NMDA receptors play dual and opposing roles in neuronal survival by mediating the activity‐dependent neurotrophic signaling and excitotoxic cell death via synaptic and extrasynaptic receptors, respectively. In this study, we demonstrate that the aryl hydrocarbon receptor (AhR), also known as the dioxin receptor, is involved in the expression and the opposing activities of NMDA receptors. In primary cultured cortical neurons, we found that NMDA excitotoxicity is significantly enhanced by an AhR agonist 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin, and AhR knockdown with small interfering RNA significantly reduces NMDA excitotoxicity. AhR knockdown also significantly reduces NMDA‐increases intracellular calcium concentration, NMDA receptor expression and surface presentation, and moderately decreases the NMDA receptor‐mediated spontaneous as well as miniature excitatory post‐synaptic currents. However, AhR knockdown significantly enhances the bath NMDA application– but not synaptic NMDA receptor‐induced brain‐derived neurotrophic factor (BDNF) gene expression, and activating AhR reduces the bath NMDA‐induced BDNF expression. Furthermore, AhR knockdown reveals the calcium dependency of NMDA‐induced BDNF expression and the binding activity of cAMP‐responsive element binding protein (CREB) and its calcium‐dependent coactivator CREB binding protein (CBP) to the BDNF promoter upon NMDA treatment. Together, our results suggest that AhR opposingly regulates NMDA receptor‐mediated excitotoxicity and neurotrophism possibly by differentially regulating the expression of synaptic and extrasynaptic NMDA receptors.

Mycotic aneurysm of the aorta is a life-threatening disease, especially when rupture occurs. The high mortality rate is due not only to the high rupture rate, but also to sepsis. When mycotic aortic aneurysm is diagnosed, early surgical intervention is mandatory.

This paper studies the amplitude-frequency characteristic of frontal steady-state visual evoked potential (SSVEP) and its feasibility as a control signal for brain computer interface (BCI). SSVEPs induced by different stimulation frequencies, from 13 ~ 31 Hz in 2 Hz steps, were measured in eight young subjects, eight elders and seven ALS patients. Each subject was requested to participate in a calibration study and an application study. The calibration study was designed to find the amplitude-frequency characteristics of SSVEPs recorded from Oz and Fpz positions, while the application study was designed to test the feasibility of using frontal SSVEP to control a two-command SSVEP-based BCI. The SSVEP amplitude was detected by an epoch-average process which enables artifact-contaminated epochs can be removed. The seven ALS patients were severely impaired, and four patients, who were incapable of completing our BCI task, were excluded from calculation of BCI performance. The averaged accuracies, command transfer intervals and information transfer rates in operating frontal SSVEP-based BCI were 96.1%, 3.43 s/command, and 14.42 bits/min in young subjects; 91.8%, 6.22 s/command, and 6.16 bits/min in elders; 81.2%, 12.14 s/command, and 1.51 bits/min in ALS patients, respectively. The frontal SSVEP could be an alternative choice to design SSVEP-based BCI.

A length polymorphism of GT repeats in the promoter region of the human heme oxygenase-1 (HO-1) gene modulates its gene transcription to protect against myocardial injury. The present study investigated the association between HO-1 promoter polymorphisms and the outcomes of catheter ablation of atrial fibrillation (AF). The allelic frequencies of GT repeats in the HO-1 gene promoter were screened in 205 random individuals who underwent catheter ablation for drug refractory AF.In the patients who received catheter ablation, those with AF recurrence had fewer GT repeats (53.4±7.1 vs. 56.1±6.5, p = 0.004), a lower incidence of hyperlipidemia, more non-paroxysmal AF, and a larger left atrial diameter. After conducting a multivariate logistic analysis, the number of GT repeats (Odds ratio: 0.94, 95% CI 0.90–0.99, p = 0.01) and the diameter of the left atrium (Odds ratio: 1.08, 95% CI 1.02–1.15, p = 0.01) remained independent predictors. The carriers of GT repeats, which were <29 in both alleles, were associated with a lower sinus maintenance rate after catheter ablation (38.5% vs. 60.1%, p = 0.003). The patients were divided into paroxysmal and non-paroxysmal AF groups; the number of GT repeats was associated with AF recurrence only in the patients with paroxysmal AF. The number of GT repeats, combined with LAD, was significant for predicting AF recurrence after catheter ablation (p = 0.01). The number of GT repeats was not found to be associated with differences in the left atrial diameter, the biatrial voltage, or the levels of bilirubin, ferritin, iron, C-reactive protein, or von-Willibrand factor. In conclusions, HO-1 gene promoter polymorphisms were associated with AF recurrence after catheter ablation.

A right-sided aortic arch with an aneurysm of the aberrant subclavian artery is a rare disease. We report a case of Kommerell's diverticulum of an aberrant left subclavian artery in a patient with a right-sided aortic arch. Fewer than 50 cases have been reported in the literature. A number of operative strategies are described. Right thoracotomy provides good exposure and avoids the morbidity associated with bilateral thoracotomy or sternotomy and thoracotomy. In our patient with symptoms of dysphagia, syncope, and left subclavian steal syndrome, a left thoracotomy was used. The repair was accomplished by division of a left ligamentum arteriosum, obliteration of the Kommerell's aneurysm, and an aorto-subclavian bypass. Postoperative complications included left vocal cord palsy and Horner's syndrome. Hoarseness and left ptosis recovered spontaneously 3 months after surgery, and the patient remained symptom-free at the 1-year follow-up. We believe a left thoracotomy for direct repair of Kommerell's diverticulum is a simple and safe method without the increased morbidity found in other procedures.