METHODS: Structural Equation Modeling (SEM) is utilized for analysis, enabling the creation of a metric set to explore intangibles such as perfectionism, learning self-efficacy, motivation, study habits, cultural influences, and introspection. The research utilizes a diverse sample from multiple universities across different regions of China, incorporating demographic factors to encompass the varied characteristics within the EFL learner community.
RESULTS: Results reveal that perfectionism (β = 0.30, p
METHODS: To achieve this goal, a systematic literature search was conducted in several databases, including Web of Science, ScienceDirect (EBSCO), SpringerLink, PubMed, and Wiley Online Library. The inclusion criteria were strictly implemented to ensure the quality of the studies included in the meta-analysis. In the end, a total of 5 studies, with 139 participants diagnosed with IGD and 139 healthy controls, were included in the analysis.
RESULTS: Meta-analysis revealed large effect sizes of N2 and P3 amplitudes in individuals with IGD, indicating that these two ERP components could be potential indicators of inhibitory control ability. Specifically, the N2 and P3 amplitude was significantly larger in individuals with IGD than in the healthy control group, suggesting deficits in inhibitory control function and increased impulsivity in the IGD group. In the inhibition control task, the IGD group required more cognitive resources to suppress impulsive responses.
CONCLUSION: Overall, the findings of this meta-analysis shed light on the potential use of N2 and P3 amplitudes as reliable indicators of inhibitory control ability in individuals with IGD. The results provide crucial insights into the neural mechanisms underlying inhibitory control impairment in IGD, which could inform the development of effective interventions for this condition. Further research is needed to explore the functional significance of these ERP components and their potential clinical applications in the diagnosis and treatment of IGD.
DESIGN: Single blinded, international, multicenter randomized controlled trial with 1:1 allocation ratio.
SETTING: Tertiary and University hospitals.
INTERVENTIONS: Patients (n=10,600) undergoing coronary artery bypass graft will be randomized to receive either volatile anesthetic as part of the anesthetic plan, or total intravenous anesthesia.
MEASUREMENTS AND MAIN RESULTS: The primary end point of the study will be one-year mortality (any cause). Secondary endpoints will be 30-day mortality; 30-day death or non-fatal myocardial infarction (composite endpoint); cardiac mortality at 30day and at one year; incidence of hospital re-admission during the one year follow-up period and duration of intensive care unit, and hospital stay. The sample size is based on the hypothesis that volatile anesthetics will reduce 1-year unadjusted mortality from 3% to 2%, using a two-sided alpha error of 0.05, and a power of 0.9.
CONCLUSIONS: The trial will determine whether the simple intervention of adding a volatile anesthetic, an intervention that can be implemented by all anesthesiologists, can improve one-year survival in patients undergoing coronary artery bypass graft surgery.
METHODS AND RESULTS: Histopathology revealed increased collagen deposition and altered fiber arrangement in the NP and isoproterenol hydrochloride (ISO) groups compared with the blank group. Systolic and diastolic functions were impaired. Western blotting and qRT-PCR demonstrated that the expression of central myofibrosis-related proteins (collagens Ι and ΙΙΙ, MMP2, MMP9, TGF-β1, α-SMA, IL-1β, and TGF-β1) and genes (Collagen Ι, Collagen ΙΙΙ, TGF-β1, and α-SMA mRNA) was upregulated in the NP and ISO groups compared with the blank group. The mRNA-seq analysis indicated differential expression of TGF-β1 signaling pathway-associated genes and proteins. Fibrosis-related protein and gene expression increased in the CFs stimulated with the recombinant human TGF-β1 and NP, which was consistent with the results of animal experiments. According to the immunofluorescence analysis and western blotting, NP exposure activated the TGF-β1/LIMK1 signaling pathway whose action mechanism in NP-induced CFs was further validated using the LIMK1 inhibitor (BMS-5). The inhibitor modulated the TGF-β1/LIMK1 signaling pathway and suppressed the NP-induced increase in fibrosis-related protein expression in the CFs. Thus, the aforementioned pathway is involved in NP-induced fibrosis.
CONCLUSION: We here provide the first evidence that perinatal NP exposure causes myocardial fibrosis in growing male rat pups and reveal the molecular mechanism and functional role of the TGF-β1/LIMK1 signaling pathway in this process.
METHODS: Analyses were conducted post hoc of this 24-month, phase III, double-blind study, in which RRMS patients were randomized (1:1:1) to once daily oral fingolimod 0.5 mg, 1.25 mg or placebo. The key outcomes were the association between baseline RNFLT and baseline clinical characteristics and clinical/imaging outcomes up to 24 months. Change of RNFLT with fingolimod versus placebo within 24 months and time to retinal nerve fiber layer (RNFL) thinning were evaluated.
RESULTS: Altogether 885 patients were included. At baseline, lower RNFLT was correlated with higher Expanded Disability Status Scale score (r = -1.085, p = 0.018), lower brain volume (r = 0.025, p = 0.006) and deep gray matter volume (r = 0.731, p