No abstract

BackgroundThe incidence of gastroesophageal reflux disease (GERD) has been shown to be elevated in individuals with epilepsy. Traditional observational studies have led to a limited understanding of the effects of GERD and BE on epilepsy due to the interference of reverse causation and potential confounders.MethodsWe conducted a bidirectional two‐sample Mendelian randomization (MR) analysis to determine whether GERD and BE can increase the risk of epilepsy. Genome‐wide association study data on epilepsy and its subgroups were obtained from the International League Against Epilepsy consortium for primary analysis using three MR approaches and the FinnGen consortium for replication and meta‑analysis. We calculated causal estimates between the two esophageal diseases and epilepsy using the inverse‐variance weighted method. Sensitivity analysis was conducted to detect heterogeneity and pleiotropy.ResultsWe found a potential effect of genetically predicted GERD on the risk of epilepsy (odds ratio [OR] = 1.078; 95% confidence interval [CI], 1.014–1.146, p = .016). Specifically, GERD showed an effect on the risk of generalized epilepsy (OR = 1.163; 95% CI, 1.048–1.290, p = .004) but not focal epilepsy (OR = 1.059, 95% CI, 0.992–1.131, p = .084). Notably, BE did not show a significant causal relationship with the risks of generalized and focal epilepsy.ConclusionsUnder MR assumptions, our findings suggest a potential risk‐increasing effect of GERD on epilepsy, especially generalized epilepsy. Considering the exploratory nature of our study, the association between GERD and epilepsy needs to be confirmed by future prospective studies.

Background Previous studies have found a correlation between coronavirus disease 2019 (COVID-19) and changes in brain structure and cognitive function, but it remains unclear whether COVID-19 causes brain structural changes and which specific brain regions are affected. Herein, we conducted a Mendelian randomization (MR) study to investigate this causal relationship and to identify specific brain regions vulnerable to COVID-19. Methods Genome-wide association study (GWAS) data for COVID-19 phenotypes (28,900 COVID-19 cases and 3,251,161 controls) were selected as exposures, and GWAS data for brain structural traits (cortical thickness and surface area from 51,665 participants and volume of subcortical structures from 30,717 participants) were selected as outcomes. Inverse-variance weighted method was used as the main estimate method. The weighted median, MR-Egger, MR-PRESSO global test, and Cochran’s Q statistic were used to detect heterogeneity and pleiotropy. Results The genetically predicted COVID-19 infection phenotype was nominally associated with reduced cortical thickness in the caudal middle frontal gyrus (β = − 0.0044, p = 0.0412). The hospitalized COVID-19 phenotype was nominally associated with reduced cortical thickness in the lateral orbitofrontal gyrus (β = − 0.0049, p = 0.0328) and rostral middle frontal gyrus (β = − 0.0022, p = 0.0032) as well as with reduced cortical surface area of the middle temporal gyrus (β = − 10.8855, p = 0.0266). These causal relationships were also identified in the severe COVID-19 phenotype. Additionally, the severe COVID-19 phenotype was nominally associated with reduced cortical thickness in the cuneus (β = − 0.0024, p = 0.0168); reduced cortical surface area of the pericalcarine (β = − 2.6628, p = 0.0492), superior parietal gyrus (β = − 5.6310, p = 0.0408), and parahippocampal gyrus (β = − 0.1473, p = 0.0297); and reduced volume in the hippocampus (β = − 15.9130, p = 0.0024). Conclusions Our study indicates a suggestively significant association between genetic predisposition to COVID-19 and atrophy in specific functional regions of the human brain. Patients with COVID-19 and cognitive impairment should be actively managed to alleviate neurocognitive symptoms and minimize long-term effects.

Introduction: Keratosis pilaris (KP) is a disfiguring disease and is resistant to treatment. Several treatment methods are available, but the efficacy is limited. This prospective, rater-blinded, split-body comparative study investigated the efficacy and safety of long-pulsed 755-nm alexandrite laser in the treatment of KP. Methods: Twenty-two patients with KP of bilateral arms were enrolled in this study. All participants were randomized and treated with a long-pulsed 755-nm alexandrite laser on the left or right arm in four sessions held 3 weeks apart. The unified moisturizing lotion was applied on both left and right arms once a day. Physicians' assessment scores and patients' selfassessment scores were recorded, and skin imaging changes in dermoscopy, high-frequency ultrasound, and skin biopsy were obtained at baseline and 4 weeks after the fourth treatment. Results: Of the 21 patients who completed the study, 15 were women and 6 were men. At 4 weeks after the fourth treatment, the laser side