The development and evaluation of a virtual, asynchronous, trauma-focused treatment program for adult survivors of childhood interpersonal trauma.

BACKGROUND: The long-term mental and physical health implications of childhood interpersonal trauma on adult survivors is immense, however, there is a lack of available trauma-focused treatment services that are widely accessible. This study, utilizing a user-centered design process, sought feedback on the initial design and development of a novel, self-paced psychoeducation and skills-based treatment intervention for this population. AIMS: To explore the views and perspectives of adult survivors of childhood interpersonal trauma on the first two modules of an asynchronous trauma-focused treatment program. METHODS: Fourteen participants from our outpatient hospital service who completed the modules consented to provide feedback on their user experience. A thematic analysis of the three focus groups was conducted. RESULTS: Four major themes emerged from the focus groups: (1) technology utilization, (2) module content, (3) asynchronous delivery, and (4) opportunity for interactivity. Participants noted the convenience of the platform and the use of multimedia content to increase engagement and did not find the modules to be emotionally overwhelming. CONCLUSIONS: Our research findings suggest that an asynchronous virtual intervention for childhood interpersonal trauma survivors may be a safe and acceptable way to provide a stabilization-focused intervention on a wider scale.

Oral glucosamine sulfate supplementation does not induce endoplasmic reticulum stress or activate the unfolded protein response in circulating leukocytes of human subjects.

Glucosamine sulfate is a dietary supplement that is marketed as a treatment for osteoarthritis. Recent evidence from animal and cell culture models have suggested that glucosamine treatment can promote the misfolding of proteins and the activation of the unfolded protein response (UPR). We investigated whether glucosamine sulfate supplementation activates the UPR in circulating leukocytes of human subjects. Cultured Thp1 human monocytes were exposed to increasing concentrations of glucosamine (0, 0.25, 1.0, 4.0 mmol · L(-1)) for 18 h. We observed a dose-dependent increase in intracellular glucosamine levels as well as the activation of UPR. To test the effect of glucosamine sulfate supplementation in humans, 14 healthy human subjects took 1500 mg · day(-1) glucosamine sulfate for 14 days. Metabolic parameters and blood samples were collected before and after supplementation. In humans, glucosamine sulfate supplementation did not alter metabolic parameters including lipid levels and glucose tolerance. Further, glucosamine sulfate supplementation did not affect intracellular glucosamine levels or activate the UPR in the leukocytes of human subjects. Our results indicate that in healthy human subjects, the recommended dose of glucosamine sulfate (1500 mg · day(-1)) for 14 days does not significantly alter intracellular glucosamine levels and does not activate the UPR in circulating leukocytes.

The Trauma PORTAL-A Blended e-Health Intervention for Survivors of Childhood Interpersonal Trauma: An Open-Label Pilot Study.

Background: Adults with mental health symptoms stemming from childhood interpersonal trauma require specialized trauma-focused psychological interventions. Limitations in accessing treatment interventions for this population necessitate innovative solutions. This study explored the feasibility of a protocol for a blended e-health psychoeducational treatment intervention for this population called the Trauma PORTAL (Providing Online tRauma Therapy using an Asynchronous Learning platform), combining asynchronous online modules and weekly live virtual group sessions. Method: From October 2021 to February 2022, this prospective, single-arm study recruited participants who were waitlisted for trauma therapy at an academic hospital. The primary outcome was protocol feasibility, including recruitment, adoption, and intervention acceptability. Secondary outcomes were pre- and post-intervention post-traumatic stress disorder (PTSD) symptoms (PTSD Checklist for DSM-5 [PCL-5]), depression/anxiety/stress (Depression and Anxiety Stress Scale [DASS-21]), and emotion regulation (Difficulties in Emotion Regulation Scale [DERS-18]), which were compared using paired t-tests and presented as mean differences (MDs) and 95% confidence intervals (CIs). Results: A total of 66 participants (median age = 37, female = 61) were enrolled, and they completed on average 53.5% of the online modules. There were 51 (77%) participants who completed post-intervention questionnaires. Acceptability was very high, with 49 respondents (98%) reporting that the intervention increased their access to health care. There were reductions from pre- to post-intervention on the PCL-5 (49.1 vs. 36.7, MD -12.4, 95% CI 8.3-16.5), DERS-18 (51.8 vs. 48.8, MD -3.3, 95% CI 0.2-6.4), and DASS-21 (60.1 vs. 50.7, MD -9.4, 95% CI 2.3-16.6). Conclusion: The Trauma PORTAL intervention was feasible to implement, well-adopted, and highly acceptable in an ambulatory trauma therapy program. The findings show promising evidence for symptom reduction. Further evaluation of the Trauma PORTAL's efficacy in a randomized trial is warranted.

Brain-Behavior Participant Similarity Networks Among Youth and Emerging Adults with Schizophrenia Spectrum, Autism Spectrum, or Bipolar Disorder and Matched Controls.

There is considerable heterogeneity in social cognitive and neurocognitive performance among people with schizophrenia spectrum disorders (SSD), autism spectrum disorders (ASD), bipolar disorder (BD), and healthy individuals. This study used Similarity Network Fusion (SNF), a novel data-driven approach, to identify participant similarity networks based on relationships among demographic, brain imaging, and behavioral data. T1-weighted and diffusion-weighted magnetic resonance images were obtained for 174 adolescents and young adults (aged 16-35 years) with an SSD (n=51), an ASD without intellectual disability (n=38), euthymic BD (n=34), and healthy controls (n=51). A battery of social cognitive and neurocognitive tasks were administered. Data integration, cluster determination, and biological group formation were then obtained using SNF. We identified four new groups of individuals, each with distinct neural circuit-cognitive profiles. The most influential variables driving the formation of the new groups were robustly reliable across embedded resampling techniques. The data-driven groups showed considerably greater differentiation on key social and neurocognitive circuit nodes than groups generated by diagnostic analyses or dimensional social cognitive analyses. The data-driven groups were validated through functional outcome and brain network property measures not included in the SNF model. Cutting across diagnostic boundaries, our approach can effectively identify new groups of people based on a profile of neuroimaging and behavioral data. Our findings bring us closer to disease subtyping that can be leveraged toward the targeting of specific neural circuitry among participant subgroups to ameliorate social cognitive and neurocognitive deficits.

Neuroimaging predictors of functional outcomes in schizophrenia at baseline and 6-month follow-up.

PURPOSE: Studies show that deficit syndrome schizophrenia patients, characterized by primary negative symptoms and poor functional outcome, have impairment in specific neural circuits. We assessed whether these same neural circuits are directly linked to functional outcomes across schizophrenia patients. METHODS: T1- and diffusion-weighted MR images were obtained for schizophrenia (n=30) and matched healthy control participants (n=30). Negative symptoms and functional outcome were assessed at baseline and 6-month follow-up. Cortical thickness and tract-wise fractional anisotropy (FA) were compared between groups. To assess relationships of neuroimaging measures with functional outcome, principal component analysis (PCA) was performed on tract-wise FA values and components were entered into a multiple regression model for schizophrenia participants. RESULTS: Consistent with the literature, schizophrenia participants showed frontotemporal reductions in cortical thickness and tract-wise FA compared to controls. The top two components from PCA explained 71% of the variance in tract-wise FA values. The second component (associated with inferior longitudinal and arcuate fasciculus FA) was significantly correlated with functional outcome (baseline: ß=0.54, p=0.03; follow-up: ß=0.74, p=0.047); further analysis revealed this effect was mediated by negative symptoms. Post-hoc network analysis revealed increased cortical coupling between right inferior frontal and supramarginal gyri (connected by the arcuate fasciculus) in schizophrenia participants with poorer functional outcome. CONCLUSIONS: Our findings indicate that impairment in the same neural circuitry susceptible in deficit syndrome schizophrenia predicts functional outcome in a continuous manner in schizophrenia participants. This relationship was mediated by negative symptom burden. Our findings provide novel evidence for brain-based biomarkers of longitudinal functional outcome in people with schizophrenia.