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Commercialization of autonomous vehicle technology is a major goal of the automotive industry, thus research in this space is rapidly expanding across the world. However, despite this high level of research activity, literature detailing a straightforward and cost-effective approach to the development of an AV research platform is sparse. To address this need, we present the methodology and results regarding the AV instrumentation and controls of a 2019 Kia Niro which was developed for a local AV pilot program. This platform includes a drive-by-wire actuation kit, Aptiv electronically scanning radar, stereo camera, MobilEye computer vision system, LiDAR, inertial measurement unit, two global positioning system receivers to provide heading information, and an in-vehicle computer for driving environment perception and path planning. Robotic Operating System software is used as the system middleware between the instruments and the autonomous application algorithms. After selection, installation, and integration of these components, our results show successful utilization of all sensors, drive-by-wire functionality, a total additional power* consumption of 242.8 Watts (*Typical), and an overall cost of $118,189 USD, which is a significant saving compared to other commercially available systems with similar functionality. This vehicle continues to serve as our primary AV research and development platform.

Laccases (E.C. 1.10.3.2) are glycoproteins widely distributed in nature. Their structural conformation includes three copper sites in their catalytic center, which are responsible for facilitating substrate oxidation, leading to the generation of H2O instead of H2O2. The measurement of laccase activity (UL−1) results may vary depending on the type of laccase, buffer, redox mediators, and substrates employed. The aim was to select the best conditions for rGILCC 1 and rPOXA 1B laccases activity assay. After sequential statistical assays, the molecular dynamics proved to support this process, and we aimed to accumulate valuable insights into the potential application of these enzymes for the degradation of novel substrates with negative environmental implications. Citrate buffer treatment T2 (CB T2) (pH 3.0 ± 0.2; λ420nm, 2 mM ABTS) had the most favorable results, with 7.315 ± 0.131 UL−1 for rGILCC 1 and 5291.665 ± 45.83 UL−1 for rPOXA 1B. The use of citrate buffer increased the enzyme affinity for ABTS since lower Km values occurred for both enzymes (1.49 × 10−2 mM for rGILCC 1 and 3.72 × 10−2 mM for rPOXA 1B) compared to those obtained in acetate buffer (5.36 × 10−2 mM for rGILCC 1 and 1.72 mM for rPOXA 1B). The molecular dynamics of GILCC 1–ABTS and POXA 1B–ABTS showed stable behavior, with root mean square deviation (RMSD) values not exceeding 2.0 Å. Enzyme activities (rGILCC 1 and rPOXA 1B) and 3D model–ABTS interactions (GILCC 1–ABTS and POXA 1B–ABTS) were under the strong influence of pH, wavelength, ions, and ABTS concentration, supported by computational studies identifying the stabilizing residues and interactions. Integration of the experimental and computational approaches yielded a comprehensive understanding of enzyme–substrate interactions, offering potential applications in environmental substrate treatments.

Genetic factors are strongly implicated in the susceptibility to develop externalizing syndromes such as attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder, conduct disorder, and substance use disorder (SUD). Variants in the ADGRL3 (LPHN3) gene predispose to ADHD and predict ADHD severity, disruptive behaviors comorbidity, long-term outcome, and response to treatment. In this study, we investigated whether variants within ADGRL3 are associated with SUD, a disorder that is frequently co-morbid with ADHD. Using family-based, case-control, and longitudinal samples from disparate regions of the world (n = 2698), recruited either for clinical, genetic epidemiological or pharmacogenomic studies of ADHD, we assembled recursive-partitioning frameworks (classification tree analyses) with clinical, demographic, and ADGRL3 genetic information to predict SUD susceptibility. Our results indicate that SUD can be efficiently and robustly predicted in ADHD participants. The genetic models used remained highly efficient in predicting SUD in a large sample of individuals with severe SUD from a psychiatric institution that were not ascertained on the basis of ADHD diagnosis, thus identifying ADGRL3 as a risk gene for SUD. Recursive-partitioning analyses revealed that rs4860437 was the predominant predictive variant. This new methodological approach offers novel insights into higher order predictive interactions and offers a unique opportunity for translational application in the clinical assessment of patients at high risk for SUD.

Attention Deficit Hyperactivity Disorder (ADHD) is a highly heritable and prevalent neurodevelopmental disorder that frequently persists into adulthood. Strong evidence from genetic studies indicates that single nucleotide polymorphisms (SNPs) harboured in the ADGRL3 (LPHN3), SNAP25, FGF1, DRD4, and SLC6A2 genes are associated with ADHD. We genotyped 26 SNPs harboured in genes previously reported to be associated with ADHD and evaluated their potential association in 386 individuals belonging to 113 nuclear families from a Caribbean community in Barranquilla, Colombia, using family-based association tests. SNPs rs362990-SNAP25 (T allele; p = 2.46 × 10−4), rs2282794-FGF1 (A allele; p = 1.33 × 10−2), rs2122642-ADGRL3 (C allele, p = 3.5 × 10−2), and ADGRL3 haplotype CCC (markers rs1565902-rs10001410-rs2122642, OR = 1.74, Ppermuted = 0.021) were significantly associated with ADHD. Our results confirm the susceptibility to ADHD conferred by SNAP25, FGF1, and ADGRL3 variants in a community with a significant African American component, and provide evidence supporting the existence of specific patterns of genetic stratification underpinning the susceptibility to ADHD. Knowledge of population genetics is crucial to define risk and predict susceptibility to disease.

Canine transmissible venereal tumour (CTVT) is a clonally transmissible cancer that originated approximately 11,000 years ago and affects dogs worldwide. Despite the clonal origin of the CTVT nuclear genome, CTVT mitochondrial genomes (mtDNAs) have been acquired by periodic capture from transient hosts. We sequenced 449 complete mtDNAs from a global population of CTVTs, and show that mtDNA horizontal transfer has occurred at least five times, delineating five tumour clades whose distributions track two millennia of dog global migration. Negative selection has operated to prevent accumulation of deleterious mutations in captured mtDNA, and recombination has caused occasional mtDNA re-assortment. These findings implicate functional mtDNA as a driver of CTVT global metastatic spread, further highlighting the important role of mtDNA in cancer evolution. A unique cancer called canine transmissible venereal tumour (CTVT) causes ugly tumours to form on the genitals of dogs. Unlike most other cancers, CTVT is contagious: the cancer cells can be directly transferred from one dog to another when they mate. The disease originated from the cancer cells of one individual dog that lived approximately 11,000 years ago. CTVT now affects dogs all over the world, which makes it the oldest and most widespread cancer known in nature. Like healthy cells, cancer cells contain compartments known as mitochondria that produce the chemical energy needed to power vital processes. Inside the mitochondria, there is some DNA that encodes the proteins that mitochondria need to perform this role. Changes (or mutations) to this mitochondrial DNA (mtDNA) may stop the mitochondria from working properly. CTVT cells have previously been found to occasionally capture mtDNA from normal dog cells, which suggests that replenishing their mtDNA may help promote CTVT cell growth. Furthermore, these captured mtDNAs act as genetic \"flags\" that can help trace the spread of the disease. Here, Strakova, Ní Leathlobhair et al. analysed the mtDNA in CTVT tumours collected from over 400 dogs in 39 countries. The analysis shows that CTVT cells have captured mtDNA from normal dog cells on at least five occasions. Over the last 2,000 years, the disease appears to have spread rapidly around the world, perhaps transported by dogs travelling on ships along historic trade routes. CTVT may have only reached the Americas within the last 500 years, possibly carried there by dogs brought by Europeans. Likewise, CTVT probably only came to Australia after European contact. The experiments also revealed that the most damaging types of mutations were absent from the mtDNA of CTVT, which suggests that fully functioning mitochondria play an important role in CTVT. Unexpectedly, Strakova, Ní Leathlobhair et al. found evidence that certain sections of mtDNA in some CTVT cells have been exchanged, or shuffled, with the mtDNA captured from normal dog cells. This type of “recombination” is not usually thought to occur in mtDNA, and has not previously been detected in cancer. Future studies will determine if this process is widespread in other types of cancer, including in humans.

Humans are now operating well outside the planetary conditions under which social and economic development has been possible. A precondition for securing equitable access to this prosperity is to safeguard the stability of the Earth system. The situation is urgent—we need a swift and profound shift in direction—a collective transformation. In response, the Earth Commission has developed a science‐based framework that integrates biophysical limits with justice considerations, aiming to enable human wellbeing for all. The Earth Commission's first assessment showed that multiple safe and just Earth system boundaries have already been transgressed, threatening the resilience of the planet and the well‐being of billions. This paper outlines the vision and scientific strategy for the Earth Commission's second phase (2024–2027), which focuses on advancing this framework and translating it into actionable budgets and exploring transformation pathways toward a safe and just future. Key components include expanding the safe and just boundary assessment to currently under‐assessed Earth system processes (e.g., novel entities and ocean change), integrating justice more deeply into the framework, modeling interactions between boundaries and tipping points, and developing practical approaches to cross‐scale translation and transformation. Special attention is given to the structural inequalities and power dynamics that shape both environmental degradation and our capacity to act. Through coordinated research, interdisciplinary collaboration, and stakeholder engagement, the Earth Commission seeks to provide knowledge to guide collective efforts toward transforming to a safe and just space for both people and the planet. Plain Language Summary People around the world are already feeling the effects of a planet under pressure‐from climate change and biodiversity loss to rising inequality. Scientists are warning that we are pushing Earth's life‐support systems beyond their safe limits, putting both nature and human well‐being at serious risk. In response, the Earth Commission has created a new science‐based framework that brings together environmental limits and fairness. This helps define what a “safe and just” future looks like‐one where the planet remains stable, and the well‐being of all people is promoted. The next phase of work focuses on improving our understanding of under‐explored threats like pollution and novel types of pollution, deepening the role of justice in our analysis, and identifying fair ways to share responsibility for staying within Earth's limits. It also looks at how big changes to systems like energy and food can help move us toward a safe and just future. The goal is to support faster, fairer action that protects both people and the planet. Key Points Human activity has pushed the planet beyond safe and just limits, endangering stability and the well‐being of billions A just and rapid transformation is needed to shift toward a liveable future for both people and the planet The Earth Commission provides a science‐based framework to guide systemic change across scales and sectors

Canine transmissible venereal tumour (CTVT) is a clonally transmissible cancer that originated approximately 11,000 years ago and affects dogs worldwide. Despite the clonal origin of the CTVT nuclear genome, CTVT mitochondrial genomes (mtDNAs) have been acquired by periodic capture from transient hosts. We sequenced 449 complete mtDNAs from a global population of CTVTs, and show that mtDNA horizontal transfer has occurred at least five times, delineating five tumour clades whose distributions track two millennia of dog global migration. Negative selection has operated to prevent accumulation of deleterious mutations in captured mtDNA, and recombination has caused occasional mtDNA re-assortment. These findings implicate functional mtDNA as a driver of CTVT global metastatic spread, further highlighting the important role of mtDNA in cancer evolution.

In a hierarchical \\(\\)CDM Universe, cosmic filaments serve as the primary channels for matter accretion into galaxy clusters, influencing the shape of their dark matter halos. We investigate whether the elongation of galaxy clusters correlates with the orientation of surrounding filaments, providing the first observational test of this relationship in large supercluster regions. We identified and characterized cosmic filaments in two dimensions within the two superclusters that are part of the low-redshift sub-survey of the Chilean Cluster Galaxy Evolution Survey (CHANCES): the Shapley supercluster and the Horologium-Reticulum supercluster. We analyzed the alignment between filament directions -- traced by galaxy distributions -- and the triaxiality of cluster gravitational potentials -- traced by X-ray emission- using publicly available optical and X-ray data. We have found that most (82%) of the X-ray clusters are associated with and interconnected by the optically detected filaments. The clusters-filaments alignment analysis shows that the elongation of most clusters is well aligned with nearby filaments, providing observational confirmation of theoretical predictions, with the alignment progressively reducing at larger cluster-centric distances (\\(> 1.6 r_200\\)). Overall, our results support the notion that filaments are the main source of galaxy accretion at redshift below 0.1 and additionally provide evidence that matter accretion through filaments shapes the gravitational potential of galaxy clusters. We propose this measurement as a simple observational proxy to determine the direction of accretion in clusters, which is key to understanding both galaxy evolution and the merger history of galaxy clusters.