Glucocorticoid signaling mediates stress-induced migraine-like behaviors in a preclinical mouse model.

Background: Stress is one of the most common precipitating factors in migraine and is identified as a trigger in nearly 70% of patients. Responses to stress include release of glucocorticoids as an adaptive mechanism, but this may also contribute to migraine attacks. Here, we investigated the role of glucocorticoids on stress-induced migraine-like behaviors.

Ultrapulse carbon dioxide dot matrix laser for facial scar treatment: A meta-analysis.

A meta-analysis was performed to investigate the efficacy of ultrapulse carbon dioxide dot matrix laser treatment for patients with facial scars. PubMed, EMBASE, Cochrane Library, China National Knowledge Infrastructure, China Biomedical Literature Database, and Wanfang Database were systematically searched for randomised controlled trials (RCTs) investigating ultrapulse carbon dioxide dot matrix laser treatment for facial scars, and the search was conducted from the time of database inception to July 2023. The retrieved literature was screened independently by two researchers, and data extraction and quality assessments were performed.

Efficacy of dual enkephalinase inhibition in a preclinical migraine model is mediated by activation of peripheral delta opioid receptors.

Objective: The aim of this study was to evaluate whether elevating levels of enkephalin by inhibiting their degradation can attenuate stress-induced migraine-like behaviors in mice.

Background: Previous studies in animals have suggested the delta opioid receptor (DOR) as a novel migraine target. The primary endogenous ligands for DOR are enkephalins and their levels can be increased by pharmacological inhibition of enkephalinases; however, it is not clear whether enkephalinase inhibition can be efficacious in preclinical migraine models through activation of DOR or whether other opioid receptors might be involved.

Molecular mechanism of microRNA-26a regulation of phosphatase and tensin homolog gene in condyloma acuminatum and penile squamous cell carcinoma.

Objective: To investigate the expression levels and mechanisms of microRNA (miRNA) 26a (miR-26a) and phosphatase and tensin homolog (PTEN) in patients with human papillomavirus (HPV)-induced condyloma acuminatum (CA) and penile squamous cell carcinoma (PSCC).

Methods: Thirty-one patients with HPV-positive CA and 28 with HPV-positive PSCC were included in this retrospective, cross-sectional study. PTEN mRNA and miR-26a levels in lesion tissues, blood, and urine were analyzed by quantitative reverse transcription polymerase chain reaction, and PTEN protein was detected by western blot and enzyme-linked immunosorbent assay.

Correction to: Soluble Epoxide Hydrolase Inhibition Attenuates Excitotoxicity Involving 14,15-Epoxyeicosatrienoic Acid-Mediated Astrocytic Survival and Plasticity to Preserve Glutamate Homeostasis.

The original version of this article unfortunately contained a mistake. The authors observed inadvertent error in Fig. 7d, in which the image of the GFAP/DAPI in the WT saline treated mice was rotated left 90-degree by mistake.

Soluble Epoxide Hydrolase Inhibition Attenuates Excitotoxicity Involving 14,15-Epoxyeicosatrienoic Acid-Mediated Astrocytic Survival and Plasticity to Preserve Glutamate Homeostasis.

Astrocytes play pivotal roles in regulating glutamate homeostasis at tripartite synapses. Inhibition of soluble epoxide hydrolase (sEHi) provides neuroprotection by blocking the degradation of 14,15-epoxyeicosatrienoic acid (14,15-EET), a lipid mediator whose synthesis can be activated downstream from group 1 metabotropic glutamate receptor (mGluR) signaling in astrocytes. However, it is unclear how sEHi regulates glutamate excitotoxicity.