Meta-analysis reveals a reduced surface area of the amygdala in individuals with attention deficit/hyperactivity disorder.

Despite the reported lack of structural alterations in the amygdala of individuals with attention deficit/hyperactivity disorder (ADHD) in previous meta-analyses, subsequent observational studies produced conflicting results. Through incorporating the updated data from observational studies on structural features of the amygdala in ADHD, the primary goal of this study was to examine the anatomical differences in amygdala between subjects with ADHD and their neurotypical controls. Using the appropriate keyword strings, we searched the PubMed, Embase, and Web of Science databases for English articles from inception to February 2022. Eligibility criteria included observational studies comparing the structure of the amygdala between ADHD subjects and their comparators using magnetic resonance imaging (MRI). Subgroup analyses were conducted focusing on the amygdala side, as well as the use of different scanners and approach to segmentation. The effects of other continuous variables, such as age, intelligence quotient, and male percentage, on amygdala size were also investigated. Of the 5703 participants in 16 eligible studies, 2928 were diagnosed with ADHD. Compared with neurotypical controls, subjects with ADHD had a smaller amygdala surface area (particularly in the left hemisphere) but without a significant difference in volume between the two groups. Subgroup analysis of MRI scanners and different approaches to segmentation showed no statistically significant difference. There was no significant correlation between continuous variables and amygdala size. Our results showed consistent surface morphological alterations of the amygdala, in particular on the left side, in subjects with ADHD. However, the preliminary findings based on the limited data available for analysis warrant future studies for verification.

DL-3-n-butylphthalide protects H9c2 cardiomyoblasts from ischemia/reperfusion injury by regulating HSP70 expression via PI3K/AKT pathway activation.

DL-3-n-butylphthalide (NBP) is commonly used to treat ischemic strokes due to its antioxidative and anti-inflammatory effects. The present study aimed to examine the protective effects of NBP on myocardial ischemia-reperfusion injury (MIRI) by establishing a MIRI model in H9c2 cells. Cell viability assay using Cell Counting Kit-8, lactate dehydrogenase (LDH) cytotoxicity and lipid peroxidation malondialdehyde (MDA) content were assessed to detect cell activity, degree of cell injury and oxidative stress reaction. Reverse transcription-quantitative PCR was used to quantify the expression of inflammatory factors in H9c2 cells. Western blotting and immunofluorescence staining were used to detect the protein expression of PI3K/AKT and heat shock protein 70 (HSP70). The present results indicated that NBP significantly increased cell viability during ischemia-reperfusion. Moreover, NBP inhibited the release of LDH and the production of MDA. NBP treatment also significantly decreased the expression of inflammatory factors at the mRNA level. Additionally, NBP activated the PI3K/AKT pathway and upregulated the expression of HSP70 compared with cells in the MIRI model. LY294002, a PI3K inhibitor, reversed the protective effects of NBP and suppressed the expression of HSP70. The present study demonstrated that NBP protected H9c2 cells from MIRI by regulating HSP70 expression via PI3K/AKT pathway activation.