Both carotid canal dehiscence (CCD) and high jugular bulb (HJB) are thought to increase the potential for disastrous consequences during middle ear surgery. Clinical co-presentation of these two great vessel variants has not yet been described. This study aims to determine the relationship between CCD and HJB based on a computed tomographic (CT) temporal bone evaluation. High-resolution CT scans of 408 temporal bones obtained from 208 adults were recruited. Carotid canal integrity, jugular bulb position, petrous apex pneumatization and the minimal thickness of the carotid canal wall (TCW) facing the tympanic cavity were examined and measured for the incidence of CCD and/or HJB. Other variables including gender, age, laterality and the presence of otitis media or mastoiditis were also collected for analysis. CCD was found in 28 ears (6.9%); 19 of these were found to also have HJB (67.9%). The presence of CCD was significantly correlated with HJB presentation. The minimal TCW in HJB ears was significantly thinner than that of normally positioned jugular bulbs. Moreover, after controlling for other candidate variables, the independent factors of age (younger or older than 50 years) and jugular bulb position (high vs. normal) were found to predict the presence of CCD. In conclusion, HJB tends to coexist with a thinner carotid canal wall. This finding emphasizes the need to be watchful for the coexistence of these two great vessel anomalies when surgeons encounter an aged patient presenting either CCD or HJB during middle ear surgery.
The capacity for perpetual self-renewal is one of the main characteristics of stem cells. Little is known about the effect of embryonic neural stem cell (NSC)-secreted factors on auditory cell proliferation in vitro. In the present work, two auditory cell types were cultured in the presence of NSC-secreted molecules and were evaluated in vitro. Our results demonstrated that both cell viability and cell proliferation were significantly enhanced upon treatment with NSC conditioned medium, which contains significantly elevated levels of leukemia inhibitory factor (LIF) secreted by NSCs. The NSC conditioned medium not only activated the expression of leukemia inhibitory factor receptor in House Ear Institute-organ of Corti 1 cells but also up-regulated the LIF downstream signal transducers and activators of transcription (STAT) 1 and STAT3. Blocking either the LIF signaling pathway with neutralizing antibodies or the downstream Janus kinase (JAK)/STAT pathway with JAK2 inhibitor AG490 resulted in a dose-dependent inhibition of cell proliferation, suggesting that NSC-secreted molecules promote auditory cell survival via the regulatory LIF/JAK/STAT signaling pathway.
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