Evidence-based design strategies to produce health promoting landscapes

Outdoor Environments for Health and Well-being is an international master’s program offered at the Swedish University of Agricultural Sciences (SLU) at Alnarp¸ leading to a Master of Science degree with a specialization in Environmental Psychology. The course Nature-Based Interventions LK0306 focuses on how different types of natural outdoor settings can be used for interventions as part of treatment, rehabilitation and programs for the prevention and promotion of healthy everyday habits in different user groups. This factsheet is the final product of the students’ work within the course during the autumn term of 2019. This year, Associate Professor John Rayner, contributed to this factsheet with his thoughts on the findings from the different groups’ work

On Being Twice Exceptional in Sweden - An Interview-Based Case Study about the Educational Situation for a Gifted Student Diagnosed with ADHD

The gifted education research area is rapidly expanding in Sweden. In the context of very limited research nationally, demands are increasing for steering documents and addressing of student and teacher needs in practice. However, Swedish research on students that are ‘twice exceptional’—students classified as being both gifted and disabled (for instance, through a neurodevelopmental disorder such as ADHD)—is nearly non-existent. In this study, we present an exploratory single case study of a female student in school year seven based on semi-structured individual interviews with the student and her two guardians regarding her educational situation. The data were first inductively coded and triangulated in collaboration between three of the authors. A fourth author later independently and deductively coded one-third of the data based on the previously inductively determined thematic structure and conducted a consensus interrater reliability check, exceeding 85% percent agreement. The three main themes are as follows: (1) multiplex perspectives on academic outcomes and expectations, (2) the intersection between twice exceptionality and academic work, and (3) information and perceptions about twice exceptionality. The results indicate several educational challenges and opportunities for twice exceptional students. Further research is needed regarding twice exceptional students in Sweden.Validerad;2023;Nivå 2;2023-11-10 (joosat);Part of special issue: Identifying and Supporting Giftedness and Talent in SchoolsCC BY 4.0 License</p

LRIG1 is a conserved EGFR regulator involved in melanoma development, survival and treatment resistance

Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a pan-negative regulator of receptor tyrosine kinase (RTK) signaling and a tumor suppressor in several cancers, but its involvement in melanoma is largely unexplored. Here, we aim to determine the role of LRIG1 in melanoma tumorigenesis, RTK signaling, and BRAF inhibitor resistance. We find that LRIG1 is downregulated during early tumorigenesis and that LRIG1 affects activation of the epidermal growth factor receptor (EGFR) in melanoma cells. LRIG1-dependent regulation of EGFR signaling is evolutionary conserved to the roundworm C. elegans, where negative regulation of the EGFR-Ras-Raf pathway by sma-10/LRIG completely depends on presence of the receptor let-23/EGFR. In a cohort of metastatic melanoma patients, we observe an association between LRIG1 and survival in the triple wild-type subtype and in tumors with high EGFR expression. During in vitro development of BRAF inhibitor resistance, LRIG1 expression decreases; and mimics LRIG1 knockout cells for increased EGFR expression. Treating resistant cells with recombinant LRIG1 suppresses AKT activation and proliferation. Together, our results show that sma-10/LRIG is a conserved regulator of RTK signaling, add to our understanding of LRIG1 in melanoma and identifies recombinant LRIG1 as a potential therapeutic against BRAF inhibitor-resistant melanoma

Regulation of YAP Promotor Accessibility in Endothelial Mechanotransduction

BACKGROUND: Endothelial cells are constantly exposed to mechanical forces in the form of fluid shear stress, extracellular stiffness, and cyclic strain. The mechanoresponsive activity of YAP (Yes-associated protein) and its role in vascular development are well described; however, whether changes to transcription or epigenetic regulation of YAP are involved in these processes remains unanswered. Furthermore, how mechanical forces are transduced to the nucleus to drive transcriptional reprogramming in endothelial cells is poorly understood. The YAP target gene, AmotL2 (angiomotin-like 2), is a junctional mechanotransducer that connects cell-cell junctions to the nuclear membrane via the actin cytoskeleton. METHODS: We applied mechanical manipulations including shear flow, stretching, and substrate stiffness to endothelial cells to investigate the role of mechanical forces in modulating YAP transcription. Using in vitro and in vivo endothelial depletion of AmotL2, we assess nuclear morphology, chromatin organization (using transposase-accessible chromatin sequencing), and whole-mount immunofluorescent staining of the aorta to determine the regulation and functionality of YAP. Finally, we use genetic and chemical inhibition to uncouple the nuclear-cytoskeletal connection to investigate the role of this pathway on YAP transcription. RESULTS: Our results reveal that mechanical forces sensed at cell-cell junctions by the YAP target gene AmotL2 are directly involved in changes in global chromatin accessibility and activity of the histone methyltransferase EZH2, leading to modulation of YAP promotor activity. Functionally, shear stress-induced proliferation of endothelial cells in vivo was reliant on AmotL2 and YAP/TAZ (transcriptional coactivator with PDZ-binding motif) expression. Mechanistically, uncoupling of the nuclear-cytoskeletal connection from junctions and focal adhesions led to altered nuclear morphology, chromatin accessibility, and YAP promotor activity. CONCLUSIONS: Our findings reveal a role for AmotL2 and nuclear-cytoskeletal force transmission in modulating the epigenetic and transcriptional regulation of YAP to maintain a mechano-enforced positive feedback loop of vascular homeostasis. These findings may offer an explanation as to the proinflammatory phenotype that leads to aneurysm formation observed in AmotL2 endothelial deletion models.Peer reviewe