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It is often taken as given that community-based disaster risk reduction (CBDRR) serves as a mechanism for the inclusion of local knowledge (LK) in disaster risk reduction (DRR). In this paper, through in-depth qualitative analysis of empirical data from Malawi, we investigate the extent to which CBDRR in practice really takes into account LK. This research argues that LK is underutilised in CBDRR and finds that current practice provides a limited opportunity for the inclusion of LK, due to five prime obstacles: i) current approach to community participation, ii) financial constraints and capacity of external stakeholders, iii) the donor landscape, iv) information consolidation and sharing, and v) external stakeholders attitudes towards LK. In CBDRR, a strong dichotomy between local and scientific knowledge is maintained, and further re-examination of community-based approaches in practice is needed to make them truly transformative.

This contributing paper aims to investigate the extent to which community-based disaster risk reduction (CBDRR) in practice really takes into account local knowledge (LK). It is often taken as given that CBDRR serves as a mechanism for the inclusion of local knowledge (LK) in disaster risk reduction (DRR). But the reality from the ground suggests that this increased attention does not result in practical inclusion of communities nor their LK in DRR. Through in-depth empirical qualitative data from Malawi, the paper explores the dynamics between the inadequate inclusion of LK and approaches to DRR. This study argues that LK is underutilised in CBDRR and finds that current practice provides a limited opportunity for the inclusion of LK, due to five prime obstacles: i) current approach to community participation, ii) financial constraints and capacity of external stakeholders, iii) the donor landscape, iv) information consolidation and sharing, and v) external stakeholders attitudes towards LK. In CBDRR, a strong dichotomy between local and scientific knowledge is maintained, and further re-examination of community-based approaches in practice is needed to make them truly transformative.

Chronic back and neck pain is a prevalent disability, often caused by degeneration of the intervertebral disc. Because current treatments for this condition are less than satisfactory, a great deal of effort is being applied to develop new solutions, including regenerative strategies. However, the path from initial promising idea to clinical use is fraught with many hurdles to overcome. Many of the keys to success are not necessarily linked to science or innovation. Successful translation to clinic will also rely on planning and awareness of the hurdles. It will be essential to plan your entire path to clinic from the outset and to do this with a multidisciplinary team. Take advice early on regulatory aspects and focus on generating the proof required to satisfy regulatory approval. Scientific demonstration and societal benefits are important, but translation cannot occur without involving commercial parties, which are instrumental to support expensive clinical trials. This will only be possible when intellectual property can be protected sufficiently to support a business model. In this manner, commercial, societal, medical, and scientific partners can work together to ultimately improve patient health. Based on literature surveys and experiences of the co-authors, this opinion paper presents this pathway, highlights the most prominent issues and hopefully will aid in your own translational endeavors.

Introduction: Degeneration of the intervertebral disc (IVD) is a frequent cause for back pain in humans and dogs. Link-N stabilizes proteoglycan aggregates in cartilaginous tissues and exerts growth factor-like effects. The human variant of Link-N facilitates IVD regeneration in several species in vitro by inducing Smad1 signaling, but it is not clear whether this is species specific. Dogs with IVD disease could possibly benefit from Link-N treatment, but Link-N has not been tested on canine IVD cells. If Link-N appears to be effective in canines, this would facilitate translation of Link-N into the clinic using the dog as an in vivo large animal model for human IVD degeneration. Materials and methods: This study’s objective was to determine the effect of the human and canine variant of Link-N and short (s) Link-N on canine chondrocyte-like cells (CLCs) and compare this to those on already studied species, i.e. human and bovine CLCs. Extracellular matrix (ECM) production was determined by measuring glycosaminoglycan (GAG) content and histological evaluation. Additionally, the micro-aggregates’ DNA content was measured. Phosphorylated (p) Smad1 and -2 levels were determined using ELISA. Results: Human (s)Link-N induced GAG deposition in human and bovine CLCs, as expected. In contrast, canine (s)Link-N did not affect ECM production in human CLCs, while it mainly induced collagen type I and II deposition in bovine CLCs. In canine CLCs, both canine and human (s)Link-N induced negligible GAG deposition. Surprisingly, human and canine (s) Link-N did not induce Smad signaling in human and bovine CLCs. Human and canine (s) Link-N only mildly increased pSmad1 and Smad2 levels in canine CLCs. Conclusions: Human and canine (s)Link-N exerted species-specific effects on CLCs from early degenerated IVDs. Both variants, however, lacked the potency as canine IVD regeneration agent. While these studies demonstrate the challenges of translational studies in large animal models, (s