A model of auditory performance and a model of ganglion cell survival in postlinguistically deafened adult cochlear implant users are suggested to describe the effects of aetiology, duration of deafness, age at implantation, age at onset of deafness, and duration of implant use. The models were compared with published data and a composite data set including 808 implant users. Qualitative agreement with the model of auditory performance was found. Duration of deafness had a strong negative effect on performance. Age at implantation had a slight negative effect on performance, increasing after age 60 years. Age at onset of deafness had little effect on performance up to age 60. Duration of implant use had a positive effect on performance. Aetiology had a relatively weak effect on performance.

A primary cause of deafness is damage of receptor cells in the inner ear. Clinically, it has been demonstrated that effective functionality can be provided by electrical stimulation of the auditory nerve, thus bypassing damaged receptor cells. However, subsequent to sensory cell loss there is a secondary degeneration of the afferent nerve fibers, resulting in reduced effectiveness of such cochlear prostheses. The effects of neurotrophic factors were tested in a guinea pig cochlear prosthesis model. After chemical deafening to mimic the clinical situation, the neurotrophic factors brain-derived neurotrophic factor and an analogue of ciliary neurotrophic factor were infused directly into the cochlea of the inner ear for 26 days by using an osmotic pump system. An electrode introduced into the cochlea was used to elicit auditory responses just as in patients implanted with cochlear prostheses. Intervention with brainderived neurotrophic factor and the ciliary neurotrophic factor analogue not only increased the survival of auditory spiral ganglion neurons, but significantly enhanced the functional responsiveness of the auditory system as measured by using electrically evoked auditory brainstem responses. This demonstration that neurotrophin intervention enhances threshold sensitivity within the auditory system will have great clinical importance for the treatment of deaf patients with cochlear prostheses. The findings have direct implications for the enhancement of responsiveness in deafferented peripheral nerves. Hearing impairment is the most frequent disability of people in industrialized countries, affecting more than one in seven individuals. Most hearing loss is caused by destruction of the sensory cells within the cochlea of the inner ear. In mammals, the auditory cells do not regenerate, nor are there currently effective interventions for their repair. Moreover, in the auditory system, as in other afferent systems, degeneration of the auditory nerve occurs secondary to the loss of the inner ear sensory cells (hair cells), thus aggravating the functional impairment. In the severely and profoundly deaf, the cochlear implant (prosthesis) has been shown to provide an effective habilitative intervention. The cochlear prosthesis consists of one or more electrodes inserted into the fluid space of the inner ear. The implant operates by directly electrically stimulating the auditory nerve, bypassing damaged or missing sensory receptor cells. This device now provides significant speech understanding, with a score for everyday sentence understanding of about 80% without lip reading in the majority of patients implanted (so far more than 40,000 worldwide) (1-3). However, the cochlear prosthesis depends on remaining excitable auditory nerve fibers, and their loss severely compromises the effectiveness of the implant and the hearing benefits it provides. Studies show a clear relationship between the total number of viable auditory neurons available for stimulation and the performance of subjects receiving cochlear implant...

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A method for the objective measurement of light dissemination in the lens was developed. There is an exponential relationship between the concentration of standard solutions and the intensity of light disseminated forwards. The light disseminated in non-pathological lenses from Sprague Dawley rats was registered as the equivalent standard concentration, C, and then transformed to log10 (C + 1) and was found not to deviate from the normal distribution. The tolerance limit for light dissemination was derived by setting the probability to classify a non-pathological lens as pathological. An analysis of variance demonstrated that the inter-animal variation was the dominating source of imprecision. It is anticipated that the developed system will be useful in experimental toxicological risk assessment.

Cytochrome oxidase (CYO), a key enzyme in the respiratory chain, was observed as an indicator of retinal metabolism after an in vivo blue light exposure. Thirty Sprague-Dawley rats were exposed to optic radiation of 404 nm with a retinal dose of 110kJ/m2. Immediately after exposure, the CYO activity in the pigment epithelium, in the outer and inner segments of photoreceptors, and in the outer plexiform layer of the exposed retina, was reduced to one-third-to-half of the control level. However, there was an increase in CYO activity in the exposed retina one day after exposure. One week after exposure, the CYO activity in the inner segment and the outer plexiform layer was higher, while the activity in the other two layers was lower, than that at one day, although still higher than in the control. Two weeks after exposure, the CYO activity in the four retinal layers returned to the level of the control retina, as did the activity four weeks after. After exposure, no ophthalmoscopically visible retinal change and no light-microscopically evident morphological alterations were found. There was no retinal edema or loss of photoreceptor cells. The observed alteration in CYO activity after blue light exposure may represent an inhibition of retinal metabolism. The inhibition was reversible. If this compensation mechanism is overwhelmed, retinal damage may occur.

The short and long-term healing of the rabbit corneal epithelium was studied after a standardized alkali wound. The wound was inflicted by applying a round filter paper, 5.5 mm in diameter, soaked in 1 N NaOH, for 60 seconds on the central cornea. The wound size and intensity was chosen not to cause melting and perforation, and not to cause vascular ingrowth. n-Heptanol corneal wounds of the same size were used as control. The eyes were followed for 8 weeks. Two phases of epithelial healing were discerned. The initial healing phase lasted 48 h during which the would was completely resurfaced. In spite of the more extensive tissue damage caused by alkali, the initial epithelial healing rate was faster than in n-heptanol wounds. The late healing phase consisted of recurrent epithelial break down, sometimes seen preceded by epithelial blister formation. Four weeks after trauma the state of epithelial healing was at its worst.