\'s ability to clearly decipher spoken language. However, systematic characterization of noise-induced impairments on supra-threshold signals in humans is difficult given the variability in noise exposure among individuals. Fortunately, the chinchilla is audiometrically similar to humans, making it an ideal animal model to investigate noise-induced supra-threshold deficits. Through a series of studies using the chinchilla, the authors have elucidated several noise-induced deficits in temporal processing that occur at supra-threshold levels. These experiments highlight the importance of the chinchilla model in developing an understanding of noise-induced deficits in temporal processing.

OBJECTIVE: To review the literature on techniques for creation of chronic tympanic membrane perforations (TMP) in animal models. Establishing such models in a laboratory setting will have value if they replicate many of the properties of the human clinical condition and can thus be used for investigation of novel grafting materials or other interventions.
METHODS: A literature search of the PubMed database (1950-August 2014) was performed. The search included all English-language literature published attempts on chronic or delayed TMP in animal models. Studies of non English-language or acute TMP were excluded.
RESULTS: Thirty-seven studies were identified. Various methods to create TMP in animals have been used including infolding technique, thermal injury, re-myringotomy, and topical agents including chemicals and growth factor receptor inhibitors. The most common type of animal utilized was chinchilla, followed by rat and guinea pig. Twenty three of the 37 studies reported success in achieving chronic TMP animal model while 14 studies solely delayed the healing of TMP. Numerous experimental limitations were identified including TMP patency duration of <8 weeks, lack of documentation of total number of animals attempted and absence of proof for chronicity with otoscopic and histologic evidence.
CONCLUSIONS: The existing literature demonstrates the need for an ideal chronic TMP animal model to allow the development of new treatments and evaluate the risk of their clinical application. Various identified techniques seem promising, however, a need was identified for standardization of experimental design and evidence to address multiple limitations.

Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive neurostimulation tool with increasing therapeutic applications in neurology, psychiatry and in the treatment of chronic tinnitus, and with a growing interest in cognitive neuroscience. One of its side effects is the loud click sound generated simultaneously to the magnetic pulse, which depends both on the equipment and rTMS intensity. This impulse sound could transiently modify peripheral hearing mechanisms, and hence hearing thresholds, both in patients and in rTMS practitioners. Furthermore, if no precautions are taken, especially in subjects with several risks factors for hearing loss, it is possible that the repetition of exposure could lead to more definitive changes in hearing thresholds. These issues are often neglected, although they could have specific relevance in rTMS treatment for tinnitus or in auditory cognitive neuroscience. This review specifically deals with noise exposure during rTMS and its potential consequences on the auditory system. It provides several practical solutions to help minimize exposure.

Quinupristin/dalfopristin is a semisynthetic parenteral streptogramin combination consisting of two components, quinupristin (RP 57669) and dalfopristin (RP 54476), in a 30:70 (w/w) ratio. These compounds act synergically against many Gram-positive bacteria that cause severe infections. Several animal models have been used to study the in-vivo efficacy and pharmacodynamics of quinupristin/dalfopristin against infections caused by Staphylococcus aureus and Streptococcus spp. Studies of its efficacy in animal models of septicaemia, thigh infection, pneumonia and aortic endocarditis have shown it to be as active as vancomycin against S. aureus, including some methicillin-resistant strains (MRSA), and as active as high doses of amoxycillin against penicillin-resistant and multi-resistant strains of Streptococcus pneumoniae. Thus, quinupristin/dalforpristin appears to have potential as an alternative to vancomycin in the management of severe staphylococcal and streptococcal infections, including those caused by MRSA and multi-resistant pneumococci.

The ultrastructure of the round window membrane of humans, monkeys, felines, and rodents discloses three basic layers: an outer epithelium, a middle core of connective tissue, and an inner epithelium. Interspecies variations are mainly in terms of thickness, being thinnest in rodents and thicker in humans. Morphologic evidence suggests that the layers of the round window participate in absorption and secretion of substances to and from the inner ear, and that the entire membrane could play a role in the defense system of the ear. Different substances, including antibiotics, local anesthetics, and tracers such as cationic ferritin, horseradish peroxidase, and 1 mu latex microspheres, are placed in the middle ear side traverse the membrane. Cationic ferritin and 1 micron microspheres placed in perilymph become incorporated by the inner epithelial cells of the membrane. Permeability is selective; factors include size, concentration, liposolubility, electrical charge, and thickness of the membrane. Passage of substances through the round window membrane is by different pathways, the nature of which is seemingly decided at the outer epithelium of the round window membrane.

We discuss several techniques of culturing middle ear epithelium from several species, which was formerly difficult but is now possible because of recent advances in culture methods. The three main methods of initiating a culture are organ culture, primary explant culture, and cell culture. Although each method has both advantages and disadvantages, investigators can choose the method most suitable to their purpose. A few researchers, including ourselves, have succeeded in obtaining serial culture of middle ear epithelium. Using 3T3 feeder layer technique or conditioned medium enabled us to develop a fibroblast-free cultured middle ear epithelium. The availability of cultured middle ear epithelium provides a potential tool in future middle ear research.

The sensory cilia of the mammalian cochlea show an orderly gradation in height along the length of the cochlea. The cilia are taller in the apex and shorter in the base. Differences in ciliary gradation also exist between the different rows of outer hair cell cilia along the length of the cochlea. There are gradations in width and thickness in the moveable portion of the tectorial membrane paralleling those in the basilar membrane. There are also gradations in the relationship between the tectorial membrane and the slope of the reticular lamina along the length of the cochlea. This suggests that there may be additional mechanical fine-tuning capability built into the organ of Corti besides the basilar membrane. The tectorial membrane is firmly attached to the outer hair cell cilia along the entire length of the cochlea in all species examined. The inner hair cell cilia do not have the same firm attachment to the tectorial membrane as outer hair cell cilia. This suggests that the modes of mechanical coupling between the tectorial membrane and the inner and outer hair cell cilia are different.

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The anatomic consequences of acoustic overstimulation are explored in this presentation, and attention is directed toward issues where improvements in technology and empirical observation are needed before further advances in our understanding can be achieved. Gains have been made in the last decade in appreciating sound-induced cochlear injury, but there is now a need to evaluate not only cochlear pathology but also the functional state of the surviving structures. There is a wealth of information about the susceptibility of inner or outer hair cells to acoustic injury; however, the etiology of this injury is not yet fully understood. In addition, current ideas concerning the effects of noise on hair-cell stereocilia, hair-cell synapses, the cochlear vascular supply, and the central auditory pathways are in a state of flux and are either undergoing revision or emerging. Other issues, such as the basis of temporary or permanent threshold shift at the cellular level, and the individual differences in susceptibility to injury are in need of a fresh approach. It would seem that the time is now ripe to review our knowledge, recognize its gaps, and develop testable hypotheses concerning the mechanisms of acoustic injury to the ear.

A review of the last 10 years of research on impulse noise reveals certain insights and perspectives on the biological and audiological effects of exposures to impulse noise. First, impulse noise may damage the cochlea by direct mechanical processes. Second, after exposure to impulse noise, hearing may recover in an erratic, nonmonotonic pattern. Third, even though the existing damage-risk criteria evaluate impulse noise in terms of level, duration, and number, often parameters such as temporal pattern, waveform, and rise time are also important in the production of a hearing loss. Fourth, the effects of impulse noise are often inconsistent with the principle of the equal energy hypothesis. Fifth, impulse noise can interact with background continuous noise to produce greater hearing loss than would have been predicted by the simple sum of the individual noises.