lipoxygenase/atrofie

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Identification of 12/15-lipoxygenase as a regulator of axon degeneration through high-content screening.

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Axon degeneration is a programed process that takes place during development, in response to neuronal injury, and as a component of neurodegenerative disease pathology, yet the molecular mechanisms that drive this process remain poorly defined. In this study, we have developed a semi-automated,

Inhibition of 12/15-Lipoxygenase Protects Against β-Cell Oxidative Stress and Glycemic Deterioration in Mouse Models of Type 1 Diabetes.

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Islet β-cell dysfunction and aggressive macrophage activity are early features in the pathogenesis of type 1 diabetes (T1D). 12/15-Lipoxygenase (12/15-LOX) is induced in β-cells and macrophages during T1D and produces proinflammatory lipids and lipid peroxides that exacerbate β-cell dysfunction and

Genetic ablation of 12/15-lipoxygenase but not 5-lipoxygenase protects against denervation-induced muscle atrophy.

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Skeletal muscle atrophy is a debilitating outcome of a number of chronic diseases and conditions associated with loss of muscle innervation by motor neurons, such as aging and neurodegenerative diseases. We previously reported that denervation-induced loss of muscle mass is associated with

Effects of lipase, lipoxygenase, peroxidase, and rutin on quality deteriorations in buckwheat flour.

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To investigate the effects of changes in lipase, lipoxygenase, peroxidase (POX), and rutin concentrations on the quality of buckwheat flour, 14 buckwheat varieties were stored for 0, 4, 10, and 30 days at 5 or 20 degrees C. During the storage period, lipase activity correlated to pH (significantly

Combination of a dual 5-lipoxygenase/cyclooxygenase inhibitor with a glucocorticoid results in synergistic topical antiinflammatory activity without inducing skin atrophy.

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Synthetic glucocorticosteroids are widely used in clinical dermatology in the treatment of a number of inflammatory skin disorders. However, cutaneous side effects such as induction of skin atrophy are among the factors that limit the chronic use of this class of agents. We have found that a

5-Lipoxygenase, but not 12/15-lipoxygenase, contributes to degeneration of retinal capillaries in a mouse model of diabetic retinopathy.

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OBJECTIVE Lipoxygenases are regulators of chronic inflammation and oxidative stress generation. We evaluated the role of 5- and 12-lipoxygenases in the development of diabetic retinopathy. METHODS Wild-type mice, 5-lipoxygenase-deficient mice, and 12/15-lipoxygenase-deficient mice were assessed 1)

Membrane deterioration in senescing carnation flowers : coordinated effects of phospholipid degradation and the action of membranous lipoxygenase.

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The lipid fluidity of microsomal membranes from the petals of cut carnation flowers decreases as the flowers senesce. A comparable change in fluidity was induced by in vitro aging of microsomal membranes from young flowers under conditions in which membranous lipoxygenase-like activity was active.

Deletion of 12/15-lipoxygenase accelerates the development of aging-associated and instability-induced osteoarthritis.

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12/15-Lipoxygenase (12/15-LOX) catalyzes the generation of various anti-inflammatory lipid mediators, and has been implicated in several inflammatory and degenerative diseases. However, there is currently no evidence that 12/15-LOX has a role in osteoarthritis (OA). The aim of this study was to

A double-blind vehicle-controlled study of R 68 151 in psoriasis: a topical 5-lipoxygenase inhibitor.

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Recently the pharmacologic role of leukotrienes (LTs), especially that of LTB4, has been intensively investigated in psoriasis. In vitro, R 68 151 is a potent 5-lipoxygenase inhibitor and consequently reduces LTB4 formation. Therefore the role of an in vitro 5-lipoxygenase inhibitor and its clinical

cDNA cloning, genomic structure, and chromosomal localization of a novel murine epidermis-type lipoxygenase.

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Using a combination of degenerate PCR technique and conventional screening procedures, we isolated a cDNA encoding a novel lipoxygenase, termed epidermis-type lipoxygenase-3 (e-LOX-3, gene symbol Aloxe3), from mouse skin. Aloxe3 mRNA is expressed in the stratified epithelia of skin, tongue, and

A chitosan induced 9-lipoxygenase in Adelostemma gracillimum seedlings.

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Oxylipins generated by the lipoxygenase (LOX) pathway play an important role in plant defense against biotic and abiotic stress. In chitosan-treated Adelostemma gracillimum seedlings, obvious accumulation of 9-LOX-derived oxylipins, namely 9,10,11-trihydroxy-12-octadecenoic acid, was detected. Using

The cloning of two tomato lipoxygenase genes and their differential expression during fruit ripening.

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A membrane-associated lipoxygenase from breaker-stage fruit of tomato (Lycopersicon esculentum Mill.) was purified and partially sequenced. Using degenerate oligonucleotides corresponding to portions of this sequence, a cDNA was amplified by PCR and used to screen a breaker fruit cDNA library. Two

Five-lipoxygenase inhibitors reduce Panc-1 survival: the mode of cell death and synergism of MK886 with gamma linolenic acid.

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The 5-lipoxygenase inhibitors ETYA, SC41661A and MK886 reduced the proliferation and viability of Panc-1 human pancreatic cancer cells. The extent of inhibition depended upon drug concentration, and with continued culture, cells detached and stained with trypan blue. Although results from flow

Role of leukotrienes and lipoxygenases in glomerular injury.

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The 5-lipoxygenated metabolites of arachidonic acid, the leukotrienes, are increasingly recognized as major mediators of early glomerular hemodynamic and structural deterioration during experimental glomerulonephritis. Generation of these metabolites is largely by infiltrating leukocytes, but can

5-Lipoxygenase gene polymorphism and onset of Alzheimer's disease.

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Přihlášení Registrace

Recently, inflammatory pathways have been recognized as possible pathophysiological mechanisms of aging-associated neurodegenerations, and slowing of the progression of Alzheimer's disease can be achieved with anti-inflammatory drugs. The formation of endogenous inflammatory lipid mediators,

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