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Background: Technology improves accessibility of psychological interventions for youth. An ecological momentary intervention (EMI) is a digital intervention geared toward intervening in daily life to enhance the generalizability and ecological validity, and to be able to intervene in moments most needed. Identifying working mechanisms of the use of ecological momentary interventions might generate insights to improve interventions., Methods: The present study investigates the working mechanisms of the use and acceptability of an ecological momentary intervention, named SELFIE, targeting self-esteem in youth exposed to childhood trauma, and evaluates under what circumstances these mechanisms of use and acceptability do or do not come into play. A realist evaluation approach was used for developing initial program theories (data: expert interviews and a stakeholders focus group), and subsequently testing (data: 15 interviews with participants, a focus group with therapists, debriefing questionnaire), and refining them., Results: The SELFIE intervention is offered through a smartphone application enabling constant availability of the intervention and thereby increasing accessibility and feasibility. When the intervention was offered on their personal smartphone, this enhanced a sense of privacy and less hesitance in engaging with the app, leading to increased disclosure and active participation. Further, the smartphone application facilitates the practice of skills in daily life, supporting the repeated practice of exercises in different situations leading to the generalizability of the effect. Buffering against technical malfunction seemed important to decrease its possible negative effects., Conclusions: This study enhanced our understanding of possible working mechanisms in EMIs, such as the constant availability supporting increased accessibility and feasibility, for which the use of the personal smartphone was experienced as a facilitating context. Hereby, the current study contributes to relatively limited research in this field. For the field to move forward, mechanisms of use, and acceptability of EMIs need to be understood. It is strongly recommended that alongside efficacy trials of an EMI on specific target mechanisms, a process evaluation is conducted investigating the working mechanisms of use., Trial Registration: The current paper reports on a realist evaluation within the SELFIE trial (Netherlands Trial Register NL7129 (NTR7475))., (© 2024. The Author(s).)

Background: Identification of non-human leukocyte antigen (HLA) genetic risk factors could improve survival after allogeneic blood or marrow transplant (BMT) through matching at additional loci or individualizing risk prediction. We hypothesized that non-HLA loci contributed significantly to 1-year overall survival (OS), disease related mortality (DRM) or transplant related mortality (TRM) after unrelated donor (URD)BMT., Methods: We performed a genome-wide association study (GWAS) in 2,887 acute myeloid leukemia (AML), myelodysplastic syndrome (MDS) and acute lymphoblastic leukemia (ALL) patients and their ≥8/8 HLA-matched URDs comprising two independent cohorts treated from 2000-2011., Findings: Using meta-analyses of both cohorts, genome-wide significant associations ( p  < 5 × 10 -8 ) were identified in: recipient genomes with OS at MBNL1 (rs9990017, HR = 1.4, 95% CI 1.24-1.56, p  = 3.3 × 10 -8 ) and donor-recipient genotype mismatch with OS at LINC02774 (rs10927108, HR = 1.34, 95% CI 1.21-1.48, p  = 2.0 × 10 -8 ); donor genomes with DRM at PCNX4 (rs79076914, HR = 1.7, 95% CI 1.41-2.05, p  = 3.15 × 10 -8 ), LINC01194 (rs79498125, HR = 1.86, 95% CI 1.49-2.31, p  = 2.84 × 10 -8 ), ARID5B (rs2167710, HR = 1.5, 95% CI 1.31-1.73, p  = 6.9 × 10 -9 ) and CT49 (rs32250, HR = 1.44, 95% CI1.26-1.64, p  = 2.6 × 10 -8 ); recipient genomes at PILRB with TRM (rs141591562, HR = 2.33, 95% CI 1.74-3.12, p  = 1.26 × 10 -8 ) and donor-recipient genotype mismatch between EPGN and MTHF2DL with TRM (rs75868097, HR = 2.66, 95% CI 1.92-3.58, p  = 4.6 × 10 -9 ). Results publicly available at https://fuma.ctglab.nl/browse., Interpretation: These data provide the first evidence that non-HLA common genetic variation at novel loci with biochemical function significantly impacts 1-year URD-BMT survival. Our findings have implications for donor selection, could guide treatment strategies and provide individualized risk prediction after future validation and functional studies., Funding: This project was funded by grants from the National Institutes of Health, USA., Competing Interests: PLM: Consulting: BlueBird Biotech, Bristol-Myers Squibb, Celgene, Fate Therapeutics, Janssen, Juno, Karyopharm, Magenta Therapeutics, Sanofi, Takeda; Honoraria: BlueBird Biotech, Bristol-Myers Squibb, Celgene, Fate Therapeutics, Janssen, Juno, Karyopharm, Magenta Therapeutics, Medscape, Takeda; Institutional Research Support: Celgene. MCP: Institutional Research Support: Bristol-Myers Squibb, Novartis, Kite, GlaxoSmithKline; Consulting: Amgen (institution), Bristol-Myers Squibb (personal). TH, LESC: report grants from NIH/NHLBI, grants from NIH/NCI, during the conduct of the study. EK: reports a Graduate Student Fellowship from Pelotonia Foundation. All other authors have nothing to declare., (© 2021 The Author(s).)

Despite empirical evidence for multifactorial causes of voice-hearing, people's own beliefs about what caused their voices are understudied. People with distressing voices (n=125) completed measures of trauma, post-traumatic stress disorder (PTSD) symptoms, and beliefs about causality. Most participants reported trauma in the past (97%) and PTSD symptoms were prevalent. Traumatic experiences were the most commonly endorsed causal factor of voice-hearing (64%), followed by distress (62%). Beliefs about biological causes, including drug use (22%), were least endorsed. Those who experienced more traumatic events and more PTSD symptoms were more likely to endorse trauma as a causal factor of voice-hearing (R 2 =0.38)., (Copyright © 2021. Published by Elsevier B.V.)

Estrogen receptor (ER)-negative tumors represent 20-30% of all breast cancers, with a higher proportion occurring in younger women and women of African ancestry. The etiology and clinical behavior of ER-negative tumors are different from those of tumors expressing ER (ER positive), including differences in genetic predisposition. To identify susceptibility loci specific to ER-negative disease, we combined in a meta-analysis 3 genome-wide association studies of 4,193 ER-negative breast cancer cases and 35,194 controls with a series of 40 follow-up studies (6,514 cases and 41,455 controls), genotyped using a custom Illumina array, iCOGS, developed by the Collaborative Oncological Gene-environment Study (COGS). SNPs at four loci, 1q32.1 (MDM4, P = 2.1 × 10(-12) and LGR6, P = 1.4 × 10(-8)), 2p24.1 (P = 4.6 × 10(-8)) and 16q12.2 (FTO, P = 4.0 × 10(-8)), were associated with ER-negative but not ER-positive breast cancer (P > 0.05). These findings provide further evidence for distinct etiological pathways associated with invasive ER-positive and ER-negative breast cancers.