Y-configuration Stent-assisted Coil Embolization for Wide-necked Intracranial Bifurcation Aneurysms

OBJECTIVE: The objective of this study was to determine the efficiency and safety of Y configuration stent-assisted coiling with double-closed stents for wide-necked intracranial aneurysms located at arterial bifurcations thorough analysis of a multicenter case series. MATERIALS AND METHODS: A retrospective chart review was done on 10 patients who underwent endovascular treatment of wide-necked intracranial aneurysms with Y-configuration stent-assisted coil embolization in three centers from August 2011 to March 2014. The degree of aneurysmal occlusion was assessed using the Raymond scale. Clinical outcomes were assessed before operation, at discharge, and at the last follow-up visit using the Glasgow outcome scale. RESULTS: The 10 patients included 6 females and 4 males with a mean age of 58.6 years. Indications for treatment included 6 unruptured intracranial aneurysms and 4 ruptured intracranial aneurysms. Five aneurysms were located at the basilar artery bifurcation, four aneurysms were located in an anterior communicating artery, and one aneurysm was in the pericallosal artery. The mean size of the 10 aneurysms was 9.7 mm. All aneurysms had a dome-to-neck ratio of < 1.5 (mean, 0.89). Immediate complications included one thromboembolic event out of the 10 cases. Immediate posttreatment angiograms showed complete occlusion in 1 aneurysm and residual necks in 9 aneurysms. Follow-up results showed 8 complete occlusions and 2 residual necks. No delayed complications were observed during the follow-up period (mean: 20 months). CONCLUSION: Y configuration using double-closed cell stents is feasible and safe in selected patients. This method is an acceptable option for managing complex wide-necked bifurcations.

Persistent Primitive Trigeminal Artery That Mimics Persistent Primitive Otic Artery on Cerebral Angiography

Persistent primitive trigeminal artery (PPTA) is the most common carotid-basilar anastomosis; on the other hand, persistent primitive otic artery (PPOA) is extremely rare. PPTA is often misdiagnosed as PPOA on cerebral angiography. We present a case of PPTA that mimicked PPOA on cerebral angiography. We further describe the utility of brain computed tomography angiography for differential diagnosis of PPTA from PPOA, together with a review of previous literature.

Effect of Resveratrol, a SIRT1 Activator, on the Interactions of the CLOCK/BMAL1 Complex

BACKGROUND: In mammals, the CLOCK/BMAL1 heterodimer is a key transcription factor complex that drives the cyclic expression of clock-controlled genes involved in various physiological functions and behavioral consequences. Recently, a growing number of studies have reported a molecular link between the circadian clock and metabolism. In the present study, we explored the regulatory effects of SIRTUIN1 (SIRT1), an NAD+-dependent deacetylase, on CLOCK/BMAL1-mediated clock gene expression. METHODS: To investigate the interaction between SIRT1 and CLOCK/BMAL1, we conducted bimolecular fluorescence complementation (BiFC) analyses supplemented with immunocytochemistry assays. BiFC experiments employing deletion-specific mutants of BMAL1 were used to elucidate the specific domains that are necessary for the SIRT1-BMAL1 interaction. Additionally, luciferase reporter assays were used to delineate the effects of SIRT1 on circadian gene expression. RESULTS: BiFC analysis revealed that SIRT1 interacted with both CLOCK and BMAL1 in most cell nuclei. As revealed by BiFC assays using various BMAL1 deletion mutants, the PAS-B domain of BMAL1 was essential for interaction with SIRT1. Activation of SIRT1 with resveratrol did not exert any significant change on the interaction with the CLOCK/BMAL1 complex. However, promoter analysis using Per1-Luc and Ebox-Luc reporters showed that SIRT1 significantly downregulated both promoter activities. This inhibitory effect was intensified by treatment with resveratrol, indicating a role for SIRT1 and its activator in CLOCK/BMAL1-mediated transcription of clock genes. CONCLUSION: These results suggest that SIRT1 may form a regulatory complex with CLOCK/BMAL1 that represses clock gene expression, probably via deacetylase activity.