Objective: Diagnosis of anxiety has relied primarily on self-report. This study aimed to investigate the neural correlates of anxiety with quantitative electroencephalography (qEEG) focusing on the state and trait anxiety defined according to the Research Domain Criteria framework existing across the differential diagnosis, rather than focusing on the diagnosis. Methods: A total of 41 participants who visited a psychiatric clinic underwent resting state EEG and completed the State-Trait Anxiety Inventory. The absolute power of six frequency bands were analyzed: delta (1–4 Hz), theta (4–8 Hz), alpha (8–10 Hz), fast alpha (10–13.5 Hz), beta (13.5–30 Hz), and gamma (30–80 Hz). Results: State anxiety scores were significantly negatively correlated with absolute gamma power in frontal (Fz, r=-0.484) and central (Cz, r=-0.523) regions, while trait anxiety scores were significantly negatively correlated with absolute gamma power in frontal (Fz, r= -0.523), central (Cz, r=-0.568), parietal (P7, r=-0.500; P8, r=-0.541), and occipital (O1, r=-0.510; O2, r=-0.480) regions. Conclusion The present study identified the significantly negative correlations between the anxiety level and gamma band power in fronto-central and posterior regions assessed at resting status. Further studies to confirm our findings and identify the neural correlates of anxiety are needed.

Syncopes are the most common non-epileptic attacks mimicking epileptic seizures. Among them, cardiogenic syncope is potentially life threatening. A 49 year old man was refered for the recurrent episodes of loss of consciousness with tonic posture and upward eyes deviation. The electrocardiogram showed polymorphologic ventricular tachycardia during attacks, which normalized after that. He was treated with isoproterenol and symptoms subsided. Here, we report a case of ventricular tachycardia manifested as epileptic seizures.
Electrocardiography ; Epilepsy* ; Isoproterenol ; Posture ; Seizures ; Syncope ; Tachycardia, Ventricular* ; Unconsciousness

Purpose: Agonists of the stimulator of interferon genes (STING) play a key role in activating the STING pathway by promoting the production of cytokines. In this study, we investigated the antitumor effects and activation of the systemic immune response of treatment with DMXAA (5,6-dimethylxanthenone-4-acetic acid), a STING agonist, in EML4-ALK lung cancer and CT26 colon cancer. Materials and Methods: The abscopal effects of DMXAA in the treatment of metastatic skin nodules were assessed. EML4-ALK lung cancer and CT26 colon cancer models were used to evaluate these effects after DMXAA treatment. To evaluate the expression of macrophages and T cells, we sacrificed the tumor-bearing mice after DMXAA treatment and obtained the formalin-fixed paraffin-embedded (FFPE) tissue and tumor cells. Immunohistochemistry and flow cytometry were performed to analyze the expression of each FFPE and tumor cell. Results: We observed that highly infiltrating immune cells downstream of the STING pathway had increased levels of chemokines after DMXAA treatment. In addition, the levels of CD80 and CD86 in antigen-presenting cells were significantly increased after STING activation. Furthermore, innate immune activation altered the systemic T cell-mediated immune responses, induced proliferation of macrophages, inhibited tumor growth, and increased numbers of cytotoxic memory T cells. Tumor-specific lymphocytes also increased in number after treatment with DMXAA. Conclusion The abscopal effect of DMXAA treatment on the skin strongly reduced the spread of EML4-ALK lung cancer and CT26 colon cancer through the STING pathway and induced the presentation of antigens.