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Muscle Sections (muscle + section)
Selected AbstractsEffects of Salt, BHA/BHT, and Differing Phosphate Types on Quality and Sensory Characteristics of Beef Longissimus MusclesJOURNAL OF FOOD SCIENCE, Issue 4 2009C.W. Rowe ABSTRACT:, USDA Select striploins (n,=,20) were cut into thirds (anterior, medial, and posterior) and randomly assigned to 1 of 6 treatments. Treatments included: (1) control (C); (2) 0.006% BHA (butylated hydroxyl anisole)/BHT (butylated hydroxytoluene) (70%/30%) (BB); (3) 0.4% trisodiumphosphate (CT); (4) 0.4% sodiumtripolyphosphate with 0.5% salt (BH); (5) sodiumtripolyphosphate, 0.5% salt, and 0.006% BHA/BHT (70%/30%) (SB); (6) 0.2% sodiumtripolyphosphate, 0.2% trisodiumphosphate, and 0.5% salt (STB). Muscle sections were injected to 110% (10% pump) of their weight with their respective treatments. Inclusion of BHA/BHT allowed for lower mean oxidation values. Regardless of phosphate type, muscles treated with both phosphate and salt had lower retail purge (P < 0.05). Sensory panelists rated (P < 0.05) STB, SB, and BH to be juicier than all other treatments. These data suggest that inclusion of both salt and phosphate can enhance palatability, lower cook loss, and retail purge. [source] HGF induction of postsynaptic specializations at the neuromuscular junctionDEVELOPMENTAL NEUROBIOLOGY, Issue 2 2006Raghavan Madhavan Abstract A critical event in the formation of vertebrate neuromuscular junctions (NMJs) is the postsynaptic clustering of acetylcholine receptors (AChRs) in muscle. AChR clustering is triggered by the activation of MuSK, a muscle-specific tyrosine kinase that is part of the functional receptor for agrin, a nerve-derived heparan sulfate proteoglycan (HSPG). At the NMJ, heparan sulfate (HS)-binding growth factors and their receptors are also localized but their involvement in postsynaptic signaling is poorly understood. In this study we found that hepatocyte growth factor (HGF), an HS-binding growth factor, surrounded muscle fibers and was localized at NMJs in rat muscle sections. In cultured Xenopus muscle cells, HGF was enriched at spontaneously occurring AChR clusters (hot spots), where HSPGs were also concentrated, and, following stimulation of muscle cells by agrin or cocultured neurons, HGF associated with newly formed AChR clusters. HGF presented locally to cultured muscle cells by latex beads induced new AChR clusters and dispersed AChR hot spots, and HGF beads also clustered phosphotyrosine, activated c-Met, and proteins of dystrophin complex; clustering of AChRs and associated proteins by HGF beads required actin polymerization. Lastly, although bath-applied HGF alone did not induce new AChR clusters, addition of HGF potentiated agrin-dependent AChR clustering in muscle. Our findings suggest that HGF promotes AChR clustering and synaptogenic signaling in muscle during NMJ development. © 2005 Wiley Periodicals, Inc. J Neurobiol, 2005 [source] Fetal programming of fat and collagen in porcine skeletal musclesJOURNAL OF ANATOMY, Issue 6 2005J. F. Karunaratne Abstract Connective tissue plays a key role in the scaffolding and development of skeletal muscle. Pilot studies carried out in our laboratory have shown that the smallest porcine littermate has a higher content of connective tissue within skeletal muscle compared with its largest littermate. The present study investigated the prenatal development of intralitter variation in terms of collagen content within connective tissue and intramuscular fat of the M. semitendinosus. Twenty-three pairs of porcine fetuses from a Large White,Landrace origin were used aged from 36 to 86 days of gestation. The largest and smallest littermates were chosen by weight and the M. semitendinosus was removed from each. Complete transverse muscle sections were stained with Oil Red O (detection of lipids) and immunocytochemistry was performed using an antibody to collagen I. Slides were analysed and paired t -Tests revealed the smallest littermate contained a significantly higher proportion of fat deposits and collagen I content compared with the largest littermate. Recent postnatal studies showing elevated levels of intramuscular lipids and low scores for meat tenderness in the smallest littermate corroborate our investigations. It can be concluded that the differences seen in connective tissue elements have a fetal origin that may continue postnatally. [source] Immunohistological intensity measurements as a tool to assess sarcolemma-associated protein expressionNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 4 2010V. Arechavala-Gomeza V. Arechavala-Gomeza, M. Kinali, L. Feng, S. C. Brown, C. Sewry, J. E. Morgan and F. Muntoni (2010) Neuropathology and Applied Neurobiology36, 265,274 Immunohistological intensity measurements as a tool to assess sarcolemma-associated protein expression Aims: The quantification of protein levels in muscle biopsies is of particular relevance in the diagnostic process of neuromuscular diseases, but is difficult to assess in cases of partial protein deficiency, particularly when information on protein localization is required. The combination of immunohistochemistry and Western blotting is often used in these cases, but is not always possible if the sample is scarce. We therefore sought to develop a method to quantify relative levels of sarcolemma-associated proteins using digitally captured images of immunolabelled sections of skeletal muscle. Methods: To validate our relative quantification method, we labelled dystrophin and other sarcolemmal proteins in transverse sections of muscle biopsies taken from Duchenne muscular dystrophy and Becker muscular dystrophy patients, a manifesting carrier of Duchenne muscular dystrophy and normal controls. Results: Using this method to quantify relative sarcolemmal protein abundance, we were able to accurately distinguish between the different patients on the basis of the relative amount of dystrophin present. Conclusions: This comparative method adds value to techniques that are already part of the diagnostic process and can be used with minimal variation of the standardized protocols, without using extra amounts of valuable biopsy samples. Comparative quantification of sarcolemmal proteins on immunostained muscle sections will be of use to establish both the abundance and localization of the protein. Moreover, it can be applied to assess the efficacy of experimental therapies where only partial restoration or upregulation of the protein may occur. [source] Acetazolamide prevents vacuolar myopathy in skeletal muscle of K+ -depleted ratsBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2008D Tricarico Background and purpose: Acetazolamide and dichlorphenamide are carbonic anhydrase (CA) inhibitors effective in the clinical condition of hypokalemic periodic paralysis (hypoPP). Whether these drugs prevent vacuolar myopathy, which is a pathogenic factor in hypoPP, is unknown. The effects of these drugs on the efflux of lactate from skeletal muscle were also investigated. Experimental approach: For 10 days, K+ -depleted rats, a model of hypoPP, were administered 5.6 mg kg,1 day,1 of acetazolamide, dichlorphenamide or bendroflumethiazide (the last is not an inhibitor of CA). Histological analysis of vacuolar myopathy and in vitro lactate efflux measurements were performed in skeletal muscles from treated and untreated K+ -depleted rats, and also from normokalemic rats. Key results: About three times as many vacuoles were found in the type II fibres of tibialis anterioris muscle sections from K+ -depleted rats as were found in the same muscle from normokalemic rats. In ex vivo experiments, a higher efflux of lactate on in vitro incubation was found in muscles of K+ -depleted rats compared with that found in muscles from normokalemic rats. After treatment of K+ -depleted rats with acetazolamide, the numbers of vacuoles in tibialis anterioris muscle decreased to near normal values. Incubation with acetazolamide in vitro inhibited efflux of lactate from muscles of K+ -depleted rats. In contrast, bendroflumethiazide and dichlorphenamide failed to prevent vacuolar myopathy after treatment in vivo and failed to inhibit lactate efflux in vitro. Conclusions and implications: Acetazolamide prevents vacuolar myopathy in K+ -depleted rats. This effect was associated with inhibition of lactate transport, rather than inhibition of CA. [source] Nitric oxide synthase in critically ischaemic muscle and alterations in isoform expression during revascularization surgery,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 1 2008J. C. S. Tsui Background: Dysfunction of the nitric oxide pathway is implicated in peripheral arterial disease. Nitric oxide synthase (NOS) isoforms and NOS activity were studied in muscle from patients with critical leg ischaemia (CLI). Alterations in NOS during revascularization surgery were also assessed. Methods: Muscle biopsies were taken from patients with CLI undergoing amputation and also from patients undergoing femorodistal bypass at the start of surgery, after arterial clamping and following reperfusion. The presence of NOS within muscle sections was confirmed using reduced nicotinamide adenine dinucleotide phosphate diaphorase histochemistry. NOS isoform distribution was studied by immunohistochemistry. NOS mRNA and protein levels were measured using real-time reverse transcriptase,polymerase chain reaction and western blotting. NOS activity was assessed with the citrulline assay. Results: All three NOS isoforms were found in muscle, associated with muscle fibres and microvessels. NOS I and III protein expression was increased in CLI (P = 0·041). During revascularization, further ischaemia and reperfusion led to a rise in NOS III protein levels (P = 0·008). NOS activity was unchanged. Conclusion: Alterations in NOS I and III occurred in muscle from patients with CLI and further changes occurred during bypass surgery. Copyright © 2007 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] | |||||||||||||