Using the dual-pathway framework (Beach et al., 2022a), we tested a Neuro-immune Network (NIN) hypothesis: i.e., that chronically elevated inflammatory processes may have delayed (i.e., incubation) effects on young adult substance use, leading to negative health outcomes. In a sample of 449 participants in the Family and Community Health Study who were followed from age 10 to age 29, we examined a non-self-report index of young adult elevated alcohol consumption (EAC). By controlling self-reported substance use at the transition to adulthood, we were able to isolate a significant delayed (incubation) effect from childhood exposure to danger to EAC (β = −.157, p = .006), which contributed to significantly worse aging outomes. Indirect effects from danger to aging outcomes via EAC were: GrimAge (IE = .010, [.002, .024]), Cardiac Risk (IE = −.004, [−.011, −.001]), DunedinPACE (IE = .002, [.000, .008]). In exploratory analyses we examined potential sex differences in effects, showing slightly stronger incubation effects for men and slightly stronger effects of EAC on aging outcomes for women. Results support the NIN hypothesis that incubation of immune pathway effects contributes to elevated alcohol consumption in young adulthood, resulting in accelerated aging and elevated cardiac risk outcomes via health behavior.

Little guidance exists for developing institutional policies and procedures that support financial management of community-engaged research, including those related to compensating community partners equitably and efficiently for their expertise and time. To address this gap at our institution, the North Carolina Translational and Clinical Sciences Institute at the University of North Carolina at Chapel Hill (UNC) pursued an iterative, multi-pronged approach to identify and address institutional barriers and facilitators related to community partner compensation for research engagement. This case study describes the approach used to involve research administrative leadership, research teams, and community partners at UNC in the identification of institutional barriers to efficient partner compensation. It also elucidates our efforts to develop policies, processes, and resources to address these barriers. The approaches and solutions described can be adapted by other academic research institutions to enhance compensation processes and to facilitate incorporation of community perspectives into the design and implementation of institutional processes that directly impact their engagement in research.

Behavioral science, once a hypernym for a collection of fields, is becoming a hyponym of itself. Nonacademic and academic practitioners alike increasingly discuss a “behavioral science,” a discipline that consolidates research from the other behavioral sciences to improve humans’ (and organizations’) predictive and manipulative powers. Despite the usefulness of a shared understanding of behavioral science, few can agree on a definition. After a brief overview of what behavioral scientists do and produce, I provide an inexhaustive list of the predicates behavioral scientists use to interpret the objects, people, and signs of their field and explore the grounding phase parts of objects’ or signs’ existence that behavioral scientists read to categorize objects or signs. I propose that behavioral scientists have begun to define behavioral science work by classifying objects or signs (which make up their work) using a partonomy in which a behavioral science-ness of a sign is directly positively correlated with the strength of its relation to the signs psychology and economics. Finally, I discuss what this definitional practice suggests for the behavioral science field now and in the future.

Children’s neural responses to emotions may play a role in the intergenerational transmission of anxiety. In a prospective longitudinal study of a community sample of N = 464 mother–child dyads, we examined relations among maternal anxiety symptoms when children were infants and age 5 years, child neural responses to emotional faces (angry, fearful, happy) at age 3 years, and child internalizing symptoms at age 5 years. Path analyses tested whether amplitudes of event-related potential (ERP) components selected a priori (N290, Nc, P400) (a) mediated associations between maternal anxiety symptoms in infancy and child internalizing symptoms at 5 years and/or (b) moderated associations between maternal anxiety symptoms at 5 years and child internalizing symptoms at 5 years. Mediating effects were not observed for any of the ERP measures. Nc and P400 amplitudes to angry faces and Nc amplitude to happy faces moderated the effect of maternal anxiety at 5 years on child internalizing symptoms at 5 years. Effects were not related to maternal depressive symptoms. Differential sex effects were not observed. The findings suggest that larger neural responses to emotional faces may represent a biological risk factor that amplifies vulnerability to the development of internalizing symptomatology in young children exposed to maternal anxiety.

Fructose-containing sugars can exaggerate postprandial lipaemia and stimulate hepatic de novo lipogenesis (DNL) when compared to glucose-based carbohydrates(1). Galactose has recently been shown to increase postprandial lipaemia compared to glucose(2), but mechanisms remain uncharacterised. The aim of this study was to assess the effect and mechanisms of lactose-induced lipaemia.

Twenty-four non-obese adults (12 male and 12 female) completed three trials in a randomised, crossover design (28 ± 7-day washout). During trials, participants consumed test drinks containing 50 g fat with 100 g of carbohydrate. The control carbohydrate was a glucose polymer (maltodextrin), the experimental carbohydrate was galactose-containing carbohydrate (lactose) and the active comparator was fructose-containing carbohydrate (sucrose). Hepatic DNL was assessed by the 2H2O method and [U-13C]-palmitate was added to the test drink to trace the fate of the ingested fat. Blood and breath samples were taken to determine plasma metabolite and hormone concentrations, in addition to plasma and breath 2H and 13C enrichments. Data were converted into incremental under the curve (iAUC) and were checked for normality by visual inspection of residuals. Differences between trials were assessed by one-way ANOVA. Where a main effect of trial was detected, post- hoc t-tests were performed to determine which trials differed from lactose according to the principle of closed-loop testing.

The plasma triacylglycerol iAUC (mean ± SD) in response to maltodextrin was 51 ± 68 mmol/L*360 min. Following lactose ingestion, plasma triacylglycerol iAUC increased to 98 ± 88 mmol/L*360 min (p<0.001 vs maltodextrin), which was comparable to sucrose [90 ± 95 mmol/L*360 min (p=0.41 vs lactose)]. Hepatic DNL in response to maltodextrin was 6.6 ± 3.0%. Following ingestion of lactose, hepatic DNL increased to 12.4 ± 6.9% (p=0.02 vs maltodextrin), which was comparable to sucrose [12.2 ± 6.9% (p=0.96 vs lactose)]. Exhaled 13CO2 in response to maltodextrin was 10.4 ± 4.1 mmol/kgFFM*360 min. Following ingestion of lactose, exhaled 13CO2 was 8.8 ± 4.9 mmol/kgFFM*360 min (p=0.09 vs maltodextrin), which was lower than sucrose [11.1 ± 3.9 mmol/kgFFM*360 min (p=0.01 vs lactose)].

These data are consistent with the hypothesis that hepatic de novo lipogenesis contributes to both lactose and sucrose-induced lipaemia and provide a rationale to investigate the longer-term effects of lactose and sucrose on metabolism.

From its inception, development and psychopathology theorists have sought to uncover the earliest forms of risk for mental health challenges in children, to prevent the development of more severe, intractable manifestations of psychopathology. Large familial risk registries have advanced our understanding of early, potentially modifiable factors that could prevent or mitigate the expression of challenging symptoms of neurodevelopmental conditions, and similar registries have been proposed to advance understanding of ADHD and related phenotypes. Data from single-site studies, largely focused on perinatal exposure to maternal mood disorders, reveal that a robust predictor of child psychopathology is parental psychopathology. However, early developmental trajectories of psychopathology risk may be better captured using transdiagnostic approaches in pregnancy, capturing the full range of mental health symptoms. We describe here the need for a parental mental health registry that begins prenatally that includes deep behavioral phenotyping across a range of transdiagnostic indicators of mental health risk to prevent psychopathology in children. This registry has the potential to uncover pathways to psychopathology risk in childhood and support the discovery of novel mechanisms to be targeted for prevention and intervention.

Research articles in the clinical and translational science literature commonly use quantitative data to inform evaluation of interventions, learn about the etiology of disease, or develop methods for diagnostic testing or risk prediction of future events. The peer review process must evaluate the methodology used therein, including use of quantitative statistical methods. In this manuscript, we provide guidance for peer reviewers tasked with assessing quantitative methodology, intended to complement guidelines and recommendations that exist for manuscript authors. We describe components of clinical and translational science research manuscripts that require assessment including study design and hypothesis evaluation, sampling and data acquisition, interventions (for studies that include an intervention), measurement of data, statistical analysis methods, presentation of the study results, and interpretation of the study results. For each component, we describe what reviewers should look for and assess; how reviewers should provide helpful comments for fixable errors or omissions; and how reviewers should communicate uncorrectable and irreparable errors. We then discuss the critical concepts of transparency and acceptance/revision guidelines when communicating with responsible journal editors.

State Medical Boards (SMBs) can take severe disciplinary actions (e.g., license revocation or suspension) against physicians who commit egregious wrongdoing in order to protect the public. However, there is noteworthy variability in the extent to which SMBs impose severe disciplinary action. In this manuscript, we present and synthesize a subset of 11 recommendations based on findings from our team’s larger consensus-building project that identified a list of 56 policies and legal provisions SMBs can use to better protect patients from egregious wrongdoing by physicians.

Although offspring of women exposed to childhood trauma exhibit elevated rates of psychopathology, many children demonstrate resilience to these intergenerational impacts. Among the variety of factors that likely contribute to resilience, epigenetic processes have been suggested to play an important role. The current study used a prospective design to test the novel hypothesis that offspring epigenetic aging – a measure of methylation differences that are associated with infant health outcomes – moderates the relationship between maternal exposure to childhood adversity and offspring symptomatology. Maternal childhood adversity was self-reported during pregnancy via the ACEs survey and the CTQ, which assessed total childhood trauma as well as maltreatment subtypes (i.e., emotional, physical, and sexual abuse). Offspring blood samples were collected at or shortly after birth and assayed on a DNA methylation microarray, and offspring symptomatology was assessed with the CBCL/1.5–5 when offspring were 2–4 years old. Results indicated that maternal childhood trauma, particularly sexual abuse, was predictive of offspring symptoms (ps = 0.003–0.03). However, the associations between maternal sexual abuse and offspring symptomatology were significantly attenuated in offspring with accelerated epigenetic aging. These findings further our understanding of how epigenetic processes may contribute to and attenuate the intergenerational link between stress and psychopathology.

The hypothesis that violence—especially gang violence—behaves like a contagious disease has grown in popularity in recent years. Scholars have long observed the tendency for violence to cluster in time and space, but little research has focused on empirically unpacking the mechanisms that make violence contagious. In the context of gang violence, retaliation is the prototypical mechanism to explain why violence begets violence. In this study, we leverage relational event models (REMs)—an underutilized yet particularly well-suited modeling technique to study the dynamics of inter-gang violence. We use REMs to examine gang violence’s tendency to replicate—for which retaliation is but one plausible mechanism—and its tendency to diffuse to other groups. We rely on data on conflicts between gangs in a region of Los Angeles over 3 years. We consider how the characteristics of gangs, their spatial proximity, networks of established rivalries, and the evolving history, directionality, and structure of conflicts predict future inter-gang conflicts. While retaliation is an important mechanism for the replication of violence, established rivalries, and inertia—a gang’s tendency to continue attacking the same group—are more important drivers of future violence. We also find little evidence for an emerging pecking order or status hierarchy between gangs suggested by other scholars. However, we find that gangs are more likely to attack multiple gangs in quick succession. We propose that gang violence is more likely to diffuse to other groups because of the boost of internal group processes an initial attack provides.

The Welfare of Farmed Animals (England) Regulations 2007 have now been approved by the UK Parliament and came into force on the 1st October 2007. The Regulations cover all farmed animals in England and have been made under the Animal Welfare Act 2006. The 2007 Regulations replace the previous Welfare of Farmed Animals (England) Regulations 2000 (as amended), and additionally Part I of the Agriculture (Miscellaneous Provisions) Act 1968 has been repealed. The changes bring farmed animal legislation into line with the Animal Welfare Act 2006.