Pulsatile tinnitus due to a sigmoid sinus diverticulum and/or dehiscence

@#<p style="text-align: justify;">In 2009, a 52-year-old man presented with a two year history of intermittent right-sided pulse-synchronous tinnitus. He noted that the tinnitus worsened when his blood pressure was elevated. Otologic exam was unremarkable, with no obvious middle ear fluid or mass. There was no neck bruit, and the tinnitus diminished on manual compression of the ipsilateral internal  jugular vein. In keeping with the recommendations for clinical imaging at that time, a non-contrast CT of the temporal bone was performed. This was to evaluate for conditions such as : a middle ear glomus, an aberrant internal carotid artery, a jugular bulb variant (e.g. a high-riding jugular bulb), otosclerosis, superior semicircular canal dehiscence syndrome, a persistent stapedial artery, or a hemangioma of the temporal bone.1 No evidence of these conditions was found. An MRI of the brain, with MR angiography and venography of the intracranial vasculature also performed to evaluate for conditions such as:  idiopathic intracranial hypertension, a dural arteriovenous fistula, an arteriovenous malformation, vascular loop syndrome, and dural sinus stenosis or thrombosis.2 All of these conditions were excluded. As no definite pathology was identified, no firm treatment reommendations were initiallly made.</p><p style="text-align: justify;">In 2011, Eisenman reported on a series of 13 patients with pulsatile tinnitus due to a sigmoid sinus diverticulum and/or dehiscence who were successfully treated surgically via an extraluminal transmastoid approach.3 This was the first relatively large series published in the otologic literature. This publication likewise reported on the subtle radiologic signs that signify the presence of a sigmoid sinus diverticulum and/or dehiscence, such as an irregularity of the normal semicircular contour of the bony sinus wall, focal thinning of the calvarial cortex overlying the adjacent sinus wall, absence of the normal thin layer of cortical bone overlying the sinus, and the "air-on-sinus" sign, where mastoid air cells directly contact the sinus wall, without overlying bone.3</p><p style="text-align: justify;">In light of this new information, the patient's imaging studies were re-evaluated, and evidence of a right-sided sigmoid sinus diverticulum and/or dehiscence was identified. The images below show the findings on an axial slice of the patient's temporal bone CT study.</p><p style="text-align: justify;"> </p><p style="text-align: justify;">How significant is this condition ? Sigmoid sinus diverticulum and/or dehiscence is being increasingly recognized as a common cause of pulsatile tinnitus. In fact, a recent study by Schoeff et al. found its prevalence to be 23% in patients with pulsatile tinnitus.4 As such, the identification of this condition is highly relevant, particularly because effective surgical management is available for its alleviation.</p>

Propofol inhibits lung cancer cell viability and induces cell apoptosis by upregulating microRNA-486 expression

Propofol is a frequently used intravenous anesthetic agent. Recent studies show that propofol exerts a number of non-anesthetic effects. The present study aimed to investigate the effects of propofol on lung cancer cell lines H1299 and H1792 and functional role of microRNA (miR)-486 in these effects. H1299 and/or H1792 cells were treated with or without propofol and transfected or not with miR-486 inhibitor, and then cell viability and apoptosis were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry. The expression of miR-486 was determined by quantitative real-time polymerase chain reaction (qRT-PCR) with or without propofol treatment. Western blot was performed to analyze the protein expression of Forkhead box, class O (FOXO) 1 and 3, Bcl-2 interacting mediator of cell death (Bim), and pro- and activated caspases-3. Results showed that propofol significantly increased the miR-486 levels in both H1299 and H1792 cells compared to untreated cells in a dose-dependent manner (P<0.05 or P<0.01). Propofol statistically decreased cell viability but increased the percentages of apoptotic cells and protein expressions of FOXO1, FOXO3, Bim, and pro- and activated caspases-3; however, miR-486 inhibitor reversed the effects of propofol on cell viability, apoptosis, and protein expression (P<0.05 or P<0.01). In conclusion, propofol might be an ideal anesthetic for lung cancer surgery by effectively inhibiting lung cancer cell viability and inducing cell apoptosis. Modulation of miR-486 might contribute to the anti-tumor activity of propofol.