heparin/воспаление

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Macrophages secrete a novel heparin-binding protein with inflammatory and neutrophil chemokinetic properties.

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We report the identification and purification of a new inflammatory monokine synthesized by the macrophage tumor cell line RAW 264.7 in response to endotoxin. This monokine, which we term "macrophage inflammatory protein" (MIP), is a doublet with an apparent molecular mass of approximately 8,000

Dalteparin, a low molecular weight heparin, attenuates inflammatory responses and reduces ischemia-reperfusion-induced liver injury in rats.

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OBJECTIVE To examine whether dalteparin, a low molecular weight heparin, prevents hepatic damage by inhibiting leukocyte activation, we analyzed its effect on ischemia/reperfusion (I/R) injury of rat liver in which activated leukocytes play a critical role. METHODS Prospective, randomized,

Possible pro-inflammatory role of heparin-binding epidermal growth factor-like growth factor in the active phase of systemic sclerosis.

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Heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) is a member of the EGF family growth factors, which affects multiple aspects of the wound healing process such as epithelialization, wound contraction and angiogenesis. In our study, we measured the serum HB-EGF levels of 51

Heparin cofactor II and thrombin Heparin-binding proteins linking hemostasis and inflammation.

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α-Thrombin is a trypsinlike serine proteinase involved in blood coagulation and wound-healing processes, which interacts with many different macromolecular substances. Heparin cofactor II is a serpin (serine proteinase inhibitor) superfamily member that specifically inhibits thrombin but no other

Heparin-coated circuits reduce the inflammatory response to cardiopulmonary bypass.

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Cardiopulmonary bypass generates a systemic inflammatory response including the activation of the complement cascade and leukocytes contributing to postoperative morbidity. To evaluate whether the use of heparin-coated extracorporeal circuits could reduce these activation processes, we performed a

Adsorption of inflammatory cytokines using a heparin-coated extracorporeal circuit.

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Cardiopulmonary bypass (CPB) surgeries cause an increase in plasma inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) along with whole-body inflammatory responses. The inflammatory responses during a CPB treatment are reduced when using a heparin-coated

Antithrombotic treatment during acute inflammatory complications of patients affected by postphlebitic syndrome: LMW-heparin versus standard heparin.

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Seventy seven patients affected by postphlebitic syndrome (PPS) during acute inflammatory and/or obstructive complications were controlled. Thirty nine patients were treated with a new low molecular weight heparin (Fluxum), 16,000 I.U. AXa/day subcutaneously for 10 days and, subsequently, 8,000 I.U.

Heparin and acute inflammation in the rat.

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The subcutaneous injection of heparin into the dorsal cervical region of rats 30 min before the intrapedal administration of carrageenin significantly impaired the local inflammatory reaction from 2 h through to 6 h. This observation implies that the release of endogenous heparins from tissue mast

Linker-free covalent immobilization of heparin, SDF-1α, and CD47 on PTFE surface for antithrombogenicity, endothelialization and anti-inflammation.

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Small-diameter vascular grafts made of biomedical polytetrafluoroethylene (PTFE) suffer from the poor long-term patency rate originating from thrombosis and intimal hyperplasia, which can be ascribed to the insufficient endothelialization and chronic inflammation of the materials. Hence,

Formation of anti-platelet factor 4/heparin antibodies after cardiac surgery: influence of perioperative platelet activation, the inflammatory response, and histocompatibility leukocyte antigen status.

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BACKGROUND Anticoagulation therapy with heparin induces antibodies that recognize multimolecular complexes of platelet factor 4 bound to heparin (anti-platelet factor 4/heparin antibodies). Considering that cardiac surgery induces an intense platelet activation and proinflammatory response, we

Anti-inflammatory effects of low molecular weight heparin derivative in a rat model of carrageenan-induced pleurisy.

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Low molecular weight heparin derivatives are characterized by low anti-coagulant activity and marked anti-inflammatory effects that allow for these molecules to be viewed as a new class of non-steroidal anti-inflammatory drugs (NSAIDs). We show here that K5NOSepiLMW, an O-sulphated heparin-like

[The role of heparin in allergic inflammation].

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Heparin is a glycosaminoglican used in prophylactic and treatment of thrombosis. Heparin possesses also non-anticoagulant properties, including modulation of various proteases, anticomplement activity, and anti-inflammatory actions. Inhaled heparin has been shown to reduce early phase of asthmatic

Structural requirements of heparin and related molecules to exert a multitude of anti-inflammatory activities.

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Chronic inflammatory diseases are common and still remain a therapeutic challenge for both efficacy and safety reasons. Hence, novel therapeutics addressing these issues would for example improve treatment of severe diseases such as psoriasis, rheumatoid arthritis, inflammatory bowel disease and

P-Selectin-mediated acute inflammation can be blocked by chemically modified heparin, RO-heparin.

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Selectins are carbohydrate-binding cell adhesion molecules that play a major role in the initiation of inflammatory responses. Heparin can bind to P-selectin, and its anti-inflammatory property is mainly due to inhibition of P-selectin. However, the strong anticoagulant activity of heparin limits

Unfractionated heparin after TBI reduces in vivo cerebrovascular inflammation, brain edema and accelerates cognitive recovery.

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Severe traumatic brain injury (TBI) may increase the risk of venous thromboembolic complications; however, early prevention with heparinoids is often withheld for its anticoagulant effect. New evidence suggests low molecular weight heparin reduces cerebral edema and improves neurological recovery

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