The Experiences of Counselors-in-Training in a School-based Counseling Practicum

Counselor education programs often must choose between providing in vivo faculty supervision or a community-based setting. Programs that combine both elements have shown positive preliminary findings related to counselor development; however, the in-depth experiences of students in such programs have not been explored. This phenomenological study examined the lived experiences of counselors-in-training who participated in a school-based counseling practicum with in vivo faculty supervision. Researchers identified six themes, including continuum of support within relationships, operational challenges and concerns, needs and challenges of the community, working with children, expectations and realities, and counselor identity development. Implications for counselor education and research are provided

The Experiences of Counselors-in-Training in a School-based Counseling Practicum

Counselor education programs often must choose between providing in vivo faculty supervision or a community-based setting. Programs that combine both elements have shown positive preliminary findings related to counselor development; however, the in-depth experiences of students in such programs have not been explored. This phenomenological study examined the lived experiences of counselors-in-training who participated in a school-based counseling practicum with in vivo faculty supervision. Researchers identified six themes, including continuum of support within relationships, operational challenges and concerns, needs and challenges of the community, working with children, expectations and realities, and counselor identity development. Implications for counselor education and research are provided

Complicated Grief: An Evolving Theoretical Landscape

The bereavement literature has proliferated in recent decades, generating a shift from conceptualizing grief as a stepwise, uniform process to an idiosyncratic experience that varies among individuals. Among the most notable developments is the empirical exploration of complicated grief—a protracted, debilitating, sometimes life-threatening response to the death of a loved one—and the testing of novel interventions to treat it. This article provides counselors with recommendations for identifying and treating complicated grief

Innovative Moments In Humanistic Therapy I: Process And Outcome Of Eminent Psychotherapists Working With Bereaved Clients

This project entailed an intensive qualitative analysis of six-session psychotherapies conducted by three eminent humanistic psychotherapists working with bereaved clients. The Innovative Moments Coding System (IMCS), rooted in narrative therapy, is designed to measure change across therapy orientations. Research using the IMCS suggests that the psychotherapy change process occurs through the emergence, elaboration, and expansion of identifiable change moments for a client—innovative moments (IMs)—which present as exceptions to a client\u27s presenting problematic narrative. There are five identified types of IMs: action, reflection, protest, reconceptualization (RC), and performing change (PC). The current study aimed to inform theory regarding the patterns of IMs across three humanistic approaches—constructivist, person-centered, and existential—when working with bereaved clients, while linking these patterns to observable change in each client\u27s functioning. The alliance between each client and therapist was also assessed across the therapy process, showing consistently strong alliances across the three cases. Findings from the current study reinforce the salience of reflection, RC, and PC IMs in successful grief therapy cases, and also suggest the importance of meaning-making interventions in grief therapy. Clinical implications and suggestions for future research are also addressed

Truncating SRCAP variants outside the Floating-Harbor syndrome locus cause a distinct neurodevelopmental disorder with a specific DNA methylation signature

Truncating variants in exons 33 and 34 of the SNF2-related CREBBP activator protein (SRCAP) gene cause the neurodevelopmental disorder (NDD) Floating-Harbor syndrome (FLHS), characterized by short stature, speech delay, and facial dysmorphism. Here, we present a cohort of 33 individuals with clinical features distinct from FLHS and truncating (mostly de novo) SRCAP variants either proximal (n = 28) or distal (n = 5) to the FLHS locus. Detailed clinical characterization of the proximal SRCAP individuals identified shared characteristics: developmental delay with or without intellectual disability, behavioral and psychiatric problems, non-specific facial features, musculoskeletal issues, and hypotonia. Because FLHS is known to be associated with a unique set of DNA methylation (DNAm) changes in blood, a DNAm signature, we investigated whether there was a distinct signature associated with our affected individuals. A machine-learning model, based on the FLHS DNAm signature, negatively classified all our tested subjects. Comparing proximal variants with typically developing controls, we identified a DNAm signature distinct from the FLHS signature. Based on the DNAm and clinical data, we refer to the condition as "non-FLHS SRCAP-related NDD." All five distal variants classified negatively using the FLHS DNAm model while two classified positively using the proximal model. This suggests divergent pathogenicity of these variants, though clinically the distal group presented with NDD, similar to the proximal SRCAP group. In summary, for SRCAP, there is a clear relationship between variant location, DNAm profile, and clinical phenotype. These results highlight the power of combined epigenetic, molecular, and clinical studies to identify and characterize genotype-epigenotype-phenotype correlations

Truncating SRCAP variants outside the Floating-Harbor syndrome locus cause a distinct neurodevelopmental disorder with a specific DNA methylation signature

Truncating variants in exons 33 and 34 of the SNF2-related CREBBP activator protein (SRCAP) gene cause the neurodevelopmental disorder (NDD) Floating-Harbor syndrome (FLHS), characterized by short stature, speech delay, and facial dysmorphism. Here, we present a cohort of 33 individuals with clinical features distinct from FLHS and truncating (mostly de novo) SRCAP variants either proximal (n = 28) or distal (n = 5) to the FLHS locus. Detailed clinical characterization of the proximal SRCAP individuals identified shared characteristics: developmental delay with or without intellectual disability, behavioral and psychiatric problems, non-specific facial features, musculoskeletal issues, and hypotonia. Because FLHS is known to be associated with a unique set of DNA methylation (DNAm) changes in blood, a DNAm signature, we investigated whether there was a distinct signature associated with our affected individuals. A machine-learning model, based on the FLHS DNAm signature, negatively classified all our tested subjects. Comparing proximal variants with typically developing controls, we identified a DNAm signature distinct from the FLHS signature. Based on the DNAm and clinical data, we refer to the condition as "non-FLHS SRCAP-related NDD." All five distal variants classified negatively using the FLHS DNAm model while two classified positively using the proximal model. This suggests divergent pathogenicity of these variants, though clinically the distal group presented with NDD, similar to the proximal SRCAP group. In summary, for SRCAP, there is a clear relationship between variant location, DNAm profile, and clinical phenotype. These results highlight the power of combined epigenetic, molecular, and clinical studies to identify and characterize genotype-epigenotype-phenotype correlations

Germline variants in tumor suppressor FBXW7 lead to impaired ubiquitination and a neurodevelopmental syndrome

Neurodevelopmental disorders are highly heterogenous conditions resulting from abnormalities of brain architecture and/or function. FBXW7 (F-box and WD-repeat-domain-containing 7), a recognized developmental regulator and tumor suppressor, has been shown to regulate cell-cycle progression and cell growth and survival by targeting substrates including CYCLIN E1/2 and NOTCH for degradation via the ubiquitin proteasome system. We used a genotype-first approach and global data-sharing platforms to identify 35 individuals harboring de novo and inherited FBXW7 germline monoallelic chromosomal deletions and nonsense, frameshift, splice-site, and missense variants associated with a neurodevelopmental syndrome. The FBXW7 neurodevelopmental syndrome is distinguished by global developmental delay, borderline to severe intellectual disability, hypotonia, and gastrointestinal issues. Brain imaging detailed variable underlying structural abnormalities affecting the cerebellum, corpus collosum, and white matter. A crystal-structure model of FBXW7 predicted that missense variants were clustered at the substrate-binding surface of the WD40 domain and that these might reduce FBXW7 substrate binding affinity. Expression of recombinant FBXW7 missense variants in cultured cells demonstrated impaired CYCLIN E1 and CYCLIN E2 turnover. Pan-neuronal knockdown of the Drosophila ortholog, archipelago, impaired learning and neuronal function. Collectively, the data presented herein provide compelling evidence of an F-Box protein-related, phenotypically variable neurodevelopmental disorder associated with monoallelic variants in FBXW7