Ultrasound-guided quadratus lumborum block (QLB) is a locoregional technique described in canine cadavers. The aim of this study was to assess a modified approach to QLB to minimise potential complications such as abdominal organ puncture. Nine canine cadavers were included and were positioned in lateral recumbency. An ultrasound-guided QLB was performed on each side. The probe was placed in the transverse position over the lumbar muscles just caudal to the last rib, and a needle was advanced in-plane from a dorso-lateral to a ventro-medial. A volume of 0.2 mL kg−1 of a mixture of iomeprol and methylene blue was injected. Computed tomography (CT) and dissection were performed to evaluate the spreading. Success was defined as staining of the nerve with a length of more than 0.6 cm. Potential complications such as intra-abdominal, epidural, or intravascular spreading of the mixture were also assessed. The CT images showed a T13 to L7 vertebra distribution, with a median of 5 (3–6). Dissection showed staining of the nerves from T13 to L4, with a median of 3 (2–5). No complications were found. This modified approach to QLB is safe and shows similar results to the previous studies in canine carcass.

Tissue fibrosis following tendon injury is a major clinical problem due to the increased risk of re-injury and limited treatment options; however, its mechanism remains unclear. Evidence suggests that insufficient resolution of inflammation contributes to fibrotic healing by disrupting tenocyte activity, with the NF-κB pathway being identified as a potential mediator. Equine embryonic stem cell (ESC) derived tenocytes may offer a potential cell-based therapy to improve tendon regeneration, but how they respond to an inflammatory environment is largely unknown. Our findings reveal for the first time that, unlike adult tenocytes, ESC-tenocytes are unaffected by IFN-γ, TNFα, and IL-1β stimulation; producing minimal changes to tendon-associated gene expression and generating 3-D collagen gel constructs indistinguishable from unstimulated controls. Inflammatory pathway analysis found these inflammatory cytokines failed to activate NF-κB in the ESC-tenocytes. However, NF-κB could be activated to induce changes in gene expression following stimulation with NF-κB pharmaceutical activators. Transcriptomic analysis revealed differences between cytokine and NF-κB signalling components between adult and ESC-tenocytes, which may contribute to the mechanism by which ESC-tenocytes escape inflammatory stimuli. Further investigation of these molecular mechanisms will help guide novel therapies to reduce fibrosis and encourage superior tendon healing.

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One contribution of 14 to a theme issue 'Challenges and opportunities in the fight against neglected tropical diseases: a decade from the London Declaration on NTDs'.

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