Conectar
Anxiety disorders, obsessive–compulsive disorder (OCD) and post-traumatic stress disorder (PTSD) are common in children and adolescents and can lead to significant impairment. Cognitive behavioural therapy (CBT) with exposure is the first-line treatment, yet approximately half of treated youth do not achieve full remission. Dysfunctional cognitions—negative automatic thoughts, maladaptive beliefs and distorted interpretations—are considered key targets of CBT, but evidence in youth is mixed and underpowered. This study will examine whether change in dysfunctional cognitions mediates treatment outcome in anxiety, OCD and PTSD symptoms and whether this association varies across individual characteristics.
An individual participant data meta-analysis (IPDMA) of randomised controlled trials of CBT for youth aged 5–18 years with anxiety disorders, OCD or PTSD will be conducted. The search strategy includes the databases APA PsycINFO, MEDLINE and Web of Science Core Collection from inception to 8 September 2025. It is supplemented by screening reference lists, trial registries, grey literature and outreach to relevant research groups. Eligible trials must include at least one validated measure of dysfunctional cognitions administered at minimum pre- and post-treatment, and clinical outcomes assessed at post-treatment and follow-up. The two primary outcomes are (1) child-reported symptom severity and (2) clinician-rated clinical severity. Data will be harmonised for dysfunctional cognition scores, moderators (age, gender, socioeconomic status, comorbidity), and primary outcomes. One-stage Bayesian mixed-effects models will examine whether changes in dysfunctional cognitions predict improvements in primary outcomes and whether these effects are moderated by individual characteristics. Missing data will be addressed using multiple imputation within the Bayesian framework, and study-level heterogeneity will be modelled using random intercepts and slopes.
All datasets will be de-identified and managed under General Data Protection Regulation standards. Each included trial will have ethical approval permitting data sharing and reuse, and the secondary analysis of the shared datasets has been approved by the University of Amsterdam. Findings will be disseminated via a peer-reviewed publication, scientific conferences and open sharing of analysis scripts and harmonisation procedures.
CRD420251139130.
by Wananit Wimuttisuk, Pisut Yotbuntueng, Pacharawan Deenarn, Punsa Tobwor, Kamonluk Kittiwongpukdee, Surasak Jiemsup, Rapeepun Vanichviriyakit, Chanadda Kasamechotchung, Suganya Yongkiettrakul, Natthinee Munkongwongsiri, Siriwan Khidprasert, Vanicha Vichai
The microsporidian Enterocytozoon hepatopenaei (EHP) is a highly contagious pathogen that causes severe growth retardation in penaeid shrimp. EHP infection damages the hepatopancreatic tubules, causes hematopoietic infiltration, and recruits granulocytes and inflammatory cells to the shrimp stomach and intestine. In this study, we investigated whether EHP infection induced the eicosanoid biosynthesis pathway in the gastrointestinal tract of the Pacific white shrimp Litopenaeus vannamei. Shrimp hepatopancreases, stomachs, and intestines were collected on days 0, 7, and 21 of the EHP cohabitation experiment for analysis. On day 7, the levels of cyclooxygenase (COX) and prostaglandin F synthase (PGFS) enzymes, which catalyze the production of prostaglandins, were elevated in the hepatopancreas of EHP-infected shrimp. The stomach of EHP-infected shrimp also contained higher levels of 12-hydroxyeicosatetraenoic acid (12-HETE) and 12-hydroxyeicosapentaenoic acid (12-HEPE) than the control shrimp. Nevertheless, the most significant impact of EHP infection on day 7 was observed in shrimp intestines, in which the levels of prostaglandin F2α (PGF2α), 8-HETE, and four isomers of HEPEs were higher in the EHP-infected shrimp than in the control shrimp. As the EHP infection progressed to day 21, the upregulation of COX and PGFS persisted in the EHP-infected hepatopancreas, leading to increasing levels of PGF2α and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2). The upregulation of prostaglandins was in contrast with the decreasing levels of HETEs and HEPEs in the hepatopancreas of EHP-infected shrimp. Meanwhile, the stomach of EHP-infected shrimp contained higher levels of prostaglandin D2, PGF2α, 15d-PGJ2, and most of the hydroxy fatty acids than the control shrimp. The levels of eicosanoid precursors, namely arachidonic acid and eicosapentaenoic acid, were upregulated in the shrimp gastrointestinal tract collected on days 7 and 21, suggesting that substrate availability contributes to the increasing levels of eicosanoids after EHP infection. Our study provides the first comprehensive analysis of the eicosanoid biosynthesis pathway in response to EHP infection. Moreover, the results indicate that eicosanoids are part of the host-pathogen interactions in crustaceans.
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