The Remote Learning Experience at Portland State University in Spring 2020

It is an endeavor to understand what we have and will learn about the impact of remote instruction on faculty, students and relevant academic support teams. Simply put: We want to learn from an experiment foisted upon us by a health crisis. We have engaged in an incredibly innovative response. And now, we ask what have we learned? How might we improve? And, most importantly, are there implications from this experiment for the future of instruction at PSU and throughout higher education? The project was organized around two stages in the Spring 2020 term. Stage One: Out of the Gate: Reflections and Lessons Learned (First half of the term) Stage Two: Reaching the Finish Line: Lessons Learned and Recommendations for moving forward (Second half of the term). The project began the week of April 20 and continued through June 12. The original plan called for the following participants: (a) ten undergraduate students to put together a group of 8-10 other students to discuss the questions posed in the study; (b) Three graduate students who would assemble 5-7 fellow graduate students; (c) Three tenured or tenure-track faculty, two non-tenure-track faculty and three adjunct faculty, each of whom would form a chat group of 5-7 other faculty to discuss the questions posed in the study. In addition, Judith Ramaley put together a chat group of a dozen student support unit leaders to explore how each unit adjusted as the university moved quickly to remote learning and remote work and then, in a second round, what lessons each had learned throughout the spring term about ways to support students and assist faculty members who were also seeking to help their students

The multifaceted functions of β-arrestins and their therapeutic potential in neurodegenerative diseases

Abstract Arrestins are multifunctional proteins that regulate G-protein-coupled receptor (GPCR) desensitization, signaling, and internalization. The arrestin family consists of four subtypes: visual arrestin1, β-arrestin1, β-arrestin2, and visual arrestin-4. Recent studies have revealed the multifunctional roles of β-arrestins beyond GPCR signaling, including scaffolding and adapter functions, and physically interacting with non-GPCR receptors. Increasing evidence suggests that β-arrestins are involved in the pathogenesis of a variety of neurodegenerative diseases, including Alzheimer’s disease (AD), frontotemporal dementia (FTD), and Parkinson’s disease (PD). β-arrestins physically interact with γ-secretase, leading to increased production and accumulation of amyloid-beta in AD. Furthermore, β-arrestin oligomers inhibit the autophagy cargo receptor p62/SQSTM1, resulting in tau accumulation and aggregation in FTD. In PD, β-arrestins are upregulated in postmortem brain tissue and an MPTP model, and the β2AR regulates SNCA gene expression. In this review, we aim to provide an overview of β-arrestin1 and β-arrestin2, and describe their physiological functions and roles in neurodegenerative diseases. The multifaceted roles of β-arrestins and their involvement in neurodegenerative diseases suggest that they may serve as promising therapeutic targets

The dimensionality and structure of species trait spaces

International audienc

The dimensionality and structure of species trait spaces

Trait- based ecology aims to understand the processes that generate the overarching diversity of organismal traits and their influence on ecosystem functioning. Achieving this goal requires simplifying this complexity in synthetic axes defining a trait space and to cluster species based on their traits while identifying those with unique combinations of traits. However, so far, we know little about the dimensionality, the robustness to trait omission and the structure of these trait spaces. Here, we propose a unified framework and a synthesis across 30 trait datasets representing a broad variety of taxa, ecosystems and spatial scales to show that a common trade- off between trait space quality and operationality appears between three and six dimensions. The robustness to trait omission is generally low but highly variable among datasets. We also highlight invariant scaling relationships, whatever organismal complexity, between the number of clusters, the number of species in the dominant cluster and the number of unique species with total species richness. When species richness increases, the number of unique species saturates, whereas species tend to disproportionately pack in the richest cluster. Based on these results, we propose some rules of thumb to build species trait spaces and estimate subsequent functional diversity indices

Study of LPIN1, LPIN2 and LPIN3 in rhabdomyolysis and exercise-induced myalgia

BACKGROUND: Recessive LPIN1 mutations were identified as a cause of severe rhabdomyolysis in pediatric patients. The human lipin family includes two other closely related members, lipin-2 and 3, which share strong homology and similar activity. The study aimed to determine the involvement of the LPIN family genes in a cohort of pediatric and adult patients (n = 171) presenting with muscular symptoms, ranging from severe (CK >10 000 UI/L) or moderate (CK <10 000 UI/L) rhabdomyolysis (n = 141) to exercise-induced myalgia (n = 30), and to report the clinical findings in patients harboring mutations. METHODS: Coding regions of LPIN1, LPIN2 and LPIN3 genes were sequenced using genomic or complementary DNAs. RESULTS: Eighteen patients harbored two LPIN1 mutations, including a frequent intragenic deletion. All presented with severe episodes of rhabdomyolysis, starting before age 6 years except two (8 and 42 years). Few patients also suffered from permanent muscle symptoms, including the eldest ones (≥ 40 years). Around 3/4 of muscle biopsies showed accumulation of lipid droplets. At least 40% of heterozygous relatives presented muscular myalgia. Nine heterozygous SNPs in LPIN family genes were identified in milder phenotypes (mild rhabdomyolysis or myalgia). These variants were non-functional in yeast complementation assay based on respiratory activity, except the LPIN3-P24L variant. CONCLUSION: LPIN1-related myolysis constitutes a major cause of early-onset rhabdomyolysis and occasionally in adults. Heterozygous LPIN1 mutations may cause mild muscular symptoms. No major defects of LPIN2 or LPIN3 genes were associated with muscular manifestations