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    ABSTRACT: There is an increasing global trend in cardiometabolic disorders being a leading cause of morbidity and mortality. Adverse dietary habits and sedentary lifestyles contribute to cardiovascular disease (CVD) and diabetes mellitus (DM). Dietary nutrients in nuts have attracted attention in recent literature due to their beneficial effects on CVD by attenuating lipid profiles, inflammation and oxidative stress. There is well-established evidence of the pharmacological properties of micronutrients that render them therapeutically effective in chronic inflammatory diseases. Although caution should be exercised in using antioxidant supplementation, antioxidant foods as dietary components play an important role in the management of cardiometabolic disorders. There is documented evidence of disease-modifying effects of nutritional compounds with anti-inflammatory and antioxidant effects. They have specific applications in ameliorating oxidative stress- induced inflammatory diseases such as DM and CVD. It is relevant that dietary components that influence risk of DM, have similar effects on inflammatory biomarkers of cardiovascular risk. Polyphenolic compounds such as flavonoids, isoflavones, phenolic acids and lignan contribute to increased plasma antioxidant capacity, decreased oxidative stress markers and reduced total and LDL cholesterol. They modulate genes associated with metabolism, stress defence, detoxification and transporter proteins. Their antioxidant and anti-inflammatory actions have specific applications for pathologies associated with chronic low-grade systemic inflammation that underpins progression of DM and CVD. Mechanisms involved depend on the structure of the compound, redox status of the inflammatory milieu and other interactions. Bioactive phytochemicals play an important therapeutic role in attenuating oxidative damage induced by metabolic syndrome associated with atherogenic dyslipidaemia and a pro-inflammatory, pro-thrombotic state, at a sub-cellular level. It would be critical to formulate optimal proportions and their combinations for therapeutic efficacy, based on synergistic interactions. Some of these mechanisms and potential actions are discussed.
    No preview · Article · Nov 2012
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    ABSTRACT: Mesenchymal stem cells (MSCs) possess great potential for use in regenerative medicine. However, their clinical application may be limited by the ability to expand their cell numbers in vitro while maintaining their differential potentials and stem cell properties. Thus the aim of this study was to test the effect of a range of medium supplements on MSC self-renewal and differentiation potential. Cells were cultured until confluent and subcultured continuously until reaching senescence. Medium supplementation with fibroblast growth factor (FGF)-2, platelet-derived growth factor (PDGF)-BB, ascorbic acid (AA), and epidermal growth factor (EGF) both increased proliferation rate and markedly increased number of cell doublings before reaching senescence, with a greater than 1,000-fold increase in total cell numbers for AA, FGF-2, and PDGF-BB compared with control cultures. Long-term culture was associated with loss of osteogenic/adipocytic differentiation potential, particularly with FGF-2 supplementation but also with AA, EGF, and PDGF-BB. In addition FGF-2 resulted in reduction in expression of CD146 and alkaline phosphatase, but this was partially reversible on removal of the supplement. Cells expressed surface markers including CD146, CD105, CD44, CD90, and CD71 by flow cytometry throughout, and expression of these putative stem cell markers persisted even after loss of differentiation potentials. Overall, medium supplementation with FGF-2, AA, EGF, and PDGF-BB greatly enhanced the total in vitro expansion capacity of MSC cultures, although differentiation potentials were lost prior to reaching senescence. Loss of differentiation potential was not reflected by changes in stem cell surface marker expression.
    No preview · Article · Nov 2012 · STEM CELLS TRANSLATIONAL MEDICINE
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    ABSTRACT: Periodontal pathogens in plaque biofilm initiate periodontitis, which is influenced by genetic and environmental factors. The resultant pro-oxidant status imposed on the periodontium, exacerbated by episodic hyperinflammatory damage contributes to progression of periodontitis and tooth loss in susceptible subjects. Increasing documentation of bi-directional connections between periodontal and cardiometabolic disorders makes it an intriguing area of therapeutic intervention for mutual benefit. Periodontitis and associated comorbidities demonstrate similar risk markers of inflammation during disease progression. Depending on the extent and severity of the inflammatory response, periodontitis could impact significantly on systemic inflammatory loading and influence the progression of endothelial dysfunction, atherosclerotic plaque instability, dyslipidaemia and insulin resistance. Some of the common mechanisms involved are discussed, relevant to periodontal and cardiometabolic disorders which have been documented as having a bidirectional relationship with periodontal disease progression; abating in response to treatment. Periodontal disease may be a useful marker of a susceptible immune system, or directly affect the progression of systemic diseases due to inflammatory loading. These mechanisms mediated by coordinated actions of cytokines, acute phase proteins, enzymes and their sequelae are addressed in the context of conventional periodontal therapy and its outcome with a modulatory role on metabolic diseases. Applications for the role of nutritional and therapeutic antioxidants as adjuncts in diseases with a distinctly prooxidant profile are discussed. Accurate therapeutic targeting as an adjunct to conventional periodontal treatment in this context, for mutual benefit to subjects with periodontitis and cardiometabolic diseases is a challenge.
    No preview · Article · Jun 2012
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International Journal of Systematic and Evolutionary Microbiology 01/2008; 57(Pt 12):2936-9. DOI:10.1099/ijs.0.65281-0
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Cochrane database of systematic reviews (Online) 02/2007; Issue 2. Art. No.(2):CD005097. DOI:10.1002/14651858.CD005097.pub2
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