Dietary advanced glycation end-products (AGEs) are a heterogeneous group of compounds formed when reducing sugars are heated with proteins, amino acids, or lipids at high temperatures for a prolonged period. The presence and accumulation of AGEs in numerous cell types and tissues are known to be prevalent in the pathology of many diseases. Modern diets, which contain a high proportion of processed foods and therefore a high level of AGE, cause deleterious effects leading to a multitude of unregulated intracellular and extracellular signalling and inflammatory pathways. Currently, many studies focus on investigating the chemical and structural aspects of AGEs and how they affect the metabolism and the cardiovascular and renal systems. Studies have also shown that AGEs affect the digestive system. However, there is no complete picture of the implication of AGEs in this area. The gastrointestinal tract is not only the first and principal site for the digestion and absorption of dietary AGEs but also one of the most susceptible organs to AGEs, which may exert many local and systemic effects. In this review, we summarise the current evidence of the association between a high-AGE diet and poor health outcomes, with a special focus on the relationship between dietary AGEs and alterations in the gastrointestinal structure, modifications in enteric neurons, and microbiota reshaping.

Anthocyanins have gained significant popularity in recent years for their diverse health benefits, yet their limited bioavailability poses a challenge. To address this concern, technologies have emerged to enhance anthocyanin concentration, often isolating these compounds from other food constituents. However, the extent to which isolated anthocyanins confer health benefits compared to their whole-food counterparts remains unclear. This review explores the current literature on anthocyanin bioavailability and metabolism in the body, with a focus on comparing bioavailability when consumed as extracts versus whole foods rich in anthocyanins, drawing from in vitro, in vivo, and human clinical studies. While direct comparisons between anthocyanin bioavailability in whole foods versus isolates are scarce, prevailing evidence favours whole-food consumption over anthocyanin extracts. Further clinical investigations, preferably with direct comparisons, are needed to validate these findings and elucidate the nuanced interplay between anthocyanins and food matrices, informing future research directions and practical recommendations.

In Duchenne muscular dystrophy (DMD), a dysregulated extracellular matrix (ECM) directly exacerbates pathology. Glucocorticoids are beneficial therapeutics in DMD, and have pleiotropic effects on the composition and processing of ECM proteins in other biological contexts. The synthesis and remodelling of a transitional versican-rich matrix is necessary for myogenesis; whether glucocorticoids modulate this transitional matrix is not known. Here, versican expression and processing were examined in hindlimb and diaphragm muscles from mdx dystrophin-deficient mice and C57BL/10 wild type mice. V0/V1 versican (Vcan) mRNA transcripts and protein levels were upregulated in dystrophic compared to wild type muscles, especially in the more severely affected mdx diaphragm. Processed versican (versikine) was detected in wild type and dystrophic muscles, and immunoreactivity was highly associated with newly regenerated myofibres. Glucocorticoids enhanced C2C12 myoblast fusion by modulating the expression of genes regulating transitional matrix synthesis and processing. Specifically, Tgfβ1, Vcan and hyaluronan synthase-2 (Has2) mRNA transcripts were decreased by 50% and Adamts1 mRNA transcripts were increased three-fold by glucocorticoid treatment. The addition of exogenous versican impaired myoblast fusion, whilst glucocorticoids alleviated this inhibition in fusion. In dystrophic mdx muscles, versican upregulation correlated with pathology. We propose that versican is a novel and relevant target gene in DMD, given its suppression by glucocorticoids and that in excess it impairs myoblast fusion, a process key for muscle regeneration.

Introduction: To create inclusive learning environments where neurodivergent students can learn and thrive, educators must appreciate their unique perspectives and experiences. This is particularly crucial in health professions courses, where students may face additional pressures as they undertake placements in clinical environments where neurodivergence is misrepresented or misunderstood. A comprehensive review of the existing literature is necessary to identify the available data to guide educators and pinpoint areas that warrant further exploration.Methods: Scoping review methodology, informed by the Joanna Briggs Institute approach, was used to guide a search of four electronic databases (MEDLINE, CINHAL, ERIC and PsycINFO), considering sources of primary data and analysis published up to June 2024. The retrieved literature was screened based on the inclusion criteria. Bibliographic data was extracted, and the included papers (n = 69) were reviewed and the themes charted using a framework approach.Results: Analysis of the included literature indicated some clear trends over time, with earlier papers predominantly focussing on dyslexia or framing neurodiverg as a form of disability. More recently there has been an increase in the number of papers specifically exploring the experiences of students identifying as neurodivergent, or the perspectives of educators. Narratives evident in the literature centred around relationships between a neurodivergent identity and a developing professional identity, challenges around disclosure, seeking effective accommodations in a stigmatising environment and the impact of educator perspectives.Discussion: Although the framing of neurodivergence has changed over time, a consistent finding is that neurodivergent students in health professions programmes are expected to conform to learning environments that exclude them and do not support their learning. Further evidence is required to inform recommendations for educators on how to provide safer learning environments which enable neurodivergent students to thrive.

Polyphenols, particularly anthocyanins, are associated with metabolic health benefits; however, whether anthocyanin extracts provide greater bioaccessibility than whole foods remain unclear. This study investigated the role of the food matrix in açaí berry, one of the richest natural sources of anthocyanins, by comparing polyphenol and anthocyanin bioaccessibility across freeze-dried whole fruit, crude extract, and purified extract. All samples underwent standardised INFOGEST in vitro digestion, and total polyphenol content (TPC), anthocyanins (ACN), and antioxidant activity were quantified using Folin–Ciocalteu, pH-differential, and DPPH assays, respectively. Intestinal-phase TPC % bioaccessibility was similar in whole fruit (58%) and crude extract (58%) but significantly lower in pure extract (43%). ACN bioaccessibility showed a pronounced matrix effect, with the highest retention in whole fruit (44%), followed by crude extract (32%), and the lowest retention in pure extract (12%). Antioxidant activity after intestinal digestion mirrored these patterns. Overall, these findings demonstrate that the natural açaí food matrix substantially preserves anthocyanin stability during digestion, resulting in higher bioaccessible levels than matrix-free extracts, suggesting that incorporating matrix components into anthocyanin-rich nutraceuticals may help support greater functional recovery during gastrointestinal digestion.

Aberrant extracellular matrix synthesis and remodeling contributes to muscle degeneration and weakness in Duchenne muscular dystrophy (DMD). ADAMTS-5, a secreted metalloproteinase with catalytic activity against versican, is implicated in myogenesis and inflammation. Here, using the mdx mouse model of DMD, we report increased ADAMTS-5 expression in dystrophic hindlimb muscles, localized to regions of regeneration and inflammation. To investigate the pathophysiological significance of this, 4-week-old mdx mice were treated with an ADAMTS-5 monoclonal antibody (mAb) or IgG2c (IgG) isotype control for 3 weeks. ADAMTS-5 mAb treatment did not reduce versican processing, as protein levels of the cleaved versikine fragment did not differ between hindlimb muscles from ADAMTS-5 mAb or IgG treated mdx mice. Nonetheless, ADAMTS-5 blockade improved ex vivo strength of isolated fast extensor digitorum longus, but not slow soleus, muscles. The underpinning mechanism may include modulation of regenerative myogenesis, as ADAMTS-5 blockade reduced the number of recently repaired desmin positive myofibers without affecting the number of desmin positive muscle progenitor cells. Treatment with the ADAMTS-5 mAb did not significantly affect markers of muscle damage, inflammation, nor fiber size. Altogether, the positive effects of ADAMTS-5 blockade in dystrophic muscles are fiber-type-specific and independent of versican processing.