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Background: In this paper the dichotic tests and the CERA (Cortical Evoked Response Audiometry) of children with dyslexia had been examined, in order to find out if there are auditory processing and perception disorders., Patients and Methods: 33 children with dyslexia had been compared with 28 children without problems of writing and reading. The mean age of the children was 9 years. All of the children had been examined by the following audiometric measurements: tympanometry, pure-tone-audiometry, speech-audiometry, dichotic Tests by Uttenweiler and Feldmann and the Cortical Evoked Response Audiometry (CERA) rated according to Esser., Results: The intelligence quotients were in the group of dyslexic children significantly lower. The Uttenweiler and Feldmann tests were in dyslexic children significantly lower in the control group as well. The late cortical responses ware normal or near normal in both groups., Conclusion: Dichotic speech tests indicate central auditory processing and perception deficits in dyslexia. These tests are confounded, however, by attention and memory deficits. The CERA rated according to Esser does not point out to these auditory disorders in dyslexia.

Malignant gliomas remain incurable brain tumors because of their diffuse-invasive growth. So far, the genetic and molecular events underlying gliomagenesis are poorly understood. In this study, we have identified the receptor tyrosine kinase Axl as a mediator of glioma growth and invasion. We demonstrate that Axl and its ligand Gas6 are overexpressed in human glioma cell lines and that Axl is activated under baseline conditions. Furthermore, Axl is expressed at high levels in human malignant glioma. Inhibition of Axl signaling by overexpression of a dominant-negative receptor mutant (AXL-DN) suppressed experimental gliomagenesis (growth inhibition >85%, P < 0.05) and resulted in long-term survival of mice after intracerebral glioma cell implantation when compared with Axl wild-type (AXL-WT) transfected tumor cells (survival times: AXL-WT, 10 days; AXL-DN, >72 days). A detailed analysis of the distinct hallmarks of glioma pathology, such as cell proliferation, migration, and invasion and tumor angiogenesis, revealed that inhibition of Axl signaling interfered with cell proliferation (inhibition 30% versus AXL-WT), glioma cell migration (inhibition 90% versus mock and AXL-WT, P < 0.05), and invasion (inhibition 62% and 79% versus mock and AXL-WT, respectively; P < 0.05). This study describes the identification, functional manipulation, in vitro and in vivo validation, and preclinical therapeutic inhibition of a target receptor tyrosine kinase mediating glioma growth and invasion. Our findings implicate Axl in gliomagenesis and validate it as a promising target for the development of approaches toward a therapy of these highly aggressive but, as yet, therapy-refractory, tumors.