Web Application for Surf Journaling

Before deciding whether to surf, many surfers consult surf forecast services. Current surf forecasting offerings provide general information such as predicted surf height and a condition rating, but these predictions are often misleading, as widely varying swell conditions can receive the same forecast. Additionally, these existing services do not incorporate user feedback into their predictions, which requires users to keep a mental mapping of trends between forecast information and real-life conditions. This report describes the design and implementation of a web application where users can record the surf conditions and assign ratings to recorded surf sessions. With historical surf conditions and rating information at their disposal, users can compare current conditions to past recorded sessions in order to more accurately predict today’s wave conditions. This increased forecast confidence will help users to choose the optimal locations and times to surf

Endocytic Sorting and Downregulation of the M2 Acetylcholine Receptor is Regulated by Ubiquitin and the ESCRT Complex

Acknowledgements The authors would like to thank Professor Mark von Zastrow from the University of California, San Francisco for sharing critical constructs. We would like to thank Kevin MacKenzie and the University of Aberdeen Microscopy core and the Iain Fraser Flow cytometry core for their assistance in the acquisition of data, and Professor Lynda Erskine for critical reading of the manuscript. This work was supported by a PhD studentship from the University of Aberdeen (DZ) and by funding from the Royal Society and Tenovus Scotland (JNH)Peer reviewedPostprin

Adapting Objective Structured Practical Examinations (OSPE’s) to assess laboratory science skills in pharmacology students

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Using Game of Thrones to teach neuroscience and neuropharmacology during lockdown

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Student perceptions of Objective Structured Practical Examination (OSPE) assessments

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Visible-Light Photoswitchable Benzimidazole Azo-Arenes as beta-Arrestin2-Biased Selective Cannabinoid 2 Receptor Agonists

Acknowledgements The authors would like to acknowledge Dr. Andrea Holme for excellent technical support and the Iain Fraser Cytometry Centre (University of Aberdeen) for providing access to their equipment. The authors would like to thank Dr. Matthias Scheiner for his contributions towards the development of the calcium mobilization assay and Dr. Valérie Jahns for her efforts towards faster automated analysis of the obtained results. Nick Verhavert is acknowledged for his assistance with the NanoBiT® assay. Diego Rodriguez-Soacha is acknowledged for establishing the rCB1R radioligand binding assay in our laboratory. Special thanks to Dr. Rangan Maitra and RTI International for providing the G16 coupled hCB1 and hCB2 CHO-K1 cell lines. The authors thank Nadine Yurdagül-Hemmrich and Annette Hannawacker for excellent technical support. This project was funded by the German Research Foundation (Deutsche Forschungsgemeinschaft under DFG DE1546/10-1). J. N. Hislop’s financing support was given by NHS Grampian. The research visit of S. A. M. Steinmüller in Dr. Hislop’s laboratory was funded by the Elite Network of Bavaria (grant N° K-BM-2013-247). J. Fender and A. Tutov were supported by the International Doctoral Program “Receptor Dynamics” funded within the framework of the Elite Network of Bavaria (grant N° K-BM-2013- 247). M. H. Deventer was funded by the Research FoundationFlanders (FWO; grant 1S54521N).Peer reviewe

Bridging the Binding Sites : Dualsteric Ligands for the Cannabinoid 2 Receptor (CB2R)

Acknowledgements This project was financially supported by the German Research Foundation (Deutsche Forschungsgemeinschaft under DFG DE1546/10-1). Gratitude is expressed to the International Doctorate Program “Receptor Dynamics” of the Elite Network of Bavaria (ENB) for financial support of A.T. and S.A.M.S. (grant No. K-BM-2013-247). Y.A.R. was granted a scholarship by the German Academic Exchange Service (Deutscher Akademischer Austauschdienst, DAAD) program “Research stays for university academics and scientists.” D.A.R.-S. was awarded a Ph.D. scholarship by the DAAD. J.N.H. was financially supported by NHS Grampian. Furthermore, the authors thank Professor Dr. Kristina Lorenz (Institute of Pharmacology and Toxicology, University of Würzburg) for enabling them to conduct in vitro experiments in her laboratory. Open access funding enabled and organized by Projekt DEAL.Peer reviewedPublisher PD

Characterization of renal cell carcinoma-associated constitutional chromosome abnormalities by genome sequencing.

Constitutional translocations, typically involving chromosome 3, have been recognized as a rare cause of inherited predisposition to renal cell carcinoma (RCC) for four decades. However, knowledge of the molecular basis of this association is limited. We have characterized the breakpoints by genome sequencing (GS) of constitutional chromosome abnormalities in five individuals who presented with RCC. In one individual with constitutional t(10;17)(q11.21;p11.2), the translocation breakpoint disrupted two genes: the known renal tumor suppressor gene (TSG) FLCN (and clinical features of Birt-Hogg-Dubé syndrome were detected) and RASGEF1A. In four cases, the rearrangement breakpoints did not disrupt known inherited RCC genes. In the second case without chromosome 3 involvement, the translocation breakpoint in an individual with a constitutional t(2;17)(q21.1;q11.2) mapped 12 Kb upstream of NLK. Interestingly, NLK has been reported to interact indirectly with FBXW7 and a previously reported RCC-associated translocation breakpoint disrupted FBXW7. In two cases of constitutional chromosome 3 translocations, no candidate TSGs were identified in the vicinity of the breakpoints. However, in an individual with a constitutional chromosome 3 inversion, the 3p breakpoint disrupted the FHIT TSG (which has been reported previously to be disrupted in two apparently unrelated families with an RCC-associated t(3;8)(p14.2;q24.1). These findings (a) expand the range of constitutional chromosome rearrangements that may be associated with predisposition to RCC, (b) confirm that chromosome rearrangements not involving chromosome 3 can predispose to RCC, (c) suggest that a variety of molecular mechanisms are involved the pathogenesis of translocation-associated RCC, and (d) demonstrate the utility of GS for investigating such cases

Dysbindin Promotes the Post-Endocytic Sorting of G Protein-Coupled Receptors to Lysosomes

BackgroundDysbindin, a cytoplasmic protein long known to function in the biogenesis of specialized lysosome-related organelles (LROs), has been reported to reduce surface expression of D2 dopamine receptors in neurons. Dysbindin is broadly expressed, and dopamine receptors are members of the large family of G protein-coupled receptors (GPCRs) that function in diverse cell types. Thus we asked if dysbindin regulates receptor number in non-neural cells, and further investigated the cellular basis of this regulation.Methodology/principal findingsWe used RNA interference to deplete endogenous dysbindin in HEK293 and HeLa cells, then used immunochemical and biochemical methods to assess expression and endocytic trafficking of epitope-tagged GPCRs. Dysbindin knockdown up-regulated surface expression of D2 receptors compared to D1 receptors, as reported previously in neurons. This regulation was not mediated by a change in D2 receptor endocytosis. Instead, dysbindin knockdown specifically reduced the subsequent trafficking of internalized D2 receptors to lysosomes. This distinct post-endocytic sorting function explained the minimal effect of dysbindin depletion on D1 receptors, which recycle efficiently and traverse the lysosomal pathway to only a small degree. Moreover, dysbindin regulated the delta opioid receptor, a more distantly related GPCR that is also sorted to lysosomes after endocytosis. Dysbindin was not required for lysosomal trafficking of all signaling receptors, however, as its depletion did not detectably affect down-regulation of the EGF receptor tyrosine kinase. Dysbindin co-immunoprecipitated with GASP-1 (or GPRASP-1), a cytoplasmic protein shown previously to modulate lysosomal trafficking of D2 dopamine and delta opioid receptors by direct interaction, and with HRS that is a core component of the conserved ESCRT machinery mediating lysosome biogenesis and sorting.Conclusions/significanceThese results identify a distinct, and potentially widespread function of dysbindin in promoting the sorting of specific GPCRs to lysosomes after endocytosis