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Objective: To analyze the clinical efficacy and possible mechanism of butylphthalide in treatment of acute ischemic stroke. Methods: In this retrospective study, 127 patients with ischemic stroke, hospitalized during Jan. 2019 to Jan. 2021, were enrolled and as assigned to observation group (n=65) and control group (n=62) according to treatment methods. The control group received routine treatment, and the observation group was treated with butylphthalide injection in addition to conventional cure. The treatments lasted for 2 weeks in both groups. Subsequently, the recovery of neurological deficits (NIHSS) and Barthel index (BI) of the two groups of patients, cerebrovascular vascular reserve function (CVR) values and pulsation index (PI) before and after treatment, and the levels of brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF) and recombinant basic fibroblast growth factor (bFGF) were detected. The expression of Keap1-Nrf2/ARE signaling pathway related molecules was detected by ELISA. Results: The overall response rate (ORR) of observation group was remarkably superior to that of control group (P0.05). Conclusion: The butylphthalide can effectively improve the clinical efficacy of acute ischemic stroke, and promote patients’ neurological function and activities of daily living. The mechanism may be that butylphthalide improves the CVR of patients, enhances the establishment of collateral compensatory vessels, and changes the expression of the Keap1-Nrf2/ARE signaling pathway, thereby exerting the neuroprotective effect. Clinically, butylphthalide may have good safety in adjuvant therapy of acute ischemic stroke.

Additional file 5. Supplementary Tables.

Additional file 2. Additional results of UPIP-qPCR.

Additional file 1. Detailed Materials and Methods for UPIP-qPCR.

Attention-deficit hyperactivity disorder (ADHD) is a complex polygenic disorder. This study aimed to discover common and rare DNA variants associated with ADHD in a large homogeneous Han Chinese ADHD case-control sample. The sample comprised 1,040 cases and 963 controls. All cases met DSM-IV ADHD diagnostic criteria. We used the Affymetrix6.0 array to assay both single nucleotide polymorphisms (SNPs) and copy number variants (CNVs). Genome-wide association analyses were performed using PLINK. SNP-heritability and SNP-genetic correlations with ADHD in Caucasians were estimated with genome-wide complex trait analysis (GCTA). Pathway analyses were performed using the Interval enRICHment Test (INRICH), the Disease Association Protein-Protein Link Evaluator (DAPPLE), and the Genomic Regions Enrichment of Annotations Tool (GREAT). We did not find genome-wide significance for single SNPs but did find an increased burden of large, rare CNVs in the ADHD sample (P=0.038). SNP-heritability was estimated to be 0.42 (standard error, 0.13, P=0.0017) and the SNP-genetic correlation with European Ancestry ADHD samples was 0.39 (SE 0.15, P=0.0072). The INRICH, DAPPLE, and GREAT analyses implicated several gene ontology cellular components, including neuron projections and synaptic components, which are consistent with a neurodevelopmental pathophysiology for ADHD. This study suggested the genetic architecture of ADHD comprises both common and rare variants. Some common causal variants are likely to be shared between Han Chinese and Caucasians. Complex neurodevelopmental networks may underlie ADHD's etiology. (c) 2013 Wiley Periodicals, Inc. Refereed/Peer-reviewed