Comparison of Grip Strength, Forearm Muscle Activity, and Shock Transmission between the Forehand Stroke Technique of Experienced and Recreational Tennis Players Using a Novel Wearable Device.

Upper limb tennis injuries are primarily chronic, resulting from repetitive overuse. We developed a wearable device which simultaneously measures risk factors (grip strength, forearm muscle activity, and vibrational data) associated with elbow tendinopathy development resulting from tennis players' technique. We tested the device on experienced (n = 18) and recreational (n = 22) tennis players hitting forehand cross-court at both flat and topspin spin levels under realistic playing conditions. Using statistical parametric mapping analysis, our results showed that all players showed a similar level of grip strength at impact, regardless of spin level, and the grip strength at impact did not influence the percentage of impact shock transfer to the wrist and elbow. Experienced players hitting with topspin exhibited the highest ball spin rotation, low-to-high swing path brushing action, and shock transfer to the wrist and elbow compared to the results obtained while hitting the ball flat, or when compared to the results obtained from recreational players. Recreational players exhibited significantly higher extensor activity during most of the follow through phase compared to the experienced players for both spin levels, potentially putting them at greater risk for developing lateral elbow tendinopathy. We successfully demonstrated that wearable technologies can be used to measure risk factors associated with elbow injury development in tennis players under realistic playing conditions.

Effects of air pollution on human health - Mechanistic evidence suggested by in vitro and in vivo modelling.

Airborne particulate matter (PM) comprises both solid and liquid particles, including carbon, sulphates, nitrate, and toxic heavy metals, which can induce oxidative stress and inflammation after inhalation. These changes occur both in the lung and systemically, due to the ability of the small-sized PM (i.e. diameters ≤2.5 µm, PM2.5) to enter and circulate in the bloodstream. As such, in 2016, airborne PM caused ∼4.2 million premature deaths worldwide. Acute exposure to high levels of airborne PM (eg. during wildfires) can exacerbate pre-existing illnesses leading to hospitalisation, such as in those with asthma and coronary heart disease. Prolonged exposure to PM can increase the risk of non-communicable chronic diseases affecting the brain, lung, heart, liver, and kidney, although the latter is less well studied. Given the breadth of potential disease, it is critical to understand the mechanisms underlying airborne PM exposure-induced disorders. Establishing aetiology in humans is difficult, therefore, in-vitro and in-vivo studies can provide mechanistic insights. We describe acute health effects (e.g. exacerbations of asthma) and long term health effects such as the induction of chronic inflammatory lung disease, and effects outside the lung (e.g. liver and renal change). We will focus on oxidative stress and inflammation as this is the common mechanism of PM-induced disease, which may be used to develop effective treatments to mitigate the adverse health effect of PM exposure.

Cell polarity defines three distinct domains in pancreatic ß-cells.

The structural organisation of pancreatic ß-cells in the islets of Langerhans is relatively unknown. Here, using three-dimensional (3D) two-photon, 3D confocal and 3D block-face serial electron microscopy, we demonstrate a consistent in situ polarisation of ß-cells and define three distinct cell surface domains. An apical domain located at the vascular apogee of ß-cells, defined by the location of PAR-3 (also known as PARD3) and ZO-1 (also known as TJP1), delineates an extracellular space into which adjacent ß-cells project their primary cilia. A separate lateral domain, is enriched in scribble and Dlg, and colocalises with E-cadherin and GLUT2 (also known as SLC2A2). Finally, a distinct basal domain, where the ß-cells contact the islet vasculature, is enriched in synaptic scaffold proteins such as liprin. This 3D analysis of ß-cells within intact islets, and the definition of distinct domains, provides new insights into understanding ß-cell structure and function.

Proximal tubular epithelial cells preferentially endocytose covalently-modified albumin compared to native albumin.

AIM: Albumin can be covalently modified at surface lysine residues and thus the circulation contains a mixture of native albumin (i.e. not modified) and albumin with varying degrees of modification. Uptake and lysosomal degradation of glomerular filtered albumin by proximal tubular cells via the megalin scavenger receptor is considered an important mechanism to limit albumin loss in the urine. However, whether this is a general mechanism of tubular uptake of albumin or if this is restricted to modified albumin is unknown. To address this question, we investigated the uptake of modified versus native albumin by proximal tubular cells. METHODS: A well-characterized proximal tubular cell model of albumin uptake was used to compare the uptake of modified albumin (covalent labelling of lysine residues with fluorescent probes) to that of native recombinant human albumin (rHA) labelled with 14 C during protein synthesis (14 C-rHA). RESULTS: Opossum kidney (OK) cells showed significant uptake of fluorescence-labelled albumin via an endocytosis mechanism. This uptake was inhibited by an equimolar ratio of different types of covalently modified albumin; however, purified bovine serum albumin and rHA failed to compete with the uptake of fluorescence-labelled albumin. In contrast, OK cells failed to endocytose native 14 C-rHA despite efficiently endocytosing covalently modified rHA. CONCLUSION: Our studies show that OK cells preferentially endocytose covalently-modified albumin compared to native albumin. This apparent selectivity of the megalin scavenger receptor complex suggests a specific role for this pathway in the removal of modified albumin from the circulation.

Reduced tubular degradation of glomerular filtered plasma albumin is a common feature in acute and chronic kidney disease.

Tubular epithelial cells take up and degrade plasma albumin filtered by the glomerulus. Tubular damage resulting in reduced albumin uptake or degradation has been suggested as one mechanism contributing to albuminuria in kidney disease. This study investigated whether tubular albumin uptake or degradation is altered in acute and chronic glomerular disease. Mouse models of acute glomerular injury (anti-GBM disease and LPS-induced albuminuria) and chronic disease (streptozotocin-induced diabetes and db/db mice) were examined. Mice were injected intravenously with Alexa-albumin plus DQ-albumin and killed 20 minutes later. Tubular uptake of albumin (Alexa-albumin) and albumin degradation (Dye Quenched (DQ)-albumin) was assessed in tissue sections via confocal microscopy. Tubular uptake of Alexa-albumin in the models of diabetic nephropathy was not different to normal mice. However, the fluorescence signal resulting from degradation of DQ-albumin was significantly reduced in db/db mice, and the ratio of degraded to intact albumin was reduced in both models. The ratio of degraded to intact albumin in tubules was also reduced in the anti-GBM model. In the LPS model, both tubular uptake and degradation of albumin were significantly reduced, with a substantial reduction in the ratio of degraded to intact albumin in tubules. LPS stimulation of cultured tubular epithelial cells inhibited albumin uptake, indicating a direct role for LPS in modifying tubular handling of albumin. In conclusion, reduced degradation of filtered albumin in the proximal tubule is a common feature of glomerular diseases. This may be a general mechanism whereby tubular dysfunction contributes to the development of albuminuria.

Chloride channel ClC-5 binds to aspartyl aminopeptidase to regulate renal albumin endocytosis.

ClC-5 is a chloride/proton exchanger that plays an obligate role in albumin uptake by the renal proximal tubule. ClC-5 forms an endocytic complex with the albumin receptor megalin/cubilin. We have identified a novel ClC-5 binding partner, cytosolic aspartyl aminopeptidase (DNPEP; EC 3.4.11.21), that catalyzes the release of N-terminal aspartate/glutamate residues. The physiological role of DNPEP remains largely unresolved. Mass spectrometric analysis of proteins binding to the glutathione-S-transferase (GST)-ClC-5 C terminus identified DNPEP as an interacting partner. Coimmunoprecipitation confirmed that DNPEP and ClC-5 also associated in cells. Further experiments using purified GST-ClC-5 and His-DNPEP proteins demonstrated that the two proteins bound directly to each other. In opossum kidney (OK) cells, confocal immunofluorescence studies revealed that DNPEP colocalized with albumin-containing endocytic vesicles. Overexpression of wild-type DNPEP increased cell-surface levels of ClC-5 and albumin uptake. Analysis of DNPEP-immunoprecipitated products from rat kidney lysate identified ß-actin and tubulin, suggesting a role for DNPEP in cytoskeletal maintenance. A DNase I inhibition assay showed a significant decrease in the amount of G actin when DNPEP was overexpressed in OK cells, suggesting a role for DNPEP in stabilizing the cytoskeleton. DNPEP was not present in the urine of healthy rats; however, it was readily detected in the urine in rat models of mild and heavy proteinuria (diabetic nephropathy and anti-glomerular basement membrane disease, respectively). Urinary levels of DNPEP were found to correlate with the severity of proteinuria. Therefore, we have identified another key molecular component of the albumin endocytic machinery in the renal proximal tubule and describe a new role for DNPEP in stabilizing the actin cytoskeleton.

Nedd4-2 (NEDD4L) controls intracellular Na(+)-mediated activity of voltage-gated sodium channels in primary cortical neurons.

Nedd4-2, a HECT (homologous with E6-associated protein C-terminus)-type ubiquitin protein ligase, has been implicated in regulating several ion channels, including Navs (voltage-gated sodium channels). In Xenopus oocytes Nedd4-2 strongly inhibits the activity of multiple Navs. However, the conditions under which Nedd4-2 mediates native Nav regulation remain uncharacterized. Using Nedd4-2-deficient mice, we demonstrate in the present study that in foetal cortical neurons Nedd4-2 regulates Navs specifically in response to elevated intracellular Na(+), but does not affect steady-state Nav activity. In dorsal root ganglia neurons from the same mice, however, Nedd4-2 does not control Nav activities. The results of the present study provide the first physiological evidence for an essential function of Nedd4-2 in regulating Navs in the central nervous system.

Developing a Framework for the Design and Deployment of Virtual Reality (VR) in Clinical Education.

The emerging cost-effective and powerful standalone VR hardware is an increasingly viable supplement to traditional clinical educational modalities. These traditional approaches are effective but can be limited by the cost of simulation infrastructure, the requirement to attend at fixed times and locations and instructor availability present challenges in meeting the needs of clinicians. One barrier facing educators looking to develop bespoke VR-based solutions is the lack of guidelines around their design, development, deployment, and evaluation. Our team has produced and deployed a number of VR-based educational applications. Through reflecting on findings from surveys, interviews, observation, we summarise a range of insights into the complexity and nuances of the clinical VR design and deployment in a framework that can inform and guide educators, clinicians and developers looking to create their own VR applications for use in healthcare.

Adipokines as a link between obesity and chronic kidney disease.

Adipocytes secrete a number of bioactive adipokines that activate a variety of cell signaling pathways in central and peripheral tissues. Obesity is associated with the altered production of many adipokines and is linked to a number of pathologies. As an increase in body weight is directly associated with an increased risk for developing chronic kidney disease (CKD), there is significant interest in the link between obesity and renal dysfunction. Altered levels of the adipokines leptin, adiponectin, resistin, and visfatin can decrease the glomerular filtration rate and increase albuminuria, which are pathophysiological changes typical of CKD. Specifically, exposure of the glomerulus to altered adipokine levels can increase its permeability, fuse the podocytes, and cause mesangial cell hypertrophy, all of which alter the glomerular filtration rate. In addition, the adipokines leptin and adiponectin can act on tubular networks. Thus, adipokines can act on multiple cell types in the development of renal pathophysiology. Importantly, most studies have been performed using in vitro models, with future studies in vivo required to further elucidate the specific roles that adipokines play in the development and progression of CKD.

Cannabinoid receptor 2 expression in human proximal tubule cells is regulated by albumin independent of ERK1/2 signaling.

BACKGROUND: The cannabinoid receptor type 2 (CB2) is reduced in podocytes of animals and humans with Type 2 Diabetes Mellitus (T2DM), with activation of CB2 ameliorating albuminuria in animals. As albuminuria also is due to proximal tubule dysfunction, the aim of this study is to investigate tubular expression of CB2 under diabetic conditions in addition to the cell signaling pathways that underlie these changes. METHODS: We characterized total CB2 protein in diabetic animals and in Human Kidney 2 (HK2) cells exposed to elevated albumin and glucose, the levels of CB2 mRNA and protein. We also used latrunculin to determine if internalization of albumin was required to regulate CB2 levels. Finally, we characterized the levels of active and total AKT, ERK1/2 and p38 in response to albumin. RESULTS: There were no changes to CB2 expression in kidney lysate from diabetic rats. In HK2 cells, expression of CB2 was unaltered following exposure to high glucose. High albumin treatment alone and in combination with high glucose, resulted in a significant reduction in CB2 receptor mRNA expression at 6 and 18 hours. CB2 protein expression was reduced at 6 and 24 hours, in high albumin and in combination with high glucose. Internalization of albumin was required to regulate CB2 levels, and inhibition of ERK1/2, did not rescue the loss of CB2 in response to albumin. CONCLUSION: We have demonstrated that internalization of albumin is required to reduce CB2 mRNA and protein expression in proximal tubules in vitro. Consequently, altered expression of CB2 in both the podocytes and tubules may contribute to the albuminuria observed in T2DM.

NHERF-1 regulation of EGF and neurotensin signalling in HT-29 epithelial cells.

Neurotensin receptors (NT-R) and the epidermal growth factor receptors (EGF-R) are commonly overexpressed in many epithelial origin tumours. In addition to their role as mitogenic mediators through specific cell signalling, recent studies indicate that the activity/expression of scaffold proteins responsible for the assembly and coordination of the signalling complexes may also have central roles in epithelial transformation. In particular, the "epithelial" PSD-95/Dlg/Zo-1 (PDZ) scaffold/adapter protein, Na(+)/H(+) exchanger regulatory factor isoform one (NHERF-1), has been identified as a potential regulator of cellular transformation. NHERF-1 is a known regulator of EGF-R function and plays numerous roles in G-protein-coupled receptor signalling. Because of the synergistic signalling between these two potent mitogens, we investigated a potential role for NHERF-1 in the molecular mechanism linking the aberrant proliferative phenotype initiated by some G-Protein-coupled receptor activators in the colon adenocarcinoma HT-29 cell line. Knockdown (80%) of endogenous NHERF-1 leads to significant reduction in proliferation rate; an effect that could not be recovered by exogenous application of either NT or EGF. Inhibition of the EGF-R with AG1487 also inhibited proliferation and this effect could not be recovered with NT. Knockdown of NHERF-1 significantly altered the expression of the EGF-R, and almost completely abolished the NT-mediated increases in intracellular free Ca(2+). Knockdown of NHERF-1 also attenuated UTP-mediated purinergic Ca(2+) signalling. Taken together, these data suggest that NHERF-1 plays a more central role in cell proliferation by modulating Gq-mediated signalling pathways.

Student responses to creative coding in biomedical science education.

Biomedical science students need to learn to code. Graduates face a future where they will be better prepared for research higher degrees and the workforce if they can code. Embedding coding in a biomedical curriculum comes with challenges. First, biomedical science students often experience anxiety learning quantitative and computational thinking skills and second biomedical faculty often lack expertise required to teach coding. In this study, we describe a creative coding approach to building coding skills in students using the packages of Processing and Arduino. Biomedical science students were taught by an interdisciplinary faculty team from Medicine and Health, Science and Architecture, Design and Planning. We describe quantitative and qualitative responses of students to this approach. Cluster analysis revealed a diversity of student responses, with a large majority of students who supported creative coding in the curriculum, a smaller but vocal cluster, who did not support creative coding because either the exercises were not sufficiently challenging or were too challenging and believed coding should not be in a Biomedical Science curriculum. We describe how two creative coding platforms, Processing and Arduino, embedded and used to visualize human physiological data, and provide responses to students, including those minority of students, who are opposed to coding in the curriculum This study found a variety of students responses in a final year capstone course of an undergraduate Biomedical Science degree where future pathways for students are either in research higher degrees or to the workforce with a future which will be increasingly data driven.

Global perspectives of the impact of the COVID-19 pandemic on learning science in higher education.

The COVID-19 pandemic required higher education institutions to rapidly transition to Emergency Remote Instruction (ERI) with little preparation. Discussions are now underway globally to learn the lessons of COVID-19 and to use this knowledge to shape the future of learning science in higher education. In this study, we examined the experiences of instructors and students to ERI in three universities across three continents-America, Europe, and Australia. We measured the instructional strategies used by instructors including assessment types, and interaction opportunities during and outside class schedules. We also measured the learning challenges experienced by students including planning, distractions, technology, learning resources, their views on educational quality and what characterized quality interactions during ERI. Our findings suggest that most instructional strategies used by instructors changed little during ERI, although the nature of instructor and student interactions during class relied more heavily on technology. Students reported significant learning challenges which included distractions from their physical and social media environments and access to technology. Both instructors and students reported that interactions with each other and their peers were concerningly low, albeit similar to pre COVID-19 pandemic levels. There were differences in the perceptions of instructors and students on whether instructor-student interactions were better or worse online. Common among all universities, there was a large proportion of students reporting mental health and work-related stress. Lessons to be learned from the COVID-19 pandemic include ensuring more support for instructors to implement effective and equitable pedagogies and an increased recognition of the importance of practicals, and the social, interactive and hands-on aspects of learning science in higher education. We predict that the incorporation of active learning pedagogies and strategies which increase student engagement and foster a sense of belonging will be ongoing global challenges for learning science in a post COVID-19 campus.

Sgk-1 is a positive regulator of constitutive albumin uptake in renal proximal tubule cells.

BACKGROUND/AIMS: Receptor-mediated endocytosis of albumin by the renal proximal tubule requires a number of proteins including megalin/cubilin, sodium/hydrogen exchanger isoform 3 (NHE3) and ClC-5, as well as the PSD-95/Dlg/Zo-1 (PDZ) scaffold sodium/hydrogen exchanger regulatory factor 2 (NHERF2). Despite members from the AGC kinase family, v-Akt Murine Thymoma Viral Oncogene (Akt or Protein Kinase B) and Serum/Glucocorticoid regulated Kinase 1 (Sgk-1) regulating a number of essential proteins in the albumin handling pathway, their role in uptake is largely unknown. METHODS: Opossum kidney (OK) cells were exposed to Texas-Red albumin, in the presence of silencing constructs against Sgk-1, Akt and NHERF2, in addition to the NHE3 inhibitor 5-(N-ethyl-N-isopropyl)-amiloride (EIPA) and NHE3 activator dexamethasone. Target protein was also measured by Western blot analysis in OK cells following exposure to dexamethasone and albumin. RESULTS: Silencing Sgk-1 or overexpression of a dominant negative mutant (DN-Sgk-1) led to a significant reduction of albumin endocytosis compared to control. Conversely, over-expression of wildtype (WT) or constitutively active (CA) Sgk-1 significantly increased uptake. Previous reports have shown Sgk-1 can activate NHE3 through an interaction mediated by NHERF2. We found that silencing both Sgk-1 and NHERF2 demonstrated no additive effect on uptake, suggesting signaling via similar endpoints. Treatment with dexamethasone increased Sgk-1 protein levels and increased albumin endocytosis in OK cells. Interestingly, silencing Akt also lead to a reduction in albumin endocytosis, however in cells silenced for both Sgk-1 and Akt, the additive change in albumin uptake demonstrated that these proteins may act via separate pathways. CONCLUSIONS: We have characterized a Sgk-dependent pathway that regulates albumin uptake in the proximal tubule which also includes NHE3 and NHERF2. These data provide further insights into this essential tubular process.

Designing Virtual Reality-Based Conversational Agents to Train Clinicians in Verbal De-escalation Skills: Exploratory Usability Study.

BACKGROUND: Violence and aggression are significant workplace challenges faced by clinicians worldwide. Traditional methods of training consist of "on-the-job learning" and role-play simulations. Although both approaches can result in improved skill levels, they are not without limitation. Interactive simulations using virtual reality (VR) can complement traditional training processes as a cost-effective, engaging, easily accessible, and flexible training tool. OBJECTIVE: In this exploratory study, we aimed to determine the feasibility of and barriers to verbal engagement with a virtual agent in the context of the Code Black VR application. Code Black VR is a new interactive VR-based verbal de-escalation trainer that we developed based on the Clinical Training Through VR Design Framework. METHODS: In total, 28 participants with varying clinical expertise from 4 local hospitals enrolled in the Western Sydney Local Health District Clinical Initiative Nurse program and Transition to Emergency Nursing Programs and participated in 1 of 5 workshops. They completed multiple playthroughs of the Code Black VR verbal de-escalation trainer application and verbally interacted with a virtual agent. We documented observations and poststudy reflection notes. After the playthroughs, the users completed the System Usability Scale and provided written comments on their experience. A thematic analysis was conducted on the results. Data were also obtained through the application itself, which also recorded the total interactions and successfully completed interactions. RESULTS: The Code Black VR verbal de-escalation training application was well received. The findings reinforced the factors in the existing design framework and identified 3 new factors-motion sickness, perceived value, and privacy-to be considered for future application development. CONCLUSIONS: Verbal interaction with a virtual agent is feasible for training staff in verbal de-escalation skills. It is an effective medium to supplement clinician training in verbal de-escalation skills. We provide broader design considerations to guide further developments in this area.

An idea to explore: Interdisciplinary capstone courses in biomedical and life science education.

While biomedical and life science research have embraced interdisciplinarity as the means to solving pressing 21st century complex challenges, interdisciplinarity in undergraduate education has been more difficult to implement. As a consequence, disciplinary rather than interdisciplinary capstones have become ubiquitous. Disciplinary capstones are valuable for students because they enable them to integrate knowledge and skills within the discipline, but they are also limiting because the integration is within rather than across disciplines. In contrast to a capstone, which involves a single discipline, interdisciplinary capstones require two or more disciplines to combine and integrate across disciplinary boundaries. Interdisciplinarity, where two of more disciplines come together, is difficult to implement in the biomedical and life science curricula because student majors and finances are administered in ways, which reinforce institutional organization of schools and faculties and prevent collaboration. Here in this "idea to explore" we provide an interdisciplinary capstone model where students enroll in disciplinary courses, but then these disciplinary courses and students collaborate on interdisciplinary real-world problems. This interdisciplinary capstone model was implemented across two diverse and large biomedical and life science schools within two faculties in a research intensive, metropolitan university. This approach allows for integration of the biomedical, social and ethical perspectives required when solving problems in the real world, such as COVID-19. Interdisciplinary learning also better prepares students for higher degree research and future careers. Overcoming disciplinary curriculum silos and faculty barriers is critical if we are to meet expectations of acquiring interdisciplinarity as a key competency.

Na+-H+ exchanger regulatory factor 1 (NHERF1) PDZ scaffold binds an internal binding site in the scavenger receptor megalin.

The scavenger receptor megalin binds to albumin in the microvilli of the renal proximal tubule, and transports the ligand to the intravillar cleft for processing by endocytosis. Albumin endocytosis in the proximal tubule is regulated by protein complexes containing a number of transmembrane and accessory proteins including PDZ scaffolds such as NHERF1 and NHERF2. PDZ scaffold proteins bind to class I PDZ binding motifs (S/T-X-Φ) in the extreme C-terminus of targets. Megalin contains a functional PDZ binding motif (SDV) in its distal terminus, however a potential interaction with the NHERF proteins has not been investigated. As megalin associates with NHE3 in the microvilli and NHE3 is tethered to the intravillar cleft via its interaction with NHERF1, we investigated if there is a direct interaction between megalin and NHERF1 in renal proximal tubule cells. Using confocal microscopy we determined that megalin and NHERF1 co-localise in the apical region in proximal tubule cells. Immunoprecipitation experiments performed using rat kidney lysate indicated that megalin bound NHERF1 in vivo. Using fusion proteins and peptides, we determined that PDZ2 of NHERF1 bound to megalin and that this interaction was via the C-terminus of megalin directly and in the absence of any accessory protein. We next investigated which domain in megalin was regulating this interaction. Using GST fusion proteins we determined that the loss of the most distal C-terminus of megalin containing the PDZ binding motif (SDV) did not alter its ability to bind to NHERF1. Significantly, we then identified an internal NHERF binding domain in the C-terminus of megalin. Using peptide studies we were able to demonstrate that NHERF1 bound to an internal PDZ binding motif in megalin and that a loss of a single threonine residue abolished the interaction between megalin and NHERF1. Finally, in proximal tubule cells, silencing NHERF1 increased megalin expression. Therefore, we have identified a novel protein interaction in proximal tubule cells and specifically identified a new internal PDZ binding motif in the C-terminus of megalin.

XR game development as a tool for authentic, experiential, and collaborative learning.

This brief review provides insights into the recent advances made by the Unity game engine into education and the ways that learning resources can be used to teach novice bioscience students to use the VR/AR affordances of the platform. We present our own practises for implementation of a novel gamification task for final-year bioscience students and reflect on the changes we have had to make in order to overcome challenges presented by the COVID-19 pandemic.

Particulate Matter, an Intrauterine Toxin Affecting Foetal Development and Beyond.

Air pollution is the 9th cause of the overall disease burden globally. The solid component in the polluted air, particulate matters (PMs) with a diameter of 2.5 µm or smaller (PM2.5) possess a significant health risk to several organ systems. PM2.5 has also been shown to cross the blood-placental barrier and circulate in foetal blood. Therefore, it is considered an intrauterine environmental toxin. Exposure to PM2.5 during the perinatal period, when the foetus is particularly susceptible to developmental defects, has been shown to reduce birth weight and cause preterm birth, with an increase in adult disease susceptibility in the offspring. However, few studies have thoroughly studied the health outcome of foetuses due to intrauterine exposure and the underlying mechanisms. This perspective summarises currently available evidence, which suggests that intrauterine exposure to PM2.5 promotes oxidative stress and inflammation in a similar manner as occurs in response to direct PM exposure. Oxidative stress and inflammation are likely to be the common mechanisms underlying the dysfunction of multiple systems, offering potential targets for preventative strategies in pregnant mothers for an optimal foetal outcome.

Bioscience education 2030 and beyond: Where will technology take the curriculum?

This brief review explores the ever-increasing role that technological affordances may play in the 21C biochemistry and molecular biology curriculum. We consider the need to develop digital and creative fluencies in our students and the importance of creativity and visualization in learning science. The potential of virtual reality (VR) platforms to complement these goals are discussed with a number of examples. Finally, we look into the future where to see how VR might fit into a future curriculum.