Search

OBJECTIVES/HYPOTHESIS: Cadherins are a superfamily of transmembrane glycoproteins, which mediate calcium-dependent intercellular adhesions. T-cadherin is an atypical member of the cadherin family in regard to its structure; it acts as a signalling receptor rather than an adhesion molecule. In this study we examine the role of T-cadherin in the mammalian cochlea. STUDY DESIGN: This study investigated the expression of T-cadherin in the inner ear under physiologic and pathologic conditions. METHODS: Expression of T-cadherin in the rat cochlea was analyzed by reverse-transcriptase polymerase chain reaction (RT-PCR), real-time RT-PCR, Western blot, and immunohistochemistry. RESULTS: We detected T-cadherin mRNA expression in three different components in the cochlea of postnatal mouse, namely the organ of Corti (OC), the spiral ganglion (SG), and the stria vascularis (SV). The SG and SV showed a higher T-cadherin mRNA level than the OC. T-cadherin protein was detected by Western blotting in the OC, SG, and SV. Immunofluorescence microscopy of adult mouse cochlea revealed the presence of T-cadherin in the apical parts of the inner and outer hair cells as well as in the SV and SG. OCs treated with gentamicin for 3, 6, or 12 hours did not show any change in T-cadherin gene expression compared to control explants maintained in culture medium alone. CONCLUSIONS: T-cadherin is expressed within the cochlea. T-cadherin seems to have a wide variety of functions in the inner ear, ranging from mechanical functions to functions in response to hair cell damage and loss.

Depression in systemic lupus erythematosus (SLE) is a common yet poorly understood phenomenon. This research adopted a biopsychosocial model in which pain and family support were hypothesized to predict depressive symptoms directly, and indirectly, through perceived helplessness. A total of 44 confirmed SLE patients recruited through the community completed a set of questionnaires in a cross-sectional, correlation design. The results confirmed our model's applicability, demonstrating that high pain and high helplessness independently contributed to depression; however, the contribution of family support was not significant. While mixed support was found for a pain-learned helplessness link, helplessness mediated the effects of patients' socio-economic status on depression such that patients of lower socio-economic status reported greater helplessness in the face of their illness. In summary, the data indicate that pain and helplessness are important concomitants of SLE-related depression. Longitudinal research is recommended to clarify the relationships among these variables over time in clinical samples.