Prior to the COVID-19 pandemic, our research group initiated a pediatric practice-based randomized trial for the treatment of childhood obesity in rural communities. Approximately 6 weeks into the originally planned 10-week enrollment period, the trial was forced to pause all study activity due to the COVID-19 pandemic. This pause necessitated a substantial revision in recruitment, enrollment, and other study methods in order to complete the trial using virtual procedures. This descriptive paper outlines methods used to recruit, enroll, and manage clinical trial participants with technology to obtain informed consent, obtain height and weight measurements by video, and maintain participant engagement throughout the duration of the trial.

The study team reviewed the IRB records, protocol team meeting minutes and records, and surveyed the site teams to document the impact of the COVID-19 shift to virtual procedures on the study. The IRB approved study changes allowed for flexibility between clinical sites given variations in site resources, which was key to success of the implementation.

All study sites faced a variety of logistical challenges unique to their location yet successfully recruited the required number of patients for the trial. Ultimately, virtual procedures enhanced our ability to establish relationships with participants who were previously beyond our reach, but presented several challenges and required additional resources.

Lessons learned from this study can assist other study groups in navigating challenges, especially when recruiting and implementing studies with rural and underserved populations or during challenging events like the pandemic.

Neuroimaging research suggests that alcohol dependency is associated with impairments in anticipating monetary rewards, but not aversive or alcohol-related cues.

We sought to investigate if reinforcement sensitivity is altered in young adults, who regularly consume harmful levels of alcohol, using a monetary incentive reinforcement (MIR) task. In light of previous research suggesting reduced motivation to obtain reward, we hypothesized that young alcohol users would show reduced motivation for monetary gain, but unimpaired loss avoidance behaviour.

We recruited 46 volunteers from the local community in Cambridge (UK), half of whom reported consuming alcohol at harmful levels, as reflected by the Alcohol Use Disorder Test. Participants completed a number of personality questionnaires, including the Barratt Impulsivity Scale (BIS-11) and Sensation-Seeking-Scale (SSS-V) and performed the MIR task, which measures participants’ efforts in avoiding punishment and gaining rewards. Data were analysed using Statistical Package for Social Sciences (SPSS) version 25 (IBM, Chicago IL). Analysis of co-variance (ANOVA) were used to explore group differences in demographics, personality traits and task performance; age and gender were included as co-variates.

The groups were well-matched in terms of socioeconomic status and education levels. As the alcohol group was significantly younger than the control group and dominated by females, age and gender were statistically controlled for. Alcohol users reported significantly higher levels of impulsivity (F1,41 = 6.0, p = 0.019) and sensation-seeking traits (F1,42 = 36.7, p < 0.001) and demonstrated normal sensitivity to monetary value (F1,41 = 1.07,p = 0.307). However, when challenged to on the MIR task to gain reward or avoid punishment, alcohol users were as equally motivated as control volunteers to take action to avoid financial loss (F1,41 = 2.6,p = 0.112) but showed less motivation to work towards financial reward (F1,41 = 4.7,p = 0.036). Especially for small rewards, alcohol users exerted significantly less efforts, as reflected by a reduced accuracy rate (F1,41 = 6.6,p = 0.014) and a significant increase in late responses (F1,41 = 7.7,p = 0.008). The lack of motivation to work for reward was negatively associated with the severity of alcohol use, as reflected by the AUDIT score (r=−.48,p < 0-05).

We observed reduced motivation to obtain financial reward, but not avoid loss in a community sample of heavy drinkers. As the observed effect was directly related to alcohol use severity, it may suggest changes in reinforcement sensitivity occur at an early stage of chronic alcohol use. Future research may want to monitor reward motivation in alcohol users longitudinally to evaluate whether it would be a suitable target for early intervention.

Schizophrenia is associated with robust hippocampal volume deficits but subregion volume deficits, their associations with cognition, and contributing genes remain to be determined.

Hippocampal formation (HF) subregion volumes were obtained using FreeSurfer 6.0 from individuals with schizophrenia (n = 176, mean age ± s.d. = 39.0 ± 11.5, 132 males) and healthy volunteers (n = 173, mean age ± s.d. = 37.6 ± 11.3, 123 males) with similar mean age, gender, handedness, and race distributions. Relationships between the HF subregion volume with the largest between group difference, neuropsychological performance, and single-nucleotide polymorphisms were assessed.

This study found a significant group by region interaction on hippocampal subregion volumes. Compared to healthy volunteers, individuals with schizophrenia had significantly smaller dentate gyrus (DG) (Cohen's d = −0.57), Cornu Ammonis (CA) 4, molecular layer of the hippocampus, hippocampal tail, and CA 1 volumes, when statistically controlling for intracranial volume; DG (d = −0.43) and CA 4 volumes remained significantly smaller when statistically controlling for mean hippocampal volume. DG volume showed the largest between group difference and significant positive associations with visual memory and speed of processing in the overall sample. Genome-wide association analysis with DG volume as the quantitative phenotype identified rs56055643 (β = 10.8, p < 5 × 10−8, 95% CI 7.0–14.5) on chromosome 3 in high linkage disequilibrium with MOBP. Gene-based analyses identified associations between SLC25A38 and RPSA and DG volume.

This study suggests that DG dysfunction is fundamentally involved in schizophrenia pathophysiology, that it may contribute to cognitive abnormalities in schizophrenia, and that underlying biological mechanisms may involve contributions from MOBP, SLC25A38, and RPSA.