Diagnostic criteria for major depressive disorder allow for heterogeneous symptom profiles but genetic analysis of major depressive symptoms has the potential to identify clinical and etiological subtypes. There are several challenges to integrating symptom data from genetically informative cohorts, such as sample size differences between clinical and community cohorts and various patterns of missing data.

We conducted genome-wide association studies of major depressive symptoms in three cohorts that were enriched for participants with a diagnosis of depression (Psychiatric Genomics Consortium, Australian Genetics of Depression Study, Generation Scotland) and three community cohorts who were not recruited on the basis of diagnosis (Avon Longitudinal Study of Parents and Children, Estonian Biobank, and UK Biobank). We fit a series of confirmatory factor models with factors that accounted for how symptom data was sampled and then compared alternative models with different symptom factors.

The best fitting model had a distinct factor for Appetite/Weight symptoms and an additional measurement factor that accounted for the skip-structure in community cohorts (use of Depression and Anhedonia as gating symptoms).

The results show the importance of assessing the directionality of symptoms (such as hypersomnia versus insomnia) and of accounting for study and measurement design when meta-analyzing genetic association data.

Dysfunctional changes in the glutamatergic system play an important role in the pathophysiology of depression. Glutamate regulates various neuronal function, such as nerve migration, excitability, plasticity, as well as long-term potentiation and long-term synaptic depression. Failures in this process might cause emotional/cognitive changes associated with stress-induced depressive symptoms, a part of our current understanding of the pathophysiology of depression. These changes might be related to deviations in biochemical blood parameters, but also to volatile organic compounds (VOCs) measured in breath.

1) To replicate our previous finding that concentration of volatile organic compounds in expiratory breath gas and metabolites derived from MR spectroscopy distinguish unmedicated depressed patients from healthy participants, (2) to determine whether the amount of these VOCs is associated with severity of depression and anxiety, and (3) to correlate breath-VOC-content with glutamatergic neurotransmission and energy metabolism derived from MR spectroscopy.

25 antidepressant-free patients with major depression according to DSM V (18-65 years of age) are recruited from our out- and inpatient clinics. The controls will consist of 25 healthy age-and-sex-matched participants. Breath gas analyses will be carried out at awakening, and 30 and 60 minutes thereafter, and at 5pm using PTR-TOF-MS with direct on time measurement through a special sampler. A 7 Tesla Siemens Terra MRI scanner will be used to undertake spectroscopic measurements. Concentrations of glutamate and β-hydroxybutyrate levels in the pregenual and dorsal anterior cingulate gyrus will subsequently be assessed.

Statistical analysis for differences between groups corrected for multiple measurements will be carried out. Concentration of VOCs will be correlated with brain metabolism and severity of symptoms.

VOCs in breath are proposed to be an efficient and non-invasive marker for depression-related biochemical changes related to disease severity, and eventually useful for personalized treatment planning.

None Declared

In the coronavirus disease 2019 (COVID-19) pandemic, child and adolescent psychiatry wards face the risk of severe acute respiratory coronavirus 2 (SARS-CoV-2) introduction and spread within the facility. In this setting, mask and vaccine mandates are hard to enforce, especially for younger children. Surveillance testing may detect infection early and enable mitigation measures to prevent viral spread. We conducted a modeling study to determine the optimal method and frequency of surveillance testing and to analyze the effect of weekly team meetings on transmission dynamics.

Simulation with an agent-based model reflecting ward structure, work processes, and contact networks from a real-world child and adolescent psychiatry clinic with 4 wards, 40 patients, and 72 healthcare workers.

We simulated the spread of 2 SARS-CoV-2 variants over 60 days under surveillance testing with polymerase chain reaction (PCR) tests and rapid antigen tests in different scenarios. We measured the size, peak, and the duration of an outbreak. We compared medians and percentage of spillover events to other wards from 1,000 simulations for each setting.

The outbreak size, peak, and duration were dependent on test frequency, test type, SARS-CoV-2 variant, and ward connectivity. Under surveillance conditions, joint staff meetings and therapists shared between wards did not significantly change median outbreak size under surveillance conditions. With daily antigen testing, outbreaks were mostly confined to 1 ward and median outbreak sizes were lower than with twice-weekly PCR testing (1 vs 22; P < .001).

Modeling can help to understand transmission patterns and guide local infection control measures.

The COVID-19 pandemic resulted in millions of deaths worldwide and is considered a significant mass-casualty disaster (MCD). The surge of patients and scarcity of resources negatively impacted hospitals, patients and medical practice. We hypothesized ICUs during this MCD had a higher acuity of illness, and subsequently had increased lengths of stay (LOS), complication rates, death rates and costs of care. The purpose of this study was to investigate those outcomes.

This was a multicenter, retrospective study that compared intensive care admissions in 2020 to those in 2019 to evaluate patient outcomes and cost of care. Data were obtained from the Vizient Clinical Data Base/Resource Manager (Vizient Inc., Irvine, Texas, USA).

Data included the number of ICU admissions, patient outcomes, case mix index and summary of cost reports. Quality outcomes were also collected, and a total of 1304981 patients from 333 hospitals were included. For all medical centers, there was a significant increase in LOS index, ICU LOS, complication rate, case mix index, total cost, and direct cost index.

The MCD caused by COVID-19 was associated with increased adverse outcomes and cost-of-care for ICU patients.

Research suggests that increasing neighbourhood social cohesion can prevent mental health problems, including depression and anxiety. However, it is unknown whether this is the case for adolescents and young adults.

To investigate whether neighbourhood social cohesion can prevent depression and anxiety, and identify interventions that can increase neighbourhood cohesion in young people.

We conducted a rapid review for an overview of the available literature. PubMed, Campbell Collaboration, KSR Ltd and grey literature databases were searched from inception up to 10 July 2020. When synthesising the results, we applied a hierarchy of evidence, prioritising study designs that allowed for the most ability to infer causality. Risk of bias was assessed with the ROBIS tool and Joanna Briggs Institute risk-of-bias assessment. A narrative review and two workshops with young people were conducted to inform what future interventions may look like.

Forty-two peer-reviewed publications, including two systematic reviews, 13 longitudinal studies and 27 cross-sectional studies, were identified. Prospective longitudinal studies found that neighbourhood social cohesion factors (safety, trust, positive social connections, helping others and a lack of crime and violence) were associated with fewer depressive symptoms. Future interventions to increase neighbourhood cohesion should involve creating safe and attractive community centres, accessible and safe outdoor spaces, community activity groups and online communities.

Neighbourhood social cohesion has the potential to protect mental health. The next step is to conduct intervention studies to evaluate the effects on onset prevention. Clinicians should consider the impact cohesion can have on mental health, and signpost to community initiatives.

Causes of childhood behavior problems remain poorly understood. Enriched family environments and corresponding brain development may reduce the risk of their onset, but research investigating white matter neurodevelopmental pathways explaining associations between the family environment and behavior remains limited. We hypothesized that more positive prenatal and mid-childhood family functioning – a measure of a family's problem solving and supportive capacity – would be associated with two markers of preadolescent white matter neurodevelopment related to reduced behavior problems: higher global fractional anisotropy (FA) and lower global mean diffusivity (MD).

Data are from 2727 families in the Generation R Study, the Netherlands. Mothers reported family functioning (McMaster Family Assessment Device, range 1–4, higher scores indicate healthier functioning) prenatally and in mid-childhood (mean age 6.1 years). In preadolescence (mean age 10.1), the study collected diffusion-weighted scans. We computed standardized global MD and FA values by averaging metrics from 27 white matter tracts, and we fit linear models adjusting for possible confounders to examine global and tract-specific outcomes.

Prenatal and mid-childhood family functioning scores were moderately correlated, r = 0.38. However, only prenatal family functioning – and not mid-childhood functioning – was associated with higher global FA and lower global MD in preadolescence in fully adjusted models: βglobal FA = 0.11 (95% CI 0.00, 0.21) and βglobal MD = −0.15 (95% CI −0.28, −0.03) per one-unit increase in functioning score. Sensitivity and tract-specific analyses supported these global findings.

These results suggest high-functioning prenatal or perinatal family environments may confer lasting white matter neurodevelopmental benefits into preadolescence.

Psychotic experiences predict adverse health outcomes, particularly if they are persistent. However, it is unclear what distinguishes persistent from transient psychotic experiences.

In a large population-based cohort, we aimed to (a) describe the course of hallucinatory experiences from childhood to adolescence, (b) compare characteristics of youth with persistent and remittent hallucinatory experiences, and (c) examine prediction models for persistence.

Youth were assessed longitudinally for hallucinatory experiences at mean ages of 10 and 14 years (n = 3473). Multi-informant-rated mental health problems, stressful life events, self-esteem, non-verbal IQ and parental psychopathology were examined in relation to absent, persistent, remittent and incident hallucinatory experiences. We evaluated two prediction models for persistence with logistic regression and assessed discrimination using the area under the curve (AUC).

The persistence rate of hallucinatory experiences was 20.5%. Adolescents with persistent hallucinatory experiences had higher baseline levels of hallucinatory experiences, emotional and behavioural problems, as well as lower self-esteem and non-verbal IQ scores than youth with remittent hallucinatory experiences. Although the prediction model for persistence versus absence of hallucinatory experiences demonstrated excellent discriminatory power (AUC-corrected = 0.80), the prediction model for persistence versus remittance demonstrated poor accuracy (AUC-corrected = 0.61).

This study provides support for the dynamic expression of childhood hallucinatory experiences and suggests increased neurodevelopmental vulnerability in youth with persistent hallucinatory experiences. Despite the inclusion of a wide array of psychosocial parameters, a prediction model discriminated poorly between youth with persistent versus remittent hallucinatory experiences, confirming that persistent hallucinatory experiences are a complex multifactorial trait.

Experimental work in animals has shown that DNA methylation (DNAm), an epigenetic mechanism regulating gene expression, is influenced by typical variation in maternal care. While emerging research in humans supports a similar association, studies to date have been limited to candidate gene and cross-sectional approaches, with a focus on extreme deviations in the caregiving environment.

Here, we explored the prospective association between typical variation in maternal sensitivity and offspring epigenome-wide DNAm, in a population-based cohort of children (N = 235). Maternal sensitivity was observed when children were 3- and 4-years-old. DNAm, quantified with the Infinium 450 K array, was extracted at age 6 (whole blood). The influence of methylation quantitative trait loci (mQTLs), DNAm at birth (cord blood), and confounders (socioeconomic status, maternal psychopathology) was considered in follow-up analyses.

Genome-wide significant associations between maternal sensitivity and offspring DNAm were observed at 13 regions (p < 1.06 × 10−07), but not at single sites. Follow-up analyses indicated that associations at these regions were in part related to genetic factors, confounders, and baseline DNAm levels at birth, as evidenced by the presence of mQTLs at five regions and estimate attenuations. Robust associations with maternal sensitivity were found at four regions, annotated to ZBTB22, TAPBP, ZBTB12, and DOCK4.

These findings provide novel leads into the relationship between typical variation in maternal caregiving and offspring DNAm in humans, highlighting robust regions of associations, previously implicated in psychological and developmental problems, immune functioning, and stress responses.

Congenital and acquired heart diseases are highly prevalent in developing countries despite limited specialised care. Namibia established a paediatric cardiac service in 2009 with significant human resource and infrastructural constraints. Therefore, patients are referred for cardiac interventions to South Africa.

To describe the diagnoses, clinical characteristics, interventions, post-operative morbidity and mortality, and follow-up of patients referred for care.

Demographics, diagnoses, interventions, intra- and post-operative morbidity and mortality, as well as longitudinal follow-up data of all patients referred to South Africa, were recorded and analysed.

The total cohort constituted 193 patients of which 179 (93%) had CHD and 7% acquired heart disease. The majority of patients (78.8%) travelled more than 400 km to Windhoek before transfer. There were 28 percutaneous interventions. Palliative and definitive surgery was performed in 27 and 129 patients, respectively. Out of 156 patients, 80 (51.3%) had post-operative complications, of which 15 (9.6%) were a direct complication of surgery. Surgical mortality was 8/156 (5.1%, 95% confidence interval 2.2–9.8), with a 30-day mortality of 3.2%. Prolonged ICU stay was associated with a 5% increased risk of death with hazard ratio 1.05, 95% confidence interval 1.02–1.08, p=0.001. Follow-up was complete in 151 (78%) patients for more than 7 years.

Despite the challenges associated with a cardiac programme for referring patients seeking intervention in a neighbouring country and the adverse characteristics of multiple lesions and complexity associated with late presentation, we report good surgical and interventional outcomes. Our goal remains to develop a comprehensive sustainable cardiac service in Namibia.

Previous studies have examined associations of cardiometabolic factors with depression and cognition separately.

To determine if depressive symptoms mediate the association between cardiometabolic factors and cognitive decline in two community studies.

Data for the analyses were drawn from the Rotterdam Study, the Netherlands (n = 2940) and the Whitehall II study, UK (n = 4469).

Mediation analyses suggested a direct association between cardiometabolic factors and cognitive decline and an indirect association through depression: poorer cardiometabolic status at time 1 was associated with a higher level of depressive symptoms at time 2 (standardised regression coefficient 0.07 and 0.06, respectively), which, in turn, was associated with greater cognitive decline between time 2 and time 3 (standardised regression coefficient of −0.15 and −0.41, respectively).

Evidence from two independent cohort studies suggest an association between cardiometabolic dysregulation and cognitive decline and that depressive symptoms tend to precede this decline.

None.