To assess the severity and evolution of sinonasal symptoms in patients following endoscopic anterior skull base surgery to define the typical postoperative course. Design: Cross sectional study. Participants include 69 patients who underwent endoscopic skull base surgery by a dual surgeon team (otolaryngologist and neurosurgeon) from January 2008 to August 2009. Main outcome measures: Sinonasal Outcomes Test (SNOT)-20 survey scores at preoperative and at three postoperative time points. An ordinal logistic regression model was used to analyze the data, summarizing the relationship between the outcome (SNOT score) and the predictor (time point) using an odds ratio. Scores for the symptoms of need to blow nose, sneezing, runny nose, postnasal discharge, thick nasal discharge, ear fullness, and facial pain showed significant worsening at the early postoperative time point. These symptoms showed significant improvement over time; however, scores for post nasal discharge remained high at the late time period compared with baseline. All patients will experience considerable sinonasal symptoms following transnasal endoscopic skull base surgery. Postnasal discharge and thick nasal discharge improve significantly over time. Symptoms approach baseline by 6 to 9 months following surgery.

In patients with CUP, survival outcomes are most significantly influenced by clinical stage at time of diagnosis. No significant 5-year survival difference was seen between patients treated with radiation or chemoradiation alone when compared to patients who also received surgical treatment.

Mitochondrial degeneration in the inner ear is likely a contributing factor in age-related hearing loss and other otopathologies such as Meniere's disease. Most mitochondrial proteins are synthesized in the cytosol and imported through the mitochondrial membranes by translocators. The translocase of the outer membrane (Tom) is the universal entry gate for all proteins that are imported into mitochondria. Altered function of the translocator could alter protein transport into the mitochondria, and disrupt function. In this study, we determined the immunolocalization of Tom20, a major mitochondrial protein import receptor, in microdissected human cochlea frozen sections obtained from postmortem autopsy and celloidin-embedded archival specimens. We used affinity purified rabbit polyclonal antibodies against Tom20. We also determined the Tom20 immunolocalization in the mouse inner ear. In the human and mouse cochlea, Tom20 was ubiquitously distributed in the organ of Corti, allowing well-delineated visualization of inner and outer hair cells. Tom20 immunoreactivity localized in the cytoplasm of spiral ganglia neurons. In the inner ear of aged subjects with Meniere's disease, there was decreased expression of Tom20. These results suggest that Tom20 can be used in the inner ear as a marker for mitochondrial protein import. Anat Rec,

Hypothesis-The histopathology of Sjogren's syndrome (SS) in the human inner ear correlates with mouse models of autoimmune inner ear disease (AIED).Background-SS is an autoimmune disease in which 25% of patients have sensorineural hearing loss (SNHL). The inner ear histology in a SS mouse model has shown degeneration of the stria vascularis (SV) and IgG deposition on the basement membrane (BM) of SV blood vessels. Correlation with human temporal bone histopathology has not been addressed.

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