133 research outputs found

    Phytosterol, tocopherol and carotenoid retention during commercial processing of brassica napus (canola) oil

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    Brassica napus (canola) seed is a rich source of phytosterols, tocopherols and carotenoids, which all have recognized health benefits, although these are reduced or lost during crude oil refinement. Many studies are now outdated, so new research to monitor bioactive retention through current processing techniques is warranted. In this work, canola seed, in-process seed, and oil samples were collected from the major stages of five commercial canola oil processes. Analysis of phytosterols, tocopherols and carotenoids indicated seed pre-treatment enhanced bioactive concentrations in the crude oil. Although the bleaching step in each process eliminated all carotenoids, high concentrations of phytosterols and tocopherols remained in the refined oil across all processes, with losses notably lower than those found in previous reports. Moreover, crude oil samples from a two-stage cold pressing process showed greatly enriched concentrations of tocopherols (+122%), sterols (+140%) and carotenoids (+217%). The results show that modern Australian canola oil processing retains high phytosterol and tocopherol concentrations and warrants further investigation into bioactive enrichment strategies. Given the growing interest in health-enhanced foods, this study provides opportunities for nutrition and health-enhanced oil products and the potential for adding value in the edible oil industry

    Effect of adeno-associated virus (AAV)-mediated overexpression of PEPCK-M (Pck2) on Clenbuterol-induced muscle growth

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    We previously identified PEPCK-M (encoded by the Pck2 gene) to be highly up-regulated in skeletal muscle of pigs treated with Ractopamine, an anabolic beta-adrenergic receptor agonist. To determine whether PEPCK-M had a causative role in modulating the skeletal muscle growth response to Ractopamine, we used adeno-associated virus 1 (AAV1) to over-express Pck2 (AAV-Pck2) in murine skeletal muscle. A contralateral limb design was employed, such that each mouse served as its own control (injected with a GFP-only expressing AAV1, labelled AAV-GFP). Daily injections of Clenbuterol (1 mg/kg for 21 days) or vehicle control were also carried out to assess the effects of AAV-Pck2 overexpression on the anabolic response to a beta-adrenergic agonist. AAV-Pck2 overexpression in leg muscles of male C57BL6/J mice for 4 weeks (6ā€“10 weeks of age) increased Pck2 mRNA (~100-fold), protein (not quantifiable) and enzyme activity (~3-fold). There was a trend (p = 0.0798) for AAV-Pck2 overexpression to reduce TA muscle weights, but there was no significant effect on muscle fibre diameters or myosin heavy chain isoform (MyHC) mRNA expression. When skeletal muscle growth was induced by daily administration of Clenbuterol (for 21 days), overexpression of AAV-Pck2 had no effect on the growth response, nor did it alter the expression of Phosphoserine Aminotransferase-1 (Psat1) or Asparagine Synthetase (Asns) mRNA or the Clenbuterol-induced decreases in MyHC IIa and IIx mRNA expression (p = 0.0065 and p = 0.0267 respectively). However AAV-Pck2 overexpression reduced TA muscle weights (p = 0.0434), particularly in the Control (vehicle treated) mice (p = 0.059 for AAV x Clenbuterol interaction) and increased the expression of Seryl-tRNA Synthetase (Sars) mRNA (p = 0.0477). Hence, contrary to the original hypothesis, AAV-Pck2 overexpression reduced TA muscle weights and did not mimic or alter the muscle hypertrophic effects of the beta-adrenergic agonist, Clenbuterol

    Implementing the battery-operated hand-held fan as an evidence-based, non-pharmacological intervention for chronic breathlessness in patients with chronic obstructive pulmonary disease (COPD): a qualitative study of the views of specialist respiratory clinicians

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    INTRODUCTION: The battery-operated hand-held fan ('fan') is an inexpensive and portable non-pharmacological intervention for chronic breathlessness. Evidence from randomised controlled trials suggests the fan reduces breathlessness intensity and improves physical activity in patients with a range of advanced chronic conditions. Qualitative data from these trials suggests the fan may also reduce anxiety and improve daily functioning for many patients. This study aimed to explore barriers and facilitators to the fan's implementation in specialist respiratory care as a non-pharmacological intervention for chronic breathlessness in patients with chronic obstructive pulmonary disease (COPD). METHODS: A qualitative approach was taken, using focus groups. Participants were clinicians from any discipline working in specialist respiratory care at two hospitals. Questions asked about current fan-related practice and perceptions regarding benefits, harms and mechanisms, and factors influencing its implementation. Analysis used a mixed inductive/deductive approach. RESULTS: Forty-nine participants from nursing (nā€‰=ā€‰30), medical (nā€‰=ā€‰13) and allied health (nā€‰=ā€‰6) disciplines participated across 9 focus groups. The most influential facilitator was a belief that the fan's benefits outweighed disadvantages. Clinicians' beliefs about the fan's mechanisms determined which patient sub-groups they targeted, for example anxious or palliative/end-stage patients. Barriers to implementation included a lack of clarity about whose role it was to implement the fan, what advice to provide patients, and limited access to fans in hospitals. Few clinicians implemented the fan for acute-on-chronic breathlessness or in combination with other interventions. CONCLUSION: Implementation of the fan in specialist respiratory care may require service- and clinician-level interventions to ensure it is routinely recommended as a first-line intervention for chronic breathlessness in patients for whom this symptom is of concern, regardless of COPD stage

    Immune Modulation by Design: Using Topography to Control Human Monocyte Attachment and Macrophage Differentiation

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    Ā© 2020 The Authors. Published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim Macrophages play a central role in orchestrating immune responses to foreign materials, which are often responsible for the failure of implanted medical devices. Material topography is known to influence macrophage attachment and phenotype, providing opportunities for the rational design of ā€œimmune-instructiveā€ topographies to modulate macrophage function and thus foreign body responses to biomaterials. However, no generalizable understanding of the inter-relationship between topography and cell response exists. A high throughput screening approach is therefore utilized to investigate the relationship between topography and human monocyteā€“derived macrophage attachment and phenotype, using a diverse library of 2176 micropatterns generated by an algorithm. This reveals that micropillars 5ā€“10Āµm in diameter play a dominant role in driving macrophage attachment compared to the many other topographies screened, an observation that aligns with studies of the interaction of macrophages with particles. Combining the pillar size with the micropillar density is found to be key in modulation of cell phenotype from pro to anti-inflammatory states. Machine learning is used to successfully build a model that correlates cell attachment and phenotype with a selection of descriptors, illustrating that materials can potentially be designed to modulate inflammatory responses for future applications in the fight against foreign body rejection of medical devices

    Immune-Instructive Polymers Control Macrophage Phenotype and Modulate the Foreign Body Response InĀ Vivo

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    Ā© 2020 The Author(s) Implantation of medical devices can result in inflammation. A large library of polymers is screened, and a selection found to promote macrophage differentiation towards pro- or anti-inflammatory phenotypes. The bioinstructive properties of these materials are validated within a rodent model. By identifying novel materials with immune-instructive properties, the relationship between material-immune cell interactions could be investigated, and this offers exciting possibilities to design novel bioinstructive materials that can be used for numerous clinical applications including medical implants

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    Spatially resolved molecular analysis of host response to medical device implantation using the 3D OrbiSIMS highlights a critical role for lipids

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    A key goal for implanted medical devices is that they do not elicit a detrimental immune response. Macrophages play critical roles in modulation of the host immune response and are the major cells responsible for persistent inflammatory reactions to implanted biomaterials. We investigate two novel immune-instructive polymers that stimulate pro- or anti-inflammatory responses from macrophages in vitro. These also modulate in vivo foreign body responses (FBR) when implanted subcutaneously in mice as coatings on biomedical grade silicone rubber. The tissue surrounding the implant is mechanically sectioned and imaged to assess the response of the polymers compared to silicone rubber. Immunofluorescent staining reveals responses consistent with pro- or anti-inflammatory responses previously described for these polymers. We apply 3D OrbiSIMS analysis to provide spatial analysis of the metabolite signature in the tissue surrounding the implant for the first time, providing molecular histology insight into the metabolite response in the host tissue. For the pro-inflammatory coating, monoacylglycerols (MG) and diacylglycerols (DG) are observed at increased intensity, while for the anti-inflammatory coating the number of phospholipid species detected decrease and pyridine and pyrimidine levels were elevated. These findings link to observations of small molecule signature from single cell studies of M2 macrophages in vitro where cell and tissue ion intensities were found to correlate suggesting potential for prediction. This illustrates the power of metabolite characterization by the 3D OrbiSIMS to gain insight into the mechanism of bio-instructive materials as medical devices and to inform on the FBR to biomaterials

    Crop Updates 1999 - Lupins

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    This article contains twenty three papers 1998 LUPIN HIGHLIGHTS LUPIN ANTHRACNOSE 1. Anthracnose overview, Greg Shea, Geoff Thomas and Mark Sweetingham, Agriculture Western Australia 2. Anthracnose ā€“ Critical seed infection levels for resistant and susceptible varieties, Geoff Thomas, Mark Sweetingham, Bill O\u27Neill and Greg Shea, Agriculture Western Australia 3. Fungicide seed treatment for anthracnose and brown spot control in lupin, G. Thomas and M. Sweetingham, Agriculture Western Australia LUPIN BREEDING AND AGRONOMY 4. Anthracnose resistance in lupins ā€“ an innovative Australian research effort 1996-1998, Wallace Cowling1\u272, Bevan Buirchell1,2 Mark Sweetinqham1,2, Hua\u27an Yang2, Geoff Thomas 1, David Luckett3, Allan Brown4 and John Hamblin2, 1 Agriculture Western Australia, 2 Centre for Legumes in Mediterranean Agriculture, University of Western Australia, 3 NSW Agriculture, Agricultural Institute, Wagga Wagga, NSW, 4 Consultant, 16 Rochester Way, Dianella, WA 5. Gene transfer to pulses: Challenges through 1989-99. Joanne E. Barton, Centre for Legumes in Mediterranean Agriculture, University of Western Australia 6. Can we select for restricted branching in narrow-leafed lupin (Lupinus angustifolius) Kedar Adhikari1, Nick Galwey1and Miles Dracup2, 1Plant Sciences, Faculty of Agriculture, The University of Western Australia,2 Agriculture Western Australia 7. Getting the beat out of new lupin varieties, Dr Bob French, Grain Legume Agronomist, Agriculture Western Australia 8. Starter nitrogen on lupins, Dr Bob French, Grain Legume Agronomist, Agriculture Western Australia APHIDS AND VIRUS CONTROL 9. Forecasting aphid and virus risk in lupins, Debbie Thackray and Roger Jones, CRC for Legumes in Mediterranean Agriculture and Agriculture Western Australia 10. Screening for resistance to cucumber mosaic virus in lupins, Roger Jones, Brenda Coutts, Narelle Reeve, Wallace Cowling and Bevan Buirchell, Agriculture Western Australia and CRC for Legumes in Mediterranean Agriculture 11. The non-necrotic strain of bean yellow mosaic virus spreads faster than the necrotic strain in lupins, Y. Cheng 1 and R.A.C. Jones 1ā€¢2, 1 Cooperative Research Centre for Legumes in Mediterranean Agriculture, 2 Agriculture Western Australia 12. Spraying to control aphid feeding damage increases yields of some lupin varieties and faba bean, Francoise Berlandier and Linnet Cartwright, Entomology, Agriculture Western Australia LUPIN NUTRITION 13. Calculated lime requirements for rotations, James Fisher1, Art Diggle 1ā€¢2 and Bill Bowden 1ā€¢2, 1 Centre for Legumes in Mediterranean Agriculture, 2 Agriculture Western Australia 14. What does lime do to acidic soils ā€“ lupin nutrition, Chris Gazey, Research Officer, Agriculture Western Australia 15. Effect of application method of manganese fertiliser and manganese concentration of seed source on seed yield of lupins grown in the West Midlands, Luigi Moreschi, CSBP Area Manager HERBICIDE TOLERANCE AND WEED CONTROL 16. Herbicide tolerance of lupins, Terry Piper, Weed Science Group, Agriculture Western Australia 17. Weed control in Wodjil yellow lupins, Terry Piper, Weed Science Group, Agriculture Western Australia 18. Herbicide tolerance of new lupin varieties, Peter Newman, Agronomist, Elders Mingenew 19. Control of volunteer canola in lupins, Terry Piper and Dave Nicholson, Weed Science Group, Agriculture Western Australia LUPIN ESTABLISHMENT 20. A new seed pressing system for healthy lupin establishment and productivity, Mohammad Amjad, Glen Riethmuller and Ron Jarvis, Agriculture Western Australia 21. Encouragement for controlled traffic farming in the Northern Wheatbelt, Paul Blackwell, Agriculture Western Australia LUPIN HARVESTING 22. Improved lupin harvesting efficiency with different knife guard extensions, Glen Riethmuller, Agriculture Western Australia LUPIN AND PULSE UTILISATION 23. The value of pulse grains for sheep, C.L. White, CSIRO Division of Animal Productio

    Discovery of a polymer resistant to bacterial biofilm, swarming, and encrustation

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    Innovative approaches to prevent catheter-associated urinary tract infections (CAUTIs) are urgently required. Here, we describe the discovery of an acrylate copolymer capable of resisting single- and multispecies bacterial biofilm formation, swarming, encrustation, and host protein deposition, which are major challenges associated with preventing CAUTIs. After screening ~400 acrylate polymers, poly(tert-butyl cyclohexyl acrylate) was selected for its biofilm- and encrustation-resistant properties. When combined with the swarming inhibitory poly(2-hydroxy-3-phenoxypropyl acrylate), the copolymer retained the bioinstructive properties of the respective homopolymers when challenged with Proteus mirabilis, Pseudomonas aeruginosa, Staphylococcus aureus, and Escherichia coli. Urinary tract catheterization causes the release of host proteins that are exploited by pathogens to colonize catheters. After preconditioning the copolymer with urine collected from patients before and after catheterization, reduced host fibrinogen deposition was observed, and resistance to diverse uropathogens was maintained. These data highlight the potential of the copolymer as a urinary catheter coating for preventing CAUTIs

    Translational pharmacology of an inhaled small molecule Ī±vĪ²6 integrin inhibitor for idiopathic pulmonary fibrosis

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    The Ī±vĪ²6 integrin plays a key role in the activation of transforming growth factor-Ī² (TGFĪ²), a pro-fibrotic mediator that is pivotal to the development of idiopathic pulmonary fibrosis (IPF). We identified a selective small molecule Ī±vĪ²6 RGD-mimetic, GSK3008348, and profiled it in a range of disease relevant pre-clinical systems. To understand the relationship between target engagement and inhibition of fibrosis, we measured pharmacodynamic and diseaserelated end points. Here we report, GSK3008348 binds to Ī±vĪ²6 with high affinity in human IPF lung and reduces downstream pro-fibrotic TGFĪ² signaling to normal levels. In human lung epithelial cells, GSK3008348 induces rapid internalization and lysosomal degradation of the Ī±vĪ²6 integrin. In the murine bleomycin-induced lung fibrosis model, GSK3008348 engages Ī±vĪ²6, induces prolonged inhibition of TGFĪ² signaling and reduces lung collagen deposition and serum C3M, a marker of IPF disease progression. These studies highlight the potential of inhaled GSK3008348 as an anti-fibrotic therapy
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