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The role of advanced glycation end products in retinal microvascular leukostasis.

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OBJECTIVE A critical event in the pathogenesis of diabetic retinopathy is the inappropriate adherence of leukocytes to the retinal capillaries. Advanced glycation end-products (AGEs) are known to play a role in chronic inflammatory processes, and the authors postulated that these adducts may play a

Inhibition of diabetic leukostasis and blood-retinal barrier breakdown with a soluble form of a receptor for advanced glycation end products.

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OBJECTIVE The interaction of advanced glycation end products (AGEs) with their receptors is hypothesized to be involved in the development of diabetic retinopathy. In the present study, the role of an AGE receptor, RAGE, was investigated in the development of diabetic retinopathy in

Inactivation of Endothelial ADAM17 Reduces Retinal Ischemia-Reperfusion Induced Neuronal and Vascular Damage

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Retinal ischemia contributes to visual impairment in ischemic retinopathies. A disintegrin and metalloproteinase ADAM17 is implicated in multiple vascular pathologies through its ability to regulate inflammatory signaling via ectodomain shedding. We investigated the role of endothelial ADAM17 in

Blockade of vascular endothelial growth factor receptor 1 prevents inflammation and vascular leakage in diabetic retinopathy.

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Diabetic retinopathy (DR) is a leading cause of blindness in working age adults. The objective of this study is to investigate the effects of vascular endothelial growth factor receptor 1 (VEGFR1) blockade on the complications of DR. Experimental models of diabetes were induced with streptozotocin

Human recombinant interleukin-2 provokes acute pulmonary vascular endothelial injury in rabbits.

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Human recombinant interleukin-2 (rIL-2), with or without lymphokine-activated killer cells, has been shown to mediate tumor regressions in animals and in humans. A well-recognized adverse effect of rIL-2 is the development of a generalized vascular leak syndrome that involves the pulmonary

The pathogenesis of clostridial myonecrosis.

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These pieces of evidence can be assimilated into a molecular and cellular model of pathogenesis which is initiated by direct toxin effects upon venous capillary endothelial cell function, leading to expression of pro-inflammatory mediators and adhesion molecules, and initiation of platelet

Effects of L-652,731, a platelet-activating factor (PAF) receptor antagonist, on PAF- and complement-induced pulmonary hypertension in sheep.

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Thromboxane-mediated pulmonary hypertension, pulmonary edema, arterial hypoxia and pulmonary leukostasis occur in response to the infusion of plasma containing zymosan-activated complement (ZAP) in sheep. Platelet-activating factor (PAF) is a potential mediator of some of these effects. We

Increased pulmonary vascular permeability after bone marrow injection in sheep.

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We determined the effects of injection of bone marrow into the pulmonary circulation on pulmonary fluid and protein exchange in sheep. We also assessed the roles of free fatty acid toxicity and secondary thrombosis as mediators of the changes in pulmonary fluid balance. Injection of small amounts of

Monokine-induced acute lung injury in rabbits.

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Interleukin-1 (IL-1) mediates components of the acute phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied in unanesthetized rabbits the effects of intravenous divided dose infusions of a murine monokine preparation containing IL-1 activity, on

Beneficial effects of a novel RAGE inhibitor on early diabetic retinopathy and tactile allodynia.

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OBJECTIVE The receptor for advanced glycation end products (RAGE) has been implicated in the pathogenesis of numerous complications of diabetes. We assessed the effect of a novel RAGE fusion protein inhibitor on retinal histopathology and nerve function, and on retinal inflammation and oxidative

MyD88-dependent pathways in leukocytes affect the retina in diabetes.

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BACKGROUND Previous studies by us and other have provided evidence that leukocytes play a critical role in the development of diabetic retinopathy, suggesting a possible role of the innate immune system in development of the retinopathy. Since MyD88 is a convergence point for signaling pathways of

Provocation of pulmonary vascular endothelial injury in rabbits by human recombinant interleukin-1 beta.

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Interleukin-1 (IL-1) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied the effects of human recombinant IL-1 beta (rIL-1 beta) or rIL-1 alpha on circulating granulocytes, their sequestration within the

[Fatal pulmonary leukoagglutination after administration of fresh frozen plasma].

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A case is reported of a 73 year old female patient who died during surgery for enlarged nephrectomy as a result of a massive non-cardiogenic pulmonary oedema. She had been given 2 red cell concentrates (450 g) and 3 fresh frozen plasma units (900 g). A postmortem examination did not reveal any

Bronchoalveolar lavage in ponies with recurrent airway obstruction (heaves).

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We performed bronchoalveolar lavage (BAL) in 2 groups of ponies. Principal ponies had a history of heaves, a disease characterized by recurrent airway obstruction and airway hyperreactivity when ponies are housed in a barn and fed hay; control ponies had no history of airway obstruction. Ponies were

The Neuropilin-1 Inhibitor, ATWLPPR Peptide, Prevents Experimental Diabetes-Induced Retinal Injury by Preserving Vascular Integrity and Decreasing Oxidative Stress.

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Neuropilin-1 (NRP-1) is a transmembrane glycoprotein. As a VEGF co-receptor, NRP1 significantly enhances VEGFR2 signaling and promotes vascular permeability and migration. The purpose of this study was to evaluate the effects of an NRP-1 inhibitor, ATWLPPR peptide, on the early stages of diabetic

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