61,598 research outputs found

    The pathogenesis of tendinopathy. A molecular perspective

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    There are many publications that discuss the aetiology, diagnosis and treatment of the various forms of tendinopathy, but few are based on conclusive scientific evidence. The pathogenesis of tendinopathy is difficult to study because tendon biopsies are rarely obtained before a tendon has ruptured. There are interesting comparisons with animal tendinopathy, particularly in the equine athlete, although many animal models do not accurately reflect the human condition—the tendon lesions usually heal. However, the application of biochemical and molecular techniques to the study of both animal and human tendinopathy has led to a greater understanding of these common and disabling conditions. This article summarizes current knowledge of the pathogenesis of tendinopathy, with particular emphasis on the molecular pathology of the tendon matrix

    Chronic tendon pathology: molecular basis and therapeutic implications

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    Tendons are frequently affected by chronic pain or rupture. Many causative factors have been implicated in the pathology, which until relatively recently was under-researched and poorly understood. There is now a greater knowledge of the molecular basis of tendon disease. Most tendon pathology (tendinopathy) is associated with degeneration, which is thought to be an active, cell-mediated process involving increased turnover and remodelling of the tendon extracellular matrix. Degradation of the tendon matrix is mediated by a variety of metalloproteinase enzymes, including matrix metalloproteinases and ‘aggrecanases’. Neuropeptides and other factors released by stimulated cells or nerve endings in or around the tendon might influence matrix turnover, and could provide novel targets for therapeutic intervention

    Correlation of Lipid Peroxidation with Glycated Haemoglobin Levels in Diabetes Mellitus

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    Reactive oxygen species are crucial to normal biological processes; they are potentially dangerous and are commonly referred to as prooxidants. The reactive oxygen intermediates can cause direct cellular injury by including lipid and protein peroxidation and damage to nucleic acid. The polyunsaturated fatty acids present in the cells are vulnerable to free radicals causing lipid peroxidation. Determination of Malondialdehyde (MDA) by using thiobarbituric acid is used as an index of the extent of lipid peroxidation. This study was done to know if lipid peroxidation correlated with the glycated haemoglobin levels. Diabetic status was assessed by estimating fasting blood sugar and glycated haemoglobin level while oxidant stress was evaluated by estimating erythrocyte MDA levels. The lipid peroxidation in erythrocyte lysates was significantly increased in diabetic individuals compared to controls (p<0.001). The result of this study indicates that in diabetic individuals are more prone to oxidative stress and glycated haemoglobin is a marker in evaluating the long term glycemic status in diabetic individuals

    ABC of chronic obstructive pulmonary disease - Acute exacerbations

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    ADAMTS proteinases: a multi-domain, multi-functional family with roles in extracellular matrix turnover and arthritis

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    Members of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family are known to influence development, angiogenesis, coagulation and progression of arthritis. As proteinases their substrates include the von Willebrand factor precursor and extracellular matrix components such as procollagen, hyalectans (hyaluronan-binding proteoglycans including aggrecan), decorin, fibromodulin and cartilage oligomeric matrix protein. ADAMTS levels and activities are regulated at multiple levels through the control of gene expression, mRNA splicing, protein processing and inhibition by TIMP (tissue inhibitor of metalloproteinases). A recent screen of human cartilage has shown that multiple members of the ADAMTS family may be important in connective tissue homeostasis and pathology

    The turning points of EU cohesion policy, Working Paper Report to Barca Report

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    In more recent discussions on the future of Cohesion policy, however, both critics and supporters have tended to agree on the need for a “modernisation” of the policy, in recognition of existing weakness in the current approach and of the emerging challenges faced by the European economy, society and broader integration process. In this context of reform, this paper will take a step back in time to examine the origins and evolution of Cohesion policy, with a view to shedding some light on its core dynamics and revealing some of the lessons of history. In doing so, the main objectives of this paper are to identify the main historical turning points in Cohesion policy, the trends and nature of changes witnessed, and the key underlying factors facilitating or obstructing policy reform over time
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