Objective: To evaluate the effects of Capsosiphon fulvescens (C. fulvescens) ethanolic extract on inflammation in lipopolysaccharide (LPS)-induced RAW296.7 macrophages. Methods: The protective effects of C. fulvescens ethanolic extract on LPS-induced inflammation in RAW264.7 macrophages were assessed using biochemical analysis, including enzyme-linked immunosorbent assay, quantitative reverse transcription-polymerase chain reaction, and Western blot analysis. To examine reactive oxygen species (ROS) production, flow cytometry analysis, and immunofluorescence staining were used. Furthermore, the modulatory effect of C. fulvescens ethanolic extract on NF-κB activation was investigated. Results: C. fulvescens ethanolic extract significantly attenuated LPS-induced levels of pro-inflammatory cytokines and notably reduced the secretion and mRNA levels of LPS-mediated matrix metalloproteinases. In addition, C. fulvescens ethanolic extract decreased ROS production and suppressed the TLR4/NF-κB signaling pathway. Conclusions: C. fulvescens ethanolic extract alleviates inflammation as well as oxidative stress by modulating the TLR4/NF-κB signaling in LPS-induced RAW264.7 macrophages. C. fulvescens can be used as a potential therapeutic agent to suppress inflammation and oxidative stress-associated diseases.

Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) is a rare primary headache disorder characterized by severe intractable stabbing headache and accompanying tearing and conjunctival injections. In this report, we present a case of a patient with SUNCT who achieved sustained remarkable improvement more than 6 months following successful treatment with a single session of botulinum toxin A, after being refractory or intolerant to several preventives for 4 months.

Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) is a rare primary headache disorder characterized by severe intractable stabbing headache and accompanying tearing and conjunctival injections. In this report, we present a case of a patient with SUNCT who achieved sustained remarkable improvement more than 6 months following successful treatment with a single session of botulinum toxin A, after being refractory or intolerant to several preventives for 4 months.

Objectives: This study aims to examine the differences in spectral analysis of waking electroencephalography (EEG) patterns between patients with moderate to severe obstructive sleep apnea (OSA) experiencing excessive daytime sleepiness (EDS) and matched healthy participants, to gain insights into the neurophysiological underpinnings of daytime impairments. Methods: A cross-sectional analysis was conducted involving 17 patients with moderate to severe OSA confirmed by overnight polysomnography (PSG). These patients had ≥15 per hour apnea–hypopnea index (AHI) and ≥11 Epworth Sleepiness Scale (ESS). EEG recordings were captured within 30 minutes of awakening. A corresponding group of the equal number of age and sex-matched healthy participants was also analyzed for comparative purposes. Spectral analysis of quantitative EEG (qEEG) of patients with OSA compared with that of an equal number of age- and sex-matched healthy participants. Results: The analysis included 17 patients (16 males, average age 57.2 years) with moderate to severe OSA experiencing EDS (mean AHI 38.1±20.5; ESS 14.4±3.2). The patients with OSA exhibited altered sleep architecture during diagnostic PSG, significantly higher EEG delta band power in the frontal regions upon awakening after night sleep, and decreased connection of delta band in frontal area than normal participants (3.78±5.53 vs. 3.22±0.98 μV2, p=0.03). Conclusions The study demonstrated difference in delta activity and connectivity in the frontal area between patients with OSA experiencing EDS and the control group. These findings suggest awakening qEEG in OSA may helpful to guide or enhance understanding of daytime functional impairment and EDS.

Objectives: This study aims to examine the differences in spectral analysis of waking electroencephalography (EEG) patterns between patients with moderate to severe obstructive sleep apnea (OSA) experiencing excessive daytime sleepiness (EDS) and matched healthy participants, to gain insights into the neurophysiological underpinnings of daytime impairments. Methods: A cross-sectional analysis was conducted involving 17 patients with moderate to severe OSA confirmed by overnight polysomnography (PSG). These patients had ≥15 per hour apnea–hypopnea index (AHI) and ≥11 Epworth Sleepiness Scale (ESS). EEG recordings were captured within 30 minutes of awakening. A corresponding group of the equal number of age and sex-matched healthy participants was also analyzed for comparative purposes. Spectral analysis of quantitative EEG (qEEG) of patients with OSA compared with that of an equal number of age- and sex-matched healthy participants. Results: The analysis included 17 patients (16 males, average age 57.2 years) with moderate to severe OSA experiencing EDS (mean AHI 38.1±20.5; ESS 14.4±3.2). The patients with OSA exhibited altered sleep architecture during diagnostic PSG, significantly higher EEG delta band power in the frontal regions upon awakening after night sleep, and decreased connection of delta band in frontal area than normal participants (3.78±5.53 vs. 3.22±0.98 μV2, p=0.03). Conclusions The study demonstrated difference in delta activity and connectivity in the frontal area between patients with OSA experiencing EDS and the control group. These findings suggest awakening qEEG in OSA may helpful to guide or enhance understanding of daytime functional impairment and EDS.

Objectives: This study aims to examine the differences in spectral analysis of waking electroencephalography (EEG) patterns between patients with moderate to severe obstructive sleep apnea (OSA) experiencing excessive daytime sleepiness (EDS) and matched healthy participants, to gain insights into the neurophysiological underpinnings of daytime impairments. Methods: A cross-sectional analysis was conducted involving 17 patients with moderate to severe OSA confirmed by overnight polysomnography (PSG). These patients had ≥15 per hour apnea–hypopnea index (AHI) and ≥11 Epworth Sleepiness Scale (ESS). EEG recordings were captured within 30 minutes of awakening. A corresponding group of the equal number of age and sex-matched healthy participants was also analyzed for comparative purposes. Spectral analysis of quantitative EEG (qEEG) of patients with OSA compared with that of an equal number of age- and sex-matched healthy participants. Results: The analysis included 17 patients (16 males, average age 57.2 years) with moderate to severe OSA experiencing EDS (mean AHI 38.1±20.5; ESS 14.4±3.2). The patients with OSA exhibited altered sleep architecture during diagnostic PSG, significantly higher EEG delta band power in the frontal regions upon awakening after night sleep, and decreased connection of delta band in frontal area than normal participants (3.78±5.53 vs. 3.22±0.98 μV2, p=0.03). Conclusions The study demonstrated difference in delta activity and connectivity in the frontal area between patients with OSA experiencing EDS and the control group. These findings suggest awakening qEEG in OSA may helpful to guide or enhance understanding of daytime functional impairment and EDS.

Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) is a rare primary headache disorder characterized by severe intractable stabbing headache and accompanying tearing and conjunctival injections. In this report, we present a case of a patient with SUNCT who achieved sustained remarkable improvement more than 6 months following successful treatment with a single session of botulinum toxin A, after being refractory or intolerant to several preventives for 4 months.

Switch/sucrose non-fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1)-deficient sinonasal carcinoma is a rare subtype of sinonasal undifferentiated carcinoma (SNUC). Due to the highly aggressive nature of the disease course, it is important to diagnose early and use multimodal treatments in the course of the disease. Two main morphologic patterns are commonly identified under the microscope: plasmacytoid/rhabdoid and basaloid. Furthermore, it demonstrates a total absence of integrase interactor 1 expression upon immunohistochemical staining. Here, we present two cases of SMARCB1-deficient sinonasal carcinoma with contrasting outcomes.

Objective: Vertebral artery dissecting aneurysm (VADA) is a rare and critical disease. VADA rupture can cause subarachnoid hemorrhage which is a major complication of VADA due to their high rebleeding rate and poor outcome. In the present study, ruptured and unruptured VADAs were compared by analyzing angiographic findings to determine useful predisposing factors for VADA rupture for appropriate treatment selection. Methods: Subjects with VADA treated during a 10-year period were retrospectively identified. The 57 cases diagnosed with VADA were divided into ruptured (n=15) and unruptured (n=42) groups. In addition, each case was analyzed using angiographic 3-dimensional (3-D) reconstructed images. Factors such as length, dilated and stenotic diameter, shape, and vessel around the vertebral artery (VA) were measured and statistically compared. Results: In the ruptured group, stenotic findings of the affected lesion were more common and severe than in the unruptured group. The average stenotic diameter was 2.27 mm (vs. 2.84 mm). And stenotic degree was 62% and 53% in the ruptured and unruptured groups, respectively. Posterior communicating artery (PcomA) flow was more common in the ruptured group (87% vs. 55%, p=0.028). Conclusions Based on angiographic findings, stenotic lesions, which may be influenced by PcomA flow, are more common in ruptured VADAs.

This study elucidates the anti-cancer potential of gallic acid (GA) as a promising therapeutic agent that exerts its effect by regulating the PI3K/Akt pathway. To prove our research rationale, we used diverse experimental methods such as cell viability assay, colony formation assay, tumor spheroid formation assay, cell cycle analysis, TUNEL assay, Western blot analysis, xenograft mouse model and histological analysis. Treatment with GA inhibited cell proliferation in dose-dependent manner as measured by cell viability assay at 48 h. GA and cisplatin (CDDP) also inhibited colony formation and tumor spheroid formation. In addition, GA and CDDP induced apoptosis, as determined by the distribution of early and late apoptotic cells and DNA fragmentation. Western blot analysis revealed that inhibition of the PI3K/Akt pathway induced upregulation of p53 (tumor suppressor protein), which in turn regulated cell cycle related proteins such as p21, p27, Cyclin D1 and E1, and intrinsic apoptotic proteins such as Bax, Bcl-2 and cleaved caspase-3. The anti-cancer effect of GA was further confirmed in an in vivo mouse model. Intraperitoneal injection with GA for 4 weeks in an A549-derived tumor xenograft model reduced the size of tumor mass. Injection of them downregulated the expression of proliferating cell nuclear antigen and p-Akt, but upregulated the expression of cleaved caspase-3 in tumor tissues. Taken together, these results indicated that GA hindered lung cancer progression by inducing cell cycle arrest and apoptosis, suggesting that GA would be a potential therapeutic agent against non-small cell lung cancer.