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diacylglycerol/edema
L'enllaç es desa al porta-retalls
Pàgina 1 des de 19 resultats
Dexamethasone effect on free fatty acid and diacylglycerol accumulation during experimentally induced vasogenic brain edema.
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Free fatty acids (FFA), diacylglycerols (DG), and water content were measured in the right and left cerebral hemispheres of rats with brain edema cryogenically induced to the right cerebral hemisphere. The effect of dexamethasone pretreatment was also studied. Twenty-four hours after lesion, maximal
Mechanisms of pulmonary edema induced by a diacylglycerol second messenger.
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We investigated the effect of dioctanoylglycerol (DOG), a second messenger of protein kinase C (PKC) activation, in the absence and presence of neutrophils in isolated perfused guinea pig lung. DOG was given after a base-line isogravimetric steady-state period. Pulmonary capillary pressure (Ppc) and
Diacylglycerol kinases are essential for hepatocyte growth factor-dependent proliferation and motility of Kaposi's sarcoma cells.
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Hepatocyte growth factor (HGF) is involved in the pathogenesis of Kaposi's sarcoma (KS), the most frequent neoplasia in patients with AIDS, characterized by proliferating spindle cells, infiltrating inflammatory cells, angiogenesis, edema, and invasiveness. In vitro, this factor sustains the
Conformationally constrained analogues of diacylglycerol. 12. Ultrapotent protein kinase C ligands based on a chiral 4,4-disubstituted heptono-1,4-lactone template.
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Conformationally constrained analogues of diacylglycerol (DAG) built on a 5(-)[(acyloxy)methyl]-5-(hydroxymethyl)tetrahydro-2-furanone template (1, Chart 1) were shown previously to bind tightly to protein kinase C alpha (PK-C alpha) in a stereospecific manner. These compounds, however, racemized
A glycosyl analogue of diacylglycerol and other antiinflammatory constituents from Inula viscosa.
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Some extracts from Inula viscosa were examined for acute antiinflammatory activity in vivo. Three flavonoids: rhamnocitrin (1), 7-O-methylaromadendrin (3), and 3-O-acetylpadmatin (4); a sesquiterpene lactone, inuviscolide (2); a sesquiterpene acid, ilicic acid (5); and a digalactosyl-diacylglycerol,
Membrane lipids in the pathogenesis of brain edema: phospholipids and arachidonic acid, the earliest membrane components changed at the onset of ischemia.
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This chapter reviews studies concerning cellular membranes in the pathogenesis of cerebral edema. The main topics discussed are membrane lipids and the observation that the concentration of endogenous free fatty acids increases rapidly and reversibly in the brain after a single electroconvulsive
Synthesis and evaluation of the anti-inflammatory effects of niflumic acid lipophilic prodrugs in brain edema.
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Five new lipophilic prodrugs of the non-steroidal anti-inflammatory drug, niflumic acid (Nifluril, CAS 4394-00-7), were synthetized and evaluated on the experimental brain edema (injection of phospholipase A2). The effect of these drugs in comparison with dexamethasone which elicits a marked effect
Inhibition of diacylglycerol kinases as a physiological way to promote diacylglycerol signaling.
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Diacylglycerol is a key regulator of cell physiology, controlling the membrane recruitment and activation of signaling molecules. Accordingly, diacylglycerol generation and metabolism are strictly controlled, allowing for localized regulation of its concentration. While the increased production of
Membrane-Binding Mechanism of Clostridium perfringens Alpha-Toxin.
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Clostridium perfringens alpha-toxin is a key mediator of gas gangrene, which is a life-threatening infection that manifests as fever, pain, edema, myonecrosis, and gas production. Alpha-toxin possesses phospholipase C and sphingomyelinase activities. The toxin is composed of an N-terminal domain
Release of polyunsaturated fatty acids from phospholipids and alteration of brain membrane integrity by oxygen-derived free radicals.
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We studied the effects of oxygen-derived free radicals on the ultrastructure of brain cortical slices and the release of fatty acids from phospholipids of crude synaptosomes. Xanthine oxidase, hypoxanthine, and ADP-Fe3+, a free-radical-generating system, caused swelling of cellular processes and
[Pharmacological treatment of diabetic retinopathy].
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Chronic overproduction of growth hormone and insulin-like growth factor 1 play an important role in the pathogenesis of diabetic retinopathy. Somatostatin receptors are the targets of somatostatin analogues such as octreotide in the treatment of diabetic retinopathy. Octreotide has shown promise as
[The role of protein kinase C in the pathophysiology of diabetic retinopathy].
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Hyperglycemic control in diabetes mellitus is a major key to prevent the development and progression of diabetic retinopathy. One important pathomechanism in the development of diabetic complications is the activation of protein kinase C (PKC) induced by high glucose due to an increased
Treatment of diabetic retinopathy with protein kinase C subtype Beta inhibitor.
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Despite better options of controlling diabetes mellitus and although the prognosis of diabetic retinopathy has markedly improved by laser treatment and vitreoretinal surgery, diabetic retinopathy is still the leading cause of blindness in working-age people in industrialized countries. Little has
Pharmacological treatment of diabetic retinopathy.
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Despite the better options of controlling diabetes mellitus and although the prognosis of diabetic retinopathy has markedly improved by laser treatment and vitreoretinal surgery, diabetic retinopathy still is the leading cause of blindness in working age people in industrialized countries. Little
Diabetic retinopathy and pregnancy.
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Diabetes mellitus and pregnancy have reciprocal influences between them, therefore diabetes mellitus may complicate the course of pregnancy as well as pregnancy can worsen the performance of diabetes especially at the fundus oculi. Several factors seem to play a role in retinal neovascularization.
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