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Borderline personality disorder (BPD) is a debilitating psychiatric illness whose symptoms frequently emerge during adolescence. Critically, self-injury and suicide attempts in BPD are often precipitated by interpersonal discord. Initial studies in adults suggest that the interpersonal difficulties common in BPD may emerge from disrupted processing of socioemotional stimuli. Less is known about these processes in adolescents with BPD symptoms, despite substantial changes in socioemotional processing during this developmental period. Eighty-six adolescents and young adults with and without BPD symptoms completed an emotional interference task involving the identification of a facial emotion expression in the presence of a conflicting or congruent emotion word. We used hierarchical drift diffusion modeling to index speed of processing and decision boundary. Using Bayesian multilevel regression, we characterized age-related differences in facial emotion processing. We examined whether BPD symptom dimensions were associated with alterations in facial emotion processing. To determine the specificity of our effects, we analyzed behavioral data from a corresponding nonemotional interference task. Emotion-related impulsivity, but not negative affectivity or interpersonal dysfunction, predicted inefficient processing when presented with conflicting negative emotional stimuli. Across both tasks, emotion-related impulsivity in adolescents, but not young adults, was further associated with a lower decision boundary - resulting in fast but inaccurate decisions. Impulsive adolescents with BPD symptoms are prone to making errors when appraising facial emotion expressions, which may potentiate or worsen interpersonal conflicts. Our findings highlight the role of lower-level social cognitive processes in interpersonal difficulties among vulnerable youth during a sensitive developmental window.

Borderline personality disorder (BPD) is a debilitating psychiatric illness whose symptoms frequently emerge during adolescence. Initial studies in adults suggest that the interpersonal difficulties common in BPD may emerge from disrupted processing of social and emotional stimuli. Less is known about these processes in adolescents with BPD symptoms, despite substantial changes in socioemotional processing during this developmental period. 86 adolescents and young adults with and without BPD symptoms completed an emotional interference task involving the identification of a facial emotion expression in the presence of a conflicting or congruent emotion word. We used hierarchical drift diffusion modeling to index speed of processing and decision boundary. Using Bayesian multilevel regression, we characterized age-related differences in facial emotion processing. We then examined whether BPD symptom dimensions were associated with facial emotion processing on this task. To determine the specificity of our effects, we analyzed behavioral data from a corresponding nonemotional interference task. Impulsivity, but not negative affectivity or interpersonal dysfunction, predicted inefficient processing when presented with conflicting negative emotional stimuli. Across both tasks, impulsivity in adolescents was further associated with a lower decision boundary. Impulsive adolescents were especially likely to make fast, but inaccurate decisions about another person's emotional state. Impulsive adolescents with BPD symptoms are prone to making errors when appraising facial expressions of emotions, which may potentiate or worsen interpersonal conflicts. Our findings highlight the role of lower-level social cognitive processes in interpersonal difficulties among vulnerable youth during a sensitive developmental window.

Key Points A rapidly growing list of rare genetic causes of autism spectrum disorders (ASDs) is being identified, giving insights into the underlying biology of these disorders. Contrary to what is generally assumed, existing genetic findings are already able to inform our current clinical practice. Genetic findings have great potential to improve the quality of health care provided to individuals with an ASD and to improve their quality of life. However, several initiatives are needed to support the translation of this knowledge into health care. It is important to promote the education of the relevant health care professionals about clinical genetic testing and its possible benefits. We must also adopt a broader view of ASDs that recognizes psychiatric and somatic comorbidity. The field would benefit greatly from unprecedented global cooperation to improve sharing of genotype–phenotype data from cross-sectional and longitudinal studies. Furthermore, researchers and clinicians must work in partnership with the autism community regarding the genetics and health care research agenda. Finally, genetic information should be used to develop future treatments and interventions for psychiatric and somatic comorbidity, and should be evaluated in clinical trials. The question is not so much when ASD genetics will start to influence our clinical practice but rather how we can optimally use the knowledge that we already have and what is required to use its full clinical potential in the future. Various large studies have provided unprecedented insights into the genetics of autism spectrum disorders (ASDs). This Review discusses the challenges and opportunities of translating genetic and biological insights into clinical progress for ASDs, in areas including genetic testing, ASD classification, genetic counselling, comorbidities and therapeutics. Genetic studies have revealed the involvement of hundreds of gene variants in autism. Their risk effects are highly variable, and they are frequently related to other conditions besides autism. However, many different variants converge on common biological pathways. These findings indicate that aetiological heterogeneity, variable penetrance and genetic pleiotropy are pervasive characteristics of autism genetics. Although this advancing insight should improve clinical care, at present there is a substantial discrepancy between research knowledge and its clinical application. In this Review, we discuss the current challenges and opportunities for the translation of autism genetics knowledge into clinical practice.

Reporting progress against targets for international biodiversity agreements is hindered by a shortage of suitable biodiversity data. We describe a cost-effective system involving Reef Life Survey citizen scientists in the systematic collection of quantitative data covering multiple phyla that can underpin numerous marine biodiversity indicators at high spatial and temporal resolution. We then summarize the findings of a continental- and decadal-scale State of the Environment assessment for rocky and coral reefs based on indicators of ecosystem state relating to fishing, ocean warming, and invasive species and describing the distribution of threatened species. Fishing impacts are widespread, whereas substantial warming-related change affected some regions between 2005 and 2015. Invasive species are concentrated near harbors in southeastern Australia, and the threatened-species index is highest for the Great Australian Bight and Tasman Sea. Our approach can be applied globally to improve reporting against biodiversity targets and enhance public and policymakers’ understanding of marine biodiversity trends.

Background High prevalence rates of β2-agonist use among athletes in competitive sports makes it tempting to speculate that illegitimate use of β2-agonists boosts performance. However, data regarding the potential performance-enhancing effects of inhaled β2-agonists and its underlying molecular basis are scarce. Methods In total, 24 competitive endurance athletes (12f/12m) participated in a clinical double-blinded balanced four-way block cross-over trial to investigate single versus combined effects of β2-agonists salbutamol (SAL) and formoterol (FOR), to evaluate the potential performance enhancement of SAL (1200 µg, Cyclocaps, Pb Pharma GmbH), FOR (36 µg, Sandoz, HEXAL AG) and SAL + FOR (1200 µg + 36 µg) compared to placebo (PLA, Gelatine capsules containing lactose monohydrate, Pharmacy of the University Hospital Ulm). Measurements included skeletal muscle gene and protein expression, endocrine regulation, urinary/serum β2-agonist concentrations, cardiac markers, cardiopulmonary and lung function testing and the 10-min time trial (TT) performance on a bicycle ergometer as outcome variables. Blood and urine samples were collected pre-, post-, 3 h post- and 24 h post-TT. Results Mean power output during TT was not different between study arms. Treatment effects regarding lung function ( p  < 0.001), echocardiographic (left ventricular end-systolic volume p  = 0.037; endocardial global longitudinal strain p  < 0.001) and metabolic variables (e.g. NR4A2 and ATF3 pathway) were observed without any influence on performance. In female athletes, total serum β2-agonist concentrations for SAL and FOR were higher. Microarray muscle gene analysis showed a treatment effect for target genes in energy metabolism with strongest effect by SAL + FOR (NR4A2; p  = 0.001). Of endocrine variables, follicle-stimulating hormone (3 h Post–Post-TT), luteinizing hormone (3 h Post–Pre-TT) and insulin (Post–Pre-TT) concentrations showed a treatment effect (all p  < 0.05). Conclusions No endurance performance-enhancing effect for SAL, FOR or SAL + FOR within the permitted dosages compared to PLA was found despite an acute effect on lung and cardiac function as well as endocrine and metabolic variables in healthy participants. The impact of combined β2-agonists on performance and sex-specific thresholds on the molecular and cardiac level and their potential long-term performance enhancing or health effects have still to be determined. Trial registration : Registered at Eudra CT with the number: 2015-005598-19 (09.12.2015) and DRKS with number DRKS00010574 (16.11.2021, retrospectively registered). Key Points • Combined β2-agonist application in threshold doses according to World Anti-Doping Agency (WADA) standards does not result in acute enhanced high-intensity endurance performance in healthy male and female athletes. • Sex-specific thresholds have to be considered as female sex showed significantly higher β2-agonist serum concentrations compared to their male counterparts. • Acute effects on lung function and cardiac variables are observed with presumably no performance-enhancing effects in competitions of short duration, but effects in longer time trials or long-term health effects have to be considered.

Blastocyst complementation combined with gene editing is an emerging approach in the field of regenerative medicine that could potentially solve the worldwide problem of organ shortages for transplantation. In theory, blastocyst complementation can generate fully functional human organs or tissues, grown within genetically engineered livestock animals. Targeted deletion of a specific gene(s) using gene editing to cause deficiencies in organ development can open a niche for human stem cells to occupy, thus generating human tissues. Within this review, we will focus on the pancreas, liver, heart, kidney, lung, and skeletal muscle, as well as cells of the immune and nervous systems. Within each of these organ systems, we identify and discuss (i) the common causes of organ failure; (ii) the current state of regenerative therapies; and (iii) the candidate genes to knockout and enable specific exogenous organ development via the use of blastocyst complementation. We also highlight some of the current barriers limiting the success of blastocyst complementation.

Affymetrix GeneChip microarrays are a powerful tool to study global gene expression profiles and have been used on many species. However, no sheep-specific Affymetrix GeneChip is currently available and the bovine array is fairly limited in its coverage and annotation. Previously, a probe-selection method based on hybridisation of genomic DNA (gDNA) was developed, which enables GeneChips to be used for species that they were not designed for. This approach can greatly increase the number of potential annotated genes that can be studied beyond that which is currently available, particularly for species that do not have comprehensively characterised genomes. In this study, we demonstrate that gDNA-based probe selection on the Affymetrix Human U133+2 GeneChip array can be used to study gene expression profiles in sheep tissues. More than 20 000 transcripts were detected in triplicate ovine skeletal muscle and liver samples, which is more than would be possible using the commercially available sheep-specific microarray. The majority of the top 15 differentially expressed genes for each tissue were known to either be expressed in a tissue-specific manner or relate to specific functions of that tissue. Gene ontology analysis of the differentially expressed genes revealed the expected differences in gene expression profiles between the two tissues. Besides demonstrating that the probe selection method can be used to study the ovine transcriptome, the benefits of this approach are that it can greatly increase the number of annotated and novel genes that can be studied beyond those currently possible using ovine- or bovine-specific microarrays. This same method also has the potential to allow the study of other species where species-specific microarrays are not available or whose genomes have not been comprehensively characterised.

[This corrects the article DOI: 10.1093/biosci/biw180.].

Theoretical neurodevelopmental models implicate increases in dopamine (DA) function and limitations in neurocognitive control in risk-taking behavior, including substance use, during the transition from adolescence to adulthood. However, developmental relationships between DA, neurocognitive control, and the emergence of substance use are poorly understood. Here, we tested the role of basal ganglia tissue iron, reflecting DA neurophysiology, as well as impulsivity and inhibitory control in longitudinal developmental trajectories of substance use. We leveraged the National Consortium on Alcohol and NeuroDevelopment in Adolescence and Adulthood (NCANDA-A) cohort, a large, multisite longitudinal neuroimaging study of 807 participants (baseline ages 12 - 22 years old, 50% female, 1 - 9 annual visits per participant, 6164 sessions total). Substance use, inhibitory control, and tissue iron increased non-linearly during adolescence into young adulthood, concurrent with decreases in impulsivity. Non-linear Growth Mixture Models identified four common trajectories of substance use: (no- or low levels of use across visits; 30% of participants), (peak use in adolescence/young adulthood followed by declines; 26%), (early, steep linear increases in use from adolescence into adulthood; 17%), and (low use in adolescence, followed by late linear increases into adulthood; 26%). We show that increased substance use was associated with a phenotype of impulsivity, inhibitory control, and basal ganglia tissue iron, particularly in early adolescence in individuals who displayed youth peak patterns in substance use trajectories. These findings highlight that early developmental differences in DA-related neurobiology and associated impulsivity and cognitive control shape distinct trajectories of adolescent substance use, underscoring adolescence as a critical window for the early identification and implementation of neurodevelopmentally sensitive interventions for substance use disorders.

We have isolated the Xenopus orthologue of the T-box gene, Tbx20, and characterized its developmental expression profile. We show that Tbx20 is one of the earliest markers of heart tissue in Xenopus, and is expressed throughout all cardiac tissue during later stages of development. In addition, we also observe expression in the cement gland, the jugular vein, the lung bud, the cloacal aperture, rhombomeres 2, 4, 6 and 8, and in a subset of motor neurons.