Embedding art in histology teaching: Visual thinking strategies (VTS) to enhance visual literacy

BACKGROUND/AIMS Histology is a visually challenging subject for novice students. Visual thinking strategies (VTS) uses the viewing of art to improve visual literacy in classroom settings (Housen, 2002), including medical programmes (Reilly, Ring, & Duke, 2005), but has not been evaluated in histology. This project assessed the impact of VTS on students' observational skills, perceptions of histological images, and practical report marks. METHODS Participants were third-year biomedical students (n=133) studying histology in 2021. Students were shown a novel histology image and wrote their observations (pre-VTS). An experienced VTS facilitator guided students through an approximately 20-minute session exploring a never-before-seen artwork. After the VTS-activity, students were shown a new histology image and wrote their observations (post-VTS). Pre- and post-VTS descriptions were scored for measures of observational richness and compared. Responses to open-ended reflective questions were analysed by inductive thematic analysis. Report marks were compared with those from a previous year. RESULTS/CONCLUSIONS While there was no significant effect of the VTS activity on the students’ pre-/post-VTS descriptions, nor on their practical report marks, 46% of students reported that VTS changed how they viewed histological images and improved their observational skills. This study suggests that a one-off VTS activity at the beginning of a histology class can benefit students’ experience of unfamiliar microscopic images and improve enjoyment of this challenging subject. REFERENCES Housen, A.C. (2002) Aesthetic thought, critical thinking and transfer. Arts and Learning Research Journal, 18, 99-132. Reilly, J. M., Ring, J., & Duke, L. (2005) Visual thinking strategies: a new role for art in medical education. Family Medicine, 37, 250-252

Final Results from U.S. FCEV Learning Demonstration: Preprint

The 'Controlled Hydrogen Fleet and Infrastructure Demonstration and Validation Project,' also known as the National Fuel Cell Electric Vehicle Learning Demonstration, is a U.S. Department of Energy (DOE) project started in 2004 and concluded in late 2011. The purpose of this project was to conduct an integrated field validation that simultaneously examined the performance of fuel cell vehicles and the supporting hydrogen fueling infrastructure. The DOE's National Renewable Energy Laboratory (NREL) received and analyzed all of the raw technical data collected by the industry partners through their participation in the project over its seven-year duration. This paper reviews highlights from the project and draws conclusions about the demonstrated status of the fuel cell vehicle and hydrogen fueling infrastructure technology

Next Steps for the FCEV Learning Demonstration Project

This presentation summarizes project goals; vehicle and H2 station deployment status, critical performance compared to targets; highlights of latest vehicle and infrastructure analysis results and progress; learning demo next steps; highlights of partner activities and summary

All Composite Data Products: National FCEV Learning Demonstration With Updates Through October 5, 2011

This technical presentation describes all composite data products: national FCEV learning demonstration with updates through October 5, 201

Early Fuel Cell Market Deployments: ARRA and Combined (IAA, DLA, ARRA); Quarter 3 2012 Composite Data Products

This report from the U.S. Department of Energy's National Renewable Energy Laboratory includes early fuel cell market composite data products for the third quarter of 2012 for American Recovery and Reinvestment Act (ARRA) and combined (IAA, DLA, ARRA) deployment projects

Spring 2013 Composite Data Products - Backup Power

This presentation from the U.S. Department of Energy's National Renewable Energy Laboratory includes 21 composite data products (CDPs) produced in Spring 2013 for fuel cell backup power systems

DGIdb 2.0: Mining clinically relevant drug-gene interactions

The Drug–Gene Interaction Database (DGIdb, www. dgidb.org) is a web resource that consolidates dis-parate data sources describing drug–gene interac-tions and gene druggability. It provides an intuitive graphical user interface and a documented applica-tion programming interface (API) for querying these data. DGIdb was assembled through an extensive manual curation effort, reflecting the combined in-formation of twenty-seven sources. For DGIdb 2.0, substantial updates have been made to increase content and improve its usefulness as a resource for mining clinically actionable drug targets. Specif-ically, nine new sources of drug–gene interactions have been added, including seven resources specifi-cally focused on interactions linked to clinical trials. These additions have more than doubled the over-all count of drug–gene interactions. The total num-ber of druggable gene claims has also increased by 30%. Importantly, a majority of the unrestricted, publicly-accessible sources used in DGIdb are now automatically updated on a weekly basis, providing the most current information for these sources. Fi-nally, a new web view and API have been developed to allow searching for interactions by drug identifiers to complement existing gene-based search function-ality. With these updates, DGIdb represents a com-prehensive and user friendly tool for mining the druggable genome for precision medicine hypothe-sis generation

Orai1 Channel Inhibition Preserves Left Ventricular Systolic Function and Normal Ca2+ Handling After Pressure Overload

Background: Orai1 is a critical ion channel subunit, best recognized as a mediator of storeoperated Ca2+ entry (SOCE) in non-excitable cells. SOCE has recently emerged as a key contributor of cardiac hypertrophy and heart failure but the relevance of Orai1 is still unclear. Methods: To test the role of these Orai1 channels in the cardiac pathophysiology, a transgenic mouse was generated with cardiomyocyte-specific expression of an ion pore-disruptive Orai1R91W mutant (C-dnO1). Synthetic chemistry and channel screening strategies were used to develop JPIII, a small-molecule Orai1 channel inhibitor suitable for in vivo delivery. Results: Adult mice subjected to transverse aortic constriction (TAC) developed cardiac hypertrophy and reduced ventricular function associated with increased Orai1 expression and Orai1-dependent SOCE (assessed by Mn2+ influx). C-dnO1 mice displayed normal cardiac electromechanical function and cellular excitation-contraction coupling despite reduced Orai1-dependent SOCE. 5 weeks after TAC, C-dnO1 mice were protected from systolic dysfunction (assessed by preserved left ventricular fractional shortening and ejection fraction) even if increased cardiac mass and pro-hypertrophic markers induction were observed. This is correlated with a protection from TAC-induced cellular Ca2+ signaling alterations (increased SOCE, decreased [Ca2+]i transients amplitude and decay rate, lower SR Ca2+ load and depressed cellular contractility) and SERCA2a downregulation in ventricular cardiomyocytes from C-dnO1 mice, associated with blunted Pyk2 signaling. There was also less fibrosis in heart sections from CdnO1 mice after TAC. Moreover, 3 weeks treatment with JPIII following 5 weeks of TAC confirmed the translational relevance of an Orai1 inhibition strategy during hypertrophic insult. Conclusions: The findings suggest a key role of cardiac Orai1 channels and the potential for Orai1 channel inhibitors as inotropic therapies for maintaining contractility reserve after hypertrophic stress

Cure of ADPKD by Selection for Spontaneous Genetic Repair Events in Pkd1-Mutated iPS Cells

Induced pluripotent stem cells (iPSCs) generated by epigenetic reprogramming of personal somatic cells have limited therapeutic capacity for patients suffering from genetic disorders. Here we demonstrate restoration of a genomic mutation heterozygous for Pkd1 (polycystic kidney disease 1) deletion (Pkd1(+/−) to Pkd1(+/R+)) by spontaneous mitotic recombination. Notably, recombination between homologous chromosomes occurred at a frequency of 1∼2 per 10,000 iPSCs. Southern blot hybridization and genomic PCR analyses demonstrated that the genotype of the mutation-restored iPSCs was indistinguishable from that of the wild-type cells. Importantly, the frequency of cyst generation in kidneys of adult chimeric mice containing Pkd1(+/R+) iPSCs was significantly lower than that of adult chimeric mice with parental Pkd1(+/−) iPSCs, and indistinguishable from that of wild-type mice. This repair step could be directly incorporated into iPSC development programmes prior to cell transplantation, offering an invaluable step forward for patients carrying a wide range of genetic disorders