Envelope versus fine structure speech coding strategy: a crossover study.

OBJECTIVE: The transmission of fine structure information to cochlear implant users is an expanding area of research. Previous studies comparing the fine structure processing (FSP) speech coding strategy to the envelope-based continuous interleaved sampling (CIS) strategy indicated improved speech perception when using the fine structure strategy. Those investigations were performed with an extended frequency spectrum in the low frequencies together with the fine structure strategy. The current study addresses the question whether these improvements are due to the presentation of fine structure per se or rather the extended frequency spectrum. Hence, this cross over study compares the two strategies using an identical frequency spectrum. STUDY DESIGN: Randomized crossover study. PATIENTS: 31 patients were randomly assigned to two groups. INTERVENTIONS: One group was fitted with a CIS map for 4 weeks, tested and subsequently fitted with a FSP map for 4 weeks. The other group followed the same pattern in reverse. MAIN OUTCOME MEASURES: Test material consisted of sentence tests in noise, monosyllables in quiet and melody recognition. RESULTS: No statistical significance was noted between the different speech coding strategies at an identical frequency spectrum. CONCLUSION: This study shows that there is no difference in speech perception with FSP compared to CIS at an extended frequency spectrum. Therefore, the extended frequency spectrum in the low frequencies might explain a benefit of FSP observed in previous studies.

Serial analysis of gene expression in the chicken otocyst.

The inner ear arises from multipotent placodal precursors that are gradually committed to the otic fate and further differentiate into all inner ear cell types, with the exception of a few immigrating neural crest-derived cells. The otocyst plays a pivotal role during inner ear development: otic progenitor cells sub-compartmentalize into non-sensory and prosensory domains, giving rise to individual vestibular and auditory organs and their associated ganglia. The genes and pathways underlying this progressive subdivision and differentiation process are not entirely known. The goal of this study was to identify a comprehensive set of genes expressed in the chicken otocyst using the serial analysis of gene expression (SAGE) method. Our analysis revealed several hundred transcriptional regulators, potential signaling proteins, and receptors. We identified a substantial collection of genes that were previously known in the context of inner ear development, but we also found many new candidate genes, such as SOX4, SOX5, SOX7, SOX8, SOX11, and SOX18, which previously were not known to be expressed in the developing inner ear. Despite its limitation of not being all-inclusive, the generated otocyst SAGE library is a practical bioinformatics tool to study otocyst gene expression and to identify candidate genes for developmental studies.

Tenth and twelfth nerve palsies in a patient with internal carotid artery dissection mistaken for cervical mass lesion.

Among the multiple causes for cranial nerve palsies, internal carotid artery dissection is rather uncommon. Patients usually present with unilateral head pain, Horner's syndrome, and signs of cerebral ischemia. We present the case of a 52-year-old male patient, who showed isolated palsies of the tenth and twelfth nerve without any other symptoms. Magnetic resonance imaging (T1) depicted a hyperintense lesion surrounding the internal carotid artery, which was mistaken for a cervical mass, and the patient underwent unnecessary surgical exploration of the neck. Angiography performed afterward could reveal the dissection of the internal carotid artery. This case shows that even in cases with mild and atypic symptoms, internal carotid artery dissection has always to be ruled out in lower cranial nerve palsies.

LIF promotes neurogenesis and maintains neural precursors in cell populations derived from spiral ganglion stem cells.

BACKGROUND: Stem cells with the ability to form clonal floating colonies (spheres) were recently isolated from the neonatal murine spiral ganglion. To further examine the features of inner ear-derived neural stem cells and their derivatives, we investigated the effects of leukemia inhibitory factor (LIF), a neurokine that has been shown to promote self-renewal of other neural stem cells and to affect neural and glial cell differentiation. RESULTS: LIF-treatment led to a dose-dependent increase of the number of neurons and glial cells in cultures of sphere-derived cells. Based on the detection of developmental and progenitor cell markers that are maintained in LIF-treated cultures and the increase of cycling nestin-positive progenitors, we propose that LIF maintains a pool of neural progenitor cells. We further provide evidence that LIF increases the number of nestin-positive progenitor cells directly in a cell cycle-independent fashion, which we interpret as an acceleration of neurogenesis in sphere-derived progenitors. This effect is further enhanced by an anti-apoptotic action of LIF. Finally, LIF and the neurotrophins BDNF and NT3 additively promote survival of stem cell-derived neurons. CONCLUSION: Our results implicate LIF as a powerful tool to control neural differentiation and maintenance of stem cell-derived murine spiral ganglion neuron precursors. This finding could be relevant in cell replacement studies with animal models featuring spiral ganglion neuron degeneration. The additive effect of the combination of LIF and BDNF/NT3 on stem cell-derived neuronal survival is similar to their effect on primary spiral ganglion neurons, which puts forward spiral ganglion-derived neurospheres as an in vitro model system to study aspects of auditory neuron development.

Laminin expression in juvenile angiofibroma indicates vessel's early developmental stage.

CONCLUSION: This study confirms the wide range of vascular architecture in juvenile angiofibromas. Proof of laminin alpha2 expression in tumour vessels is suggested to indicate presence of vessels of early developmental stage in juvenile angiofibromas, supporting the concept that plexus remnants of the first branchial arch artery contribute to the vascular tumour component. OBJECTIVES: Laminins, one of the major components of vascular wall basement membranes, have been implicated in tumour growth and have been shown to have developmentally regulated expression patterns. The goal of this study was to analyse the expression of laminins in juvenile angiofibromas. MATERIALS AND METHODS: A detailed analysis of the laminin isoform expression was performed by immunofluorescence staining for laminin chains alpha1, alpha2, alpha3, alpha4, alpha5, beta1, beta2, beta3, gamma1, gamma2, and gamma3 on cryosections of 10 juvenile angiofibromas and inferior nasal turbinate tissue for control. RESULTS: Vascular staining of the different laminin chains revealed areas of differential vessel density in juvenile angiofibromas and irregularities in vessel size, configuration and architecture. Similar to vessels in nasal turbinates, laminins alpha4, alpha5, beta1, beta2 and gamma1 were found to be expressed in juvenile angiofibroma vessels. In contrast to vessels of nasal turbinates, staining for alpha2 and alpha3 chains was only detected in vessels of juvenile angiofibromas.

Delayed formation of actin filaments in the outer pillar head plate of VASP-/- mice.

Pillar cells with their rich network of tubulin and actin filaments have been reported to contribute to the rigidity of the organ of Corti. As the earliest expression of the actin filament enhancer vasodilator-stimulated phosphoprotein (VASP) in the outer pillar head plate has been found to be associated with the onset of hearing, we tested hearing development in VASP-/- compared to wild-type mice. Performing measurements of auditory brainstem responses on postnatal days (P) P14 and P21, we detected statistically significantly higher thresholds in VASP-/- compared to wild-type mice at P14, but no hearing differences at P21. Staining for prestin and synaptophysin at P12 in morphologically regularly developed cochleae of VASP-/- mice provided an immature prestin protein pattern but no evidence of developmental delay in hair cell innervations. Regularly intense staining of actin filaments in the outer pillar head plate was found only in wild-type but not in VASP-/- mice at P14. At P21, intensive actin filament staining was also observed in the outer pillar head plates of VASP-/- mice. The delayed hearing development in VASP-/- mice is supposed to be caused by a delayed formation of actin filaments in the outer pillar head plate indicating the importance of appropriate pillar cell stiffness in cochlear mechanics.

Dynamic regulation of Na(+)-K(+)-2Cl(-) cotransporter surface expression by PKC-{epsilon} in Cl(-)--secretory epithelia.

In secretory epithelia, activation of PKC by phorbol ester and carbachol negatively regulates Cl(-) secretion, the transport event of secretory diarrhea. Previous studies have implicated the basolateral Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) as a target of PKC-dependent inhibition of Cl(-) secretion. In the present study, we examined the regulation of surface expression of NKCC1 in response to the activation of PKC. Treatment of confluent T84 intestinal epithelial cells with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (PMA) reduced the amount of NKCC1 accessible to basolateral surface biotinylation. Loss of cell surface NKCC1 was due to internalization as shown by 1) the resistance of biotinylated NKCC1 to surface biotin stripping after incubation with PMA and 2) indirect immunofluorescent labeling. PMA-induced internalization of NKCC1 is dependent on the epsilon-isoform of PKC as determined on the basis of sensitivity to a panel of PKC inhibitors. The effect of PMA on surface expression of NKCC1 was specific because PMA did not significantly alter the amount of Na(+)-K(+)-ATPase or E-cadherin available for surface biotinylation. After extended PMA exposure (>2 h), NKCC1 became degraded in a proteasome-dependent fashion. Like PMA, carbachol reduced the amount of NKCC1 accessible to basolateral surface biotinylation in a PKC-epsilon-dependent manner. However, long-term exposure to carbachol did not result in degradation of NKCC1; rather, NKCC1 that was internalized after exposure to carbachol was recycled back to the cell membrane. PKC-epsilon-dependent alteration of NKCC1 surface expression represents a novel mechanism for regulating Cl(-) secretion.