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Clin Neurophysiol 2021 Apr 28;132(4):977-983. Epub 2021 Jan 28.

Department of Anesthesiology, Washington University School of Medicine in St. Louis, St. Louis, MO, USA; Division of Biology and Biomedical Sciences, Washington University School of Medicine in St. Louis, St. Louis, MO, USA; Department of Psychiatry, Washington University School of Medicine in St. Louis, St. Louis, MO, USA; Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, MO, USA. Electronic address:

Objective: Postictal generalized electroencephalographic suppression (PGES) has been defined as electroencephalographic (EEG) activity of less than 10 microvolts following a generalized seizure. PGES is associated with an increased risk of sudden unexplained death in epilepsy, as well as treatment efficacy of electroconvulsive therapy (ECT). We investigated the impact of anesthetic on PGES expression and temporal characteristics. Read More

Reprod Fertil Dev 2021 Feb;33(3):209-219

College of Animal Science and Technology, No. 61 Daizong Street, Taian, Shandong Province, 271018, PR China; and Corresponding authors. Email:

Previous studies demonstrated that progesterone (P4) can promote prostaglandin (PG) E2 production; however, how P4 mediates the synthesis of PGE2 remains unclear. In this study, cervical epithelial cells from mice during the follicular phase were cultured invitro and treated with different concentrations of P4 (5, 10, and 20nM). The results of the present study suggest that treatment of murine cervical epithelial cells with 10nM P4 for 24h contributed to: (1) significantly increased expression of protein kinase A (PKA), cytosolic phospholipase A2 (cPLA2) and PGE synthase (PGES)-1; (2) higher phosphorylated (p-) to total extracellular signal-regulated kinase (ERK) 1/2 and hormone-sensitive lipase (HSL) ratios; (3) a significant decrease in the number of lipid droplets (LDs) and fatty acid content within LDs in epithelial cells; and (4) enhanced arachidonic acid and PGE2 levels in cells compared with the control (0nM P4) group (P<0. Read More

Mediators Inflamm 2020 12;2020:4301072. Epub 2020 Nov 12.

Department of Anaesthesiology and Intensive Care Medicine, Charité-University Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Campus Benjamin Franklin, Berlin, Germany.

A complex inflammatory process mediated by proinflammatory cytokines and prostaglandins commonly occurs in the synovial tissue of patients with joint trauma (JT), osteoarthritis (OA), and rheumatoid arthritis (RA). This study systematically investigated the distinct expression profile of prostaglandin E2 (PGE2), its processing enzymes (COX-2), and microsomal PGES-1 (mPGES-1) as well as the corresponding prostanoid receptor subtypes (EP1-4) in representative samples of synovial tissue from these patients (JT, OA, and RA). Quantitative TaqMan®-PCR and double immunofluorescence confocal microscopy of synovial tissue determined the abundance and exact immune cell types expressing these target molecules. Read More

Neuroscience 2021 01 24;453:206-221. Epub 2020 Nov 24.

Interdisciplinary Graduate Program in Neuroscience, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, United States; Department of Neurology, Carver College of Medicine, Carver College of Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, United States; Iowa Neuroscience Institute, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, United States. Electronic address:

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in patients with refractory epilepsy. A proposed risk marker for SUDEP is the duration of post-ictal generalized EEG suppression (PGES). The mechanisms underlying PGES are unknown. Read More

Front Pharmacol 2020 25;11:532199. Epub 2020 Sep 25.

Department of Microbiology, Faculty of Medicine, Kuwait University, Kuwait City, Kuwait.

Despite significant advances, asthma remains a cause of premature death, and current treatments are suboptimal. Antigen-specific Th2 cells and their cytokines are primary mediators of the pathophysiological changes seen in asthma. Studies in animal models have shown that mycobacteria can suppress the asthma phenotype by alteration of the Th1/Th2 cytokines ratio. Read More