Melbourne Veterinary School - Research Publications
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ItemImmunohistochemical analysis of laryngeal muscle of horses clinically affected with recurrent laryngeal neuropathy(WILEY, 2020-10-27)Background As myosin heavy chain (MyHC) profile of muscle fibres is heavily influenced by neural input, changes in MyHC expression are expected in horses clinically affected with recurrent laryngeal neuropathy (RLN) yet, this has not been thoroughly investigated. Objectives To describe the changes in MyHC and fibre diameter in left cricoarytenoideus dorsalis (L-CAD) muscle of horses with clinical signs of RLN. Study design Observational cohort study. Methods Immunohistochemistry was used to assess the MyHC-based fibre-type proportion, size and grouping in the L-CAD of 10 Thoroughbred horses, five clinically affected with RLN and five unaffected controls based on resting endoscopic examination. The Mann-Whitney U test was used to compare the two groups. Results Compared to controls (of mean age 3.0 ± 1.7 years) which only expressed type I, IIA and IIX MyHC, the L-CAD of affected horses (of mean age 2.8 ± 0.8 years) had obvious fibre-type grouping, and despite apparent compensatory hypertrophy of a small number of fibres, a decrease in overall fibre diameter (median difference −35.2 µm, 95% CI −47.4 to −7.9, P = .02) and diameter of type IIA fibres (median difference −46.8 µm, 95% CI −52.1 to −5.0, P = .03) was observed. Anti-fast MyHC (MY32) cross-immunoreacted with embryonic-MyHC. Whereas MY32-positive fibres were identified as type IIX in controls, in affected horses these fibres were less than 50 µm diameter with internal nuclei and were MYH3-positive for embryonic myosin indicating depletion of type IIX fibres, yet active regeneration and fibre renewal. Main limitations Small sample size that did not include subclinical cases. Fibre size and appearance rather than staining colour were relied upon to differentiate embryonic from type IIX MyHC. Conclusions Horses clinically affected with RLN have overall atrophy of fibres, loss of IIX fibres and expression of embryonic myosin indicating regenerative capacity. Despite hypertrophy of some remaining fibres, the overall decline in the bulk of fibres, including those most fatigue-resistant, may be the critical change that results in failure to maintain arytenoid abduction during exercise although direct comparison to subclinical cases is needed to confirm this.
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ItemMuscle, Ageing and Temperature Influence the Changes in Texture, Cooking Loss and Shrinkage of Cooked Beef(MDPI AG, 2020-09-01)This study aimed to quantify the effect of muscle, ageing and cooking temperature on the texture, cooking loss and shrinkage of cooked beef. Cuboids from unaged (1 day post mortem) and aged (14 days post mortem) semitendinosus, biceps femoris and psoas major muscles, from both sides of five beef carcasses, were cooked at four different cooking temperatures (50, 60, 70 and 80 °C) for 30 min. and their Warner–Bratzler shear force (WBSF), cooking loss and shrinkage (longitudinal and transverse) were quantified. The WBSF was reduced by ageing in the muscles at the specific cooking temperatures: psoas major (cooked at 50, 60 and 80 °C), semitendinosus (70 and 80 °C) and biceps femoris (80 °C). The cooking loss was 3% greater in aged compared to unaged muscles. The longitudinal shrinkage was greatest in psoas major at 80 °C amongst the muscle types and it was reduced by ageing in psoas major (70 and 80 °C) and biceps femoris (80 °C). The transverse shrinkage was reduced by ageing only in biceps femoris, across all temperatures; and the diameter of homogenized fibre fragments from semitendinosus and biceps femoris was reduced more by cooking at 50 °C in unaged compared to aged condition. WBSF was related to transverse shrinkage, and cooking loss was related to longitudinal shrinkage. The effect of muscle type on the physical changes occurring during cooking of beef is dependent on ageing and cooking temperature.
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ItemAdenylosuccinic acid therapy ameliorates murine Duchenne Muscular Dystrophy(NATURE PUBLISHING GROUP, 2020-01-24)Arising from the ablation of the cytoskeletal protein dystrophin, Duchenne Muscular Dystrophy (DMD) is a debilitating and fatal skeletal muscle wasting disease underpinned by metabolic insufficiency. The inability to facilitate adequate energy production may impede calcium (Ca2+) buffering within, and the regenerative capacity of, dystrophic muscle. Therefore, increasing the metabogenic potential could represent an effective treatment avenue. The aim of our study was to determine the efficacy of adenylosuccinic acid (ASA), a purine nucleotide cycle metabolite, to stimulate metabolism and buffer skeletal muscle damage in the mdx mouse model of DMD. Dystrophin-positive control (C57BL/10) and dystrophin-deficient mdx mice were treated with ASA (3000 µg.mL-1) in drinking water. Following the 8-week treatment period, metabolism, mitochondrial density, viability and superoxide (O2-) production, as well as skeletal muscle histopathology, were assessed. ASA treatment significantly improved the histopathological features of murine DMD by reducing damage area, the number of centronucleated fibres, lipid accumulation, connective tissue infiltration and Ca2+ content of mdx tibialis anterior. These effects were independent of upregulated utrophin expression in the tibialis anterior. ASA treatment also increased mitochondrial viability in mdx flexor digitorum brevis fibres and concomitantly reduced O2- production, an effect that was also observed in cultured immortalised human DMD myoblasts. Our data indicates that ASA has a protective effect on mdx skeletal muscles.