Peer-mentorship and first-year inclusion: building belonging in higher education.

BACKGROUND: An inclusive academic environment is pivotal to ensure student well-being and a strong sense of belonging and authenticity. Specific attention for an inclusive learning environment is particularly important during a student's transition to higher education. At Utrecht University's Medical School, explorative interviews with students from minority groups indicated they did not always feel included during the orientation programme of their academic education. We, therefore, developed a bias awareness training with theoretical and practical components on diversity and inclusion for peer-mentors who are assigned to each first-year student at the start of university. METHODS: At the end of the orientation programme, we investigated the effectiveness of the training for two consecutive years using two measurements. Firstly, we investigated the behavioural changes in the peer-mentors through a (self-reporting) questionnaire. Additionally, we measured the perceived inclusion of the first-year students, divided into belonging and authenticity, using a validated questionnaire. RESULTS: Our results show that peer-mentors found the training useful and indicated it enabled them to create an inclusive atmosphere. Overall, students experienced a high level of inclusion during the orientation programme. After the first year, the bias training was adjusted based on the evaluations. This had a positive effect, as mentors felt they were significantly more able to provide an inclusive orientation in the second year of this study. In line with this, students experienced an increased level of authenticity specifically due to the peer-mentor in the second year as compared to the first. CONCLUSIONS: We conclude that training peer-mentors is an effective way to increase awareness and to ensure an inclusive atmosphere during the start of higher education.

'A role model is like a mosaic': reimagining URiM students' role models in medical school.

BACKGROUND: Role modelling is a widely acknowledged element of medical education and it is associated with a range of beneficial outcomes for medical students, such as contributing to professional identity development and a sense of belonging. However, for students who are racially and ethnically underrepresented in medicine (URiM), identification with clinical role models may not be self-evident, as they have no shared ethnic background as a basis for social comparison. This study aims to learn more about the role models of URiM students during medical school and about the added value of representative role models. METHODS: In this qualitative study we used a concept-guided approach to explore URiM alumni's experiences with role models during medical school. We conducted semi-structured interviews with ten URiM alumni about their perception of role models, who their own role models were during medical school and why they considered these figures as role models. Sensitizing concepts guided the topic list, interview questions and finally served as deductive codes in the first round of coding. RESULTS: The participants needed time to think about what a role model is and who their own role models are. Having role models was not self-evident as they had never thought about it before, and participants appeared hesitant and uncomfortable discussing representative role models. Eventually, all participants identified not one, but multiple people as their role model. These role models served different functions: role models from outside medical school, such as parents, motivated them to work hard. Clinical role models were fewer and functioned primarily as examples of professional behaviour. The participants experienced a lack of representation rather than a lack of role models. CONCLUSIONS: This study presents us with three ways to reimagine role models in medical education. First, as culturally embedded: having a role model is not as self-evident as it appears in existing role model literature, which is largely based on research conducted in the U.S. Second, as cognitive constructs: the participants engaged in selective imitation, where they did not have one archetypical clinical role model, but rather approach role models as a mosaic of elements from different people. Third, role models carry not only a behavioural but also a symbolical value, the latter of which is particularly important for URiM students because it relies heavier on social comparison.

[Deeper skin tones rarely depicted in Dutch dermatology textbooks]. / Donkere huid zelden afgebeeld in Nederlandse dermatologieboeken.

OBJECTIVE: Within diverse populations such as in the Netherlands, medical education must prepare students to diagnose skin conditions on a broad range of skin tones. To develop the visual pattern recognition skills to do so, medical students need exposure to skin conditions on deeper skin tones. The purpose of this study is to assess the inclusion of images of brown skin in Dutch dermatology textbooks. DESIGN: Observational study. METHOD: Two large Dutch student textbook web shops were searched for dermatology textbooks, and all available general dermatology textbooks explicitly aimed at medical students were selected. All images of skin were examined and divided into the categories 'light skin', 'light to medium brown skin', 'medium to deep brown skin', 'deep to very deep brown skin', and 'indeterminate'. RESULTS: Five textbooks, with a total of 2060 images of skin, were examined. 87.6% of images showed light skin, 7.0% showed light to medium brown skin, 2.9% showed medium to deep brown skin, and 0.5% showed deep to very deep brown skin. 2.0% was categorized as 'indeterminate'. CONCLUSION: Dutch dermatology textbooks currently include only small percentages of images of brown skin. Unfamiliarity with disease presentation on deeper skin tones can lead to delayed diagnosis and worse outcomes in Black and Brown patients. Future textbooks should include images of different skin tones, including deeper ones, for every skin condition.

Inclusion and diversity within medical education: a focus group study of students' experiences.

BACKGROUND/INTRODUCTION: As patient populations become more diverse, it is imperative that future physicians receive proper training in order to provide the best quality of care. This study examines medical students' perceptions of how prepared they are in dealing with a diverse population and assesses how included and supported the students felt during their studies. METHODS: Four semi-structured focus groups were held with medical students across all years of the medical study program of a Dutch university. Focus group transcripts were analyzed thematically. RESULTS: Students' experiences could be categorized as follows: (1) (Minority) identities and personal motivations, (2) Understanding of diversity and an inclusive learning environment, (3) Diversity in education, (4) Experiences of exclusion, (5) Experiences of inclusion, and (6) Lack of awareness. The key findings from the focus groups were that students perceived a lack of diversity and awareness in medical education and were convinced of the need to incorporate diversity to a greater extent and were personally motivated to contribute to incorporating diversity in the curriculum. Students also shared exclusion experiences such as stereotypes and prejudices but also some inclusion experiences such as feelings of belonging. CONCLUSION: Based on our findings, it is recommended that medical schools incorporate diversity education into their curriculum so that health professionals can provide the best quality of care for their diverse patient populations. This education should also ensure that all students feel included in their medical education program.

PTPRR protein tyrosine phosphatase isoforms and locomotion of vesicles and mice.

Protein tyrosine phosphatases (PTPs) are central players in many different cellular processes and their aberrant activity is associated with multiple human pathologies. In this review, we present current knowledge on the PTPRR subfamily of classical PTPs that is expressed in neuronal cells and comprises receptor-type (PTPBR7, PTP-SL) as well as cytosolic (PTPPBSgamma-37, PTPPBSgamma-42) isoforms. The two receptor-type isoforms PTPBR7 and PTP-SL both localize in late endosomes and the Golgi area. PTPBR7, however, is additionally localized at the cell surface and on early endosomes. During cerebellar maturation, PTPBR7 expression in developing Purkinje cells ceases and is replaced by PTP-SL expression in the mature Purkinje cells. All PTPRR isoforms contain a kinase interacting motif that makes them mitogen-activated protein kinase phosphatases. The distinct subcellular localization of the different PTPRR isoforms may reflect differential roles in growth-factor-induced MAPK-mediated retrograde signaling cascades. Studies in PTPRR-deficient mice established that PTPRR isoforms are physiological regulators of MAPK phosphorylation levels. Surprisingly, PTPRR-deficient mice display defects in motor coordination and balancing skills, while cerebellar morphological abnormalities, which are often encountered in ataxic mouse models, are absent. This is reminiscent of the phenotype observed in a handful of mouse mutants that have alterations in cerebellar calcium ion homeostasis. Elucidation of the molecular mechanisms by which PTPRR deficiency imposes impairment of cerebellar neurons and motor coordination may provide candidate molecules for hereditary cerebellar ataxias that still await identification of the corresponding disease genes.

Proteolytic processing of the receptor-type protein tyrosine phosphatase PTPBR7.

The single-copy mouse gene Ptprr gives rise to different protein tyrosine phosphatase (PTP) isoforms in neuronal cells through the use of distinct promoters, alternative splicing, and multiple translation initiation sites. Here, we examined the array of post-translational modifications imposed on the PTPRR protein isoforms PTPBR7, PTP-SL, PTPPBSgamma42 and PTPPBSgamma37, which have distinct N-terminal segments and localize to different parts of the cell. All isoforms were found to be short-lived, constitutively phosphorylated proteins. In addition, the transmembrane isoform, PTPBR7, was subject to N-terminal proteolytic processing, in between amino acid position 136 and 137, resulting in an additional, 65-kDa transmembrane PTPRR isoform. Unlike for some other receptor-type PTPs, the proteolytically produced N-terminal ectodomain does not remain associated with this PTPRR-65. Shedding of PTPBR7-derived polypeptides at the cell surface further adds to the molecular complexity of PTPRR biology.

Characterization of multiple transcripts and isoforms derived from the mouse protein tyrosine phosphatase gene Ptprr.

The use of alternative splice sites, promoters and translation start sites considerably adds to the complexity of organisms. Four mouse cDNAs (PTPBR7, PTP-SL, PTPPBSgamma+ and PTPPBSgamma-) have been cloned that contain different 5' parts but encode identical protein tyrosine phosphatase PTPRR catalytic domains. We investigated the genomic origin and coding potential of these transcripts to elucidate their interrelationship. Mouse gene Ptprr exons were identified within a 260 kbp segment on chromosome 10, revealing PTP-SL- and PTPPBSgamma-specific transcription start sites within introns two and four, respectively, relative to the 14 PTPBR7 exons. Northern and RT-PCR analyses demonstrated differential expression patterns for these promoters. Furthermore, transfection studies and AUG codon mutagenesis demonstrated that in PTP-SL and PTPPBSgamma messengers multiple translation initiation sites are being used. Resulting 72, 60, 42 and 37 kDa PTPRR protein isoforms differ not only in the length of their N-terminal part but also in their subcellular localization, covering all major PTP subtypes; receptor-like, membrane associated and cytosolic. In summary, mouse gene Ptprr gives rise to multiple isoforms through the use of distinct promoters, alternative splicing and differential translation starts. These results set the stage for further investigations on the physiological roles of PTPRR proteins.

Colocalisation of the protein tyrosine phosphatases PTP-SL and PTPBR7 with beta4-adaptin in neuronal cells.

The mouse gene Ptprr encodes the neuronal protein tyrosine phosphatases PTP-SL and PTPBR7. These proteins differ in their N-terminal domains, with PTP-SL being a cytosolic, membrane-associated phosphatase and PTPBR7 a type I transmembrane protein. In this study, we further explored the nature of the PTP-SL-associated vesicles in neuronal cells using a panel of organelle markers and noted a comparable subcellular distribution for PTP-SL and the beta4-adaptin subunit of the AP4 complex. PTP-SL, PTPBR7 and beta4-adaptin are localised at the Golgi apparatus and at vesicles throughout the cytoplasm. Immunohistochemical analysis demonstrated that PTP-SL, PTPBR7 and beta4-adaptin are all endogenously expressed in brain. Interestingly, coexpression of PTP-SL and beta4-adaptin leads to an altered subcellular localisation for PTP-SL. Instead of the Golgi and vesicle-type staining pattern, still observable for beta4-adaptin, PTP-SL is now distributed throughout the cytoplasm. Although beta4-adaptin was found to interact with the phosphatase domain of PTP-SL and PTPBR7 in the yeast two-hybrid system, it failed to do so in transfected neuronal cells. Our data suggest that the tyrosine phosphatases PTP-SL and PTPBR7 may be involved in the formation and transport of AP4-coated vesicles or in the dephosphorylation of their transmembrane cargo molecules at or near the Golgi apparatus.