Casual analysis

  • 文章类型: Journal Article
    尽管先前的研究报道了缺血性卒中(IS)和癫痫之间的双向关系,因果关系的存在及其方向性仍然是一个有争议的话题。
    与IS相关的单核苷酸多态性(SNP)从全基因组关联研究(GWAS)数据库中提取。包含所有癫痫病例的汇总遗传数据,以及全身性和局灶性癫痫亚型,是从国际抗癫痫联盟的GWAS研究中获得的。在这项研究中,主要分析方法使用方差逆加权(IVW)方法作为主要分析技术。为了增强研究结果对潜在多效性的稳健性,进行了额外的敏感性分析.
    在正向分析中,IVW方法显示IS与所有癫痫(比值比(OR)=1.127,95%置信区间(CI)=1.038~1.224,P=0.004)和全身性癫痫(IVW:OR=1.340,95%CI=1.162~1.546,P=5.70×10~5)的风险增加相关.IS与局灶性癫痫之间无显著因果关系(P>0.05)。此外,全身性癫痫,局灶性癫痫,所有癫痫均未显示与IS有因果关系.
    这项孟德尔随机化(MR)分析表明,IS会增加患癫痫的风险,尤其是全身性癫痫.相反,在癫痫发作和卒中发作之间没有明确的因果关系.因此,癫痫对IS发病机制的影响可能机制仍需进一步研究。
    UNASSIGNED: Although previous studies have reported a bidirectional relationship between ischemic stroke (IS) and epilepsy, the existence of a causal nexus and its directionality remains a topic of controversy.
    UNASSIGNED: The single nucleotide polymorphisms (SNPs) associated with IS were extracted from the Genome-Wide Association Study (GWAS) database. Pooled genetic data encompassing all epilepsy cases, as well as generalized and focal epilepsy subtypes, were acquired from the International League Against Epilepsy\'s GWAS study. In this study, the primary analysis approach utilized the inverse variance weighting (IVW) method as the main analytical technique. To enhance the robustness of the findings against potential pleiotropy, additional sensitivity analyses were conducted.
    UNASSIGNED: In the forward analysis, the IVW method demonstrated that IS was associated with an increased risk of all epilepsy (odds ratio (OR) = 1.127, 95 % confidence interval (CI) = 1.038-1.224, P = 0.004) and generalized epilepsy (IVW: OR = 1.340, 95 % CI = 1.162-1.546, P = 5.70 × 10-5). There was no substantial causal relationship observed between IS and focal epilepsy (P > 0.05). Furthermore, generalized epilepsy, focal epilepsy, and all epilepsy did not show a causal relationship with IS.
    UNASSIGNED: This Mendelian randomization (MR) analysis demonstrates that IS increases the risk of developing epilepsy, especially generalized epilepsy. Conversely, no clear causal association was found between epilepsy and the onset of stroke. Therefore, the possible mechanisms of the effect of epilepsy on the pathogenesis of IS still need to be further investigated.
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  • 文章类型: Journal Article
    生态瞬时评估(EMA)研究为人们在积极和消极情绪下饮酒的情绪调节原则提供了相互矛盾的证据。当前的研究以特定的方式检查了情绪与酒精的关系,以量化个体之间积极和消极情绪与饮酒之间的关系的患病率和强度。
    我们使用了两个EMA样本:96名重度饮酒的大学生(样本1)和19名完成生态瞬时干预(EMI)以应对饮酒的年轻人(样本2)。每天多次测量情绪和酒精的使用,持续4-6周。使用三种不同的分析方法检查情绪-酒精关系:标准多级建模,群体因果建模,和具体因果建模。
    多水平建模和群体因果建模均表明,两个样本中的参与者仅在积极情绪下饮酒。然而,具体因果分析显示,只有63%和21%的受试者(分别在样本1和2中)在任何积极情绪后饮酒。许多受试者(24%和58%)在日常生活中不喝酒以应对积极或消极的情绪,在整个EMA方案中,很少有人(5%和16%)因负面情绪而喝酒,尽管样本2被特别选择,因为他们支持饮酒来应对负面情绪。
    传统的群体水平分析和相应的全人群理论假设在情绪-酒精关系中人群的相对同质性,但在两个人口统计和临床均一的样本中,这种方法未能准确描述大约一半受试者的情绪和酒精使用之间的关系。鉴于迄今为止情绪与酒精关系的不一致发现,我们得出的结论是,具体的因果分析可以为更准确的情绪和酒精使用理论提供基础。此外,通过在临床环境中直接使用,个体因果模型也可能有助于改善社会心理治疗。
    Ecological momentary assessment (EMA) studies have provided conflicting evidence for the mood regulation tenet that people drink in response to positive and negative moods. The current study examined mood-to-alcohol relationships idiographically to quantify the prevalence and intensity of relationships between positive and negative moods and drinking across individuals.
    We used two EMA samples: 96 heavy drinking college students (sample 1) and 19 young adults completing an ecological momentary intervention (EMI) for drinking to cope (sample 2). Mood and alcohol use were measured multiple times per day for 4-6 weeks. Mood-alcohol relationships were examined using three different analytic approaches: standard multilevel modeling, group causal modeling, and idiographic causal modeling.
    Both multilevel modeling and group causal modeling showed that participants in both samples drank in response to positive moods only. However, idiographic causal analyses revealed that only 63% and 21% of subjects (in samples 1 and 2, respectively) drank following any positive mood. Many subjects (24% and 58%) did not drink in response to either positive or negative mood in their daily lives, and very few (5% and 16%) drank in response to negative moods throughout the EMA protocol, despite sample 2 being selected specifically because they endorse drinking to cope with negative mood.
    Traditional group-level analyses and corresponding population-wide theories assume relative homogeneity within populations in mood-alcohol relationships, but this nomothetic approach failed to characterize accurately the relationship between mood and alcohol use in approximately half of the subjects in two samples that were demographically and clinically homogeneous. Given inconsistent findings in the mood-alcohol relationships to date, we conclude that idiographic causal analyses can provide a foundation for more accurate theories of mood and alcohol use. In addition, idiographic causal models may also help improve psychosocial treatments through direct use in clinical settings.
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