Sleep and Epilepsy

Sleep and epilepsy have a complex interrelationship that is influenced by various factors, including the distinct stages of sleep. Non-rapid eye movement sleep promotes epileptic activity, while rapid eye movement sleep suppresses it. Seizures can be triggered by sleep, while sleep deprivation increases seizure susceptibility. Epilepsy disrupts sleep architecture and quality, leading to sleep disturbances and comorbidities, like sleep apnea and restless legs syndrome. Excessive daytime sleepiness and fatigue can result from epilepsy and the sedating effects of antiseizure medications. Sleep-related epilepsy exhibits seizures predominantly during sleep, with specific patterns related to sleep stages. Antiseizure medications can directly impact sleep quality and should be carefully considered when treating epilepsy patients with comorbid sleep disorders. Understanding the bidirectional relationship between sleep and epilepsy is crucial for effective management. Optimizing treatment strategies requires recognizing the effects of antiseizure medications on sleep, and addressing sleep-related issues in individuals with epilepsy

Transient cortical visual impairment after video-assisted thoracic surgery: a case report

This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.Abstract Background Visual loss associated with thoracic surgery has been reported mostly after coronary angiography or bypass surgery. The position of video-assisted thoracic surgery (VATS) is usually lateral, thus not compressive to the globe. Visual loss after VATS has not been reported. Herein we report a patient without any cardiovascular risk factors who experienced transient cortical blindness after an uneventful VATS. Case presentation A 40-year-old man noticed a visual loss at the recovery room after VATS. He showed normal pupillary reflex, normal optic disc appearance, and homonymous hemianopia respecting the vertical meridian, thus was typical for cortical visual impairment. Conclusions Transient cortical visual impairment could be encountered after an uneventful VATS in a patient without any cardiovascular risk factors

Two Distinct Filopodia Populations at the Growth Cone Allow to Sense Nanotopographical Extracellular Matrix Cues to Guide Neurite Outgrowth

The process of neurite outgrowth is the initial step in producing the neuronal processes that wire the brain. Current models about neurite outgrowth have been derived from classic two-dimensional (2D) cell culture systems, which do not recapitulate the topographical cues that are present in the extracellular matrix (ECM) in vivo. Here, we explore how ECM nanotopography influences neurite outgrowth

Curcumin induces expression of 15-hydroxyprostaglandin dehydrogenase in gastric mucosal cells and mouse stomach in vivo: AP-1 as a potential target

15-Hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the conversion of oncogenic prostaglandin E-2 to non-tumerigenic 15-keto prostaglandin E-2. In the present study, we found that curcumin, a yellow coloring agent present in the rhizome of Curcuma Tonga Linn (Zingiberaceae), induced expression of 15-PGDH at the both transcriptional and translational levels in normal rat gastric mucosal cells. By using deletion constructs of 15-PGDH promoter, we were able to demonstrate that activator protein-1 (AP-1) is the principal transcription factor responsible for regulating curcumin-induced 15-PGDH expression. Curcumin enhanced the expression of c-jun and cFos that are functional subunits of AP-1, in the nuclear fraction of cells. Silencing of c-jun suppressed curcumin-induced expression of 15-PGDH. Moreover, the chromatin immunoprecipitation assay revealed curcumin-induced binding of c-Jun to the AP-1 consensus sequence present in the 15-PGDH promoter. Curaimin increased phosphorylation of ERK1/2 and JNK. and pharmacologic inhibition of these kinases abrogated the curcumin-induced phosphorylation of clun and 15-PGDH expression. In contrast, tetrahydrocurcumin which lacks the alpha,beta-unsaturated carbonyl group failed to induce 15-PGDH expression, suggesting that the electrophilic carbonyl group of curcumin is essential for its induction of 15-PGDH expression. Curcumin restored the expression of 15-PGDH which is down-regulated by Helicobater pylori through suppression of DNA methyltransferase 1. In addition, oral administration of curcumin increased the expression of 15-PGDH and its regulators such as p-ERK1/2, p-JNK and c-Jun in the mouse stomach. Taken together, these findings suggest that curcumin-induced upregulation of 15-PGDH may contribute to chemopreventive effects of this phytochemical on inflammation-associated gastric carcinogenesis. (C) 2020 Elsevier Inc. All rights reserved.

A Study of Micronucleus Induction with Methyl Formate and 2-Methylbutane in Bone Marrow Cells of Male ICR Mice

Objectives: We investigated the genotoxicity of two chemicals, methyl formate and 2-methylbutane, using male ICR mice bone marrow cells for the screening of micronucleus induction. Although these two chemicals have already been tested numerous times, a micronucleus test has not been conducted and the amounts used have recently been increased.Methods: 7 week male ICR mice were tested at dosages of 250, 500, and 1,000mg/kg for methyl formate and 500, 1,000, and 2,000mg/kg for 2-methlybutane, respectively. After 24 hours of oral administration with the two chemicals, the mice were sacrificed and their bone marrow cells were prepared for smearing slides.Results: As a result of counting the micronucleated polychromatic erythrocyte (MNPCE) of 2,000 polychromatic erythrocytes (PCE), all treated groups expressed no statistically significant increase of MNPCE compared to the negative control group. There were no clinical signs related with the oral exposure of these two chemicals.Conclusion: It was concluded that the two chemicals did not induce micronucleus in the bone marrow cells of ICR mice, and there was no direct proportion with dosage. These results indicate that the two chemicals have no mutagenic potential under each study condition

Combined Brown syndrome and superior oblique palsy without a trochlear nerve: case report

CCDD: congenital cranial dysinnervation disorder; MRI: magnetic resonance imaging; RHT: right hypertropia; SO: superior obliqueAbstract Background Congenital Brown syndrome is characterized by limited elevation particularly during adduction. The pathogenesis of congenital Brown syndrome is still controversial. Case presentation A 6-year-old boy had been tilting his head to the left since infancy. He showed right hypertropia (RHT) of 2 prism diopters (Δ) in the primary position. He showed RHT 6Δ in right gaze, RHT 2Δ in left gaze, RHT 12Δ in right head tilt, and orthotropia in left head tilt. The right eye showed limitation of elevation and depression on adduction, and the left eye showed overdepression on adduction. MR images showed an absent right trochlear nerve with a hypoplastic ipsilateral superior oblique muscle. Conclusions Congenital Brown syndrome may be associated with an absent trochlear nerve and hypoplastic superior oblique muscle suggesting an etiologic mechanism of congenital cranial dysinnervation disorder

Predictive Scale for Amyloid PET Positivity Based on Clinical and MRI Variables in Patients with Amnestic Mild Cognitive Impairment

The presence of amyloid-β (Aβ) deposition is considered important in patients with amnestic mild cognitive impairment (aMCI), since they can progress to Alzheimer's disease dementia. Amyloid positron emission tomography (PET) has been used for detecting Aβ deposition, but its high cost is a significant barrier for clinical usage. Therefore, we aimed to develop a new predictive scale for amyloid PET positivity using easily accessible tools. Overall, 161 aMCI patients were recruited from six memory clinics and underwent neuropsychological tests, brain magnetic resonance imaging (MRI), apolipoprotein E (APOE) genotype testing, and amyloid PET. Among the potential predictors, verbal and visual memory tests, medial temporal lobe atrophy, APOE genotype, and age showed significant differences between the Aβ-positive and Aβ-negative groups and were combined to make a model for predicting amyloid PET positivity with the area under the curve (AUC) of 0.856. Based on the best model, we developed the new predictive scale comprising integers, which had an optimal cutoff score ≥ 3. The new predictive scale was validated in another cohort of 98 participants and showed a good performance with AUC of 0.835. This new predictive scale with accessible variables may be useful for predicting Aβ positivity in aMCI patients in clinical practice