Diversifying the dental curriculum: A review of the Bachelor of Dental Surgery degree reading lists in a UK dental school.

INTRODUCTION: Analysis of the diversity of reading lists on courses offered by universities is one way to assess what is being taught and how it shapes our understanding of the world. Very little work has been carried out so far within dentistry on decolonising the curriculum. Existing work looks at the representation of women or ethnic minorities but not at the dental curriculum per se. This article starts to address this. METHODS: The reading lists within the 5 year Bachelor of Dental Surgery curriculum in a large UK dental school were collected and assessed. A data extraction spreadsheet was developed and journal articles on every course reading list across the 5 year curriculum were read in detail. Information on authorship and author affiliations, alongside patient and population representation within the article itself, were collected and collated. RESULTS: We found that there are 2.5 times more male authors than female authors, and almost three times more male lead authors in the articles evaluated. The majority of journal articles included in the reading lists are written by academics and/or clinicians affiliated with institutions in the United Kingdom and most articles are from the global north. In addition, 65% of articles do not specify the focus patient or population group studied. DISCUSSION: It is unlikely that current reading lists within dentistry fully reflect the composition of the profession itself, the variety of knowledge needed to provide evidence-based practice in a globalised oral health arena or the heterogeneous nature of the patient population.

Role of the redox state of the Pirin-bound cofactor on interaction with the master regulators of inflammation and other pathways.

Persistent cellular stress induced perpetuation and uncontrolled amplification of inflammatory response results in a shift from tissue repair toward collateral damage, significant alterations of tissue functions, and derangements of homeostasis which in turn can lead to a large number of acute and chronic pathological conditions, such as chronic heart failure, atherosclerosis, myocardial infarction, neurodegenerative diseases, diabetes, rheumatoid arthritis, and cancer. Keeping the vital role of balanced inflammation in maintaining tissue integrity in mind, the way to combating inflammatory diseases may be through identification and characterization of mediators of inflammation that can be targeted without hampering normal body function. Pirin (PIR) is a non-heme iron containing protein having two different conformations depending on the oxidation state of the iron. Through exploration of the Pirin interactome and using molecular docking approaches, we identified that the Fe2+-bound Pirin directly interacts with BCL3, NFKBIA, NFIX and SMAD9 with more resemblance to the native binding pose and higher affinity than the Fe3+-bound form. In addition, Pirin appears to have a function in the regulation of inflammation, the transition between the canonical and non-canonical NF-κB pathways, and the remodeling of the actin cytoskeleton. Moreover, Pirin signaling appears to have a critical role in tumor invasion and metastasis, as well as metabolic and neuro-pathological complications. There are regulatory variants in PIR that can influence expression of not only PIR but also other genes, including VEGFD and ACE2. Disparity exists between South Asian and European populations in the frequencies of variant alleles at some of these regulatory loci that may lead to differential occurrence of Pirin-mediated pathogenic conditions.

Deciphering the role of predicted miRNAs of polyomaviruses in carcinogenesis.

Human polyomaviruses are relatively common in the general population. Polyomaviruses maintain a persistent infection after initial infection in childhood, acting as an opportunistic pathogen in immunocompromised populations and their association has been linked to carcinogenesis. A comprehensive understanding of the underlying molecular mechanisms of carcinogenesis in consequence of polyomavirus infection remains elusive. However, the critical role of viral miRNAs and their potential targets in modifying the transcriptome profile of the host remains largely unknown. Polyomavirus-derived miRNAs have the potential to play a substantial role in carcinogenesis. Employing computational approaches, putative viral miRNAs along with their target genes have been predicted and possible roles of the targeted genes in many significant biological processes have been obtained. Polyomaviruses have been observed to target intracellular signal transduction pathways through miRNA-mediated epigenetic regulation, which may contribute to cancer development. In addition, BKPyV-infected human renal cell microarray data was coupled with predicted target genes and analysis of the downregulated genes indicated that viruses target multiple signaling pathways (e.g. MAPK signaling pathway, PI3K-Akt signaling pathway, PPAR signaling pathway) in the host as well as turning off several tumor suppression genes (e.g. FGGY, EPHX2, CACNA2D3, CDH16) through miRNA-induced mechanisms, assuring cell transformation. This study provides a conceptual framework for the underlying molecular mechanisms involved in the course of carcinogenesis upon polyomavirus infection.