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fucoidan/slagtilfælde

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ArtiklerKliniske forsøgPatenter
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BACKGROUND P-selectin is activated early after stroke, followed by a rapid decline. This time course can be used to generate important information on stroke onset. The latter is crucial for therapeutic decision-making of wake-up strokes (i.e. thrombolysis or not). Here, we evaluated the specific

Fucoidan from Fucus vesiculosus Fails to Improve Outcomes Following Intracerebral Hemorrhage in Mice.

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Intracerebral hemorrhage (ICH) is the most fatal stroke subtype, with no effective therapies. Hematoma expansion and inflammation play major roles in the pathophysiology of ICH, contributing to primary and secondary brain injury, respectively. Fucoidan, a polysaccharide from the brown seaweed Fucus

Amino-Fucoidan as a Vector for rtPA-Induced Fibrinolysis in Experimental Thrombotic Events.

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Acute ischaemic stroke, myocardial infarction and pulmonary embolism are the main causes of mortality and morbidity worldwide. Thrombolysis by intravenous injection of recombinant tissue plasminogen activator (rtPA) remains the most common non-interventional treatment to recanalize occluded vessels.
Despite major scientific advances in its prevention, treatment and care, hypertension remains a serious condition that might lead to long-term complications such as heart disease and stroke. The great majority of forms of hypertension eventually result from an increased vasomotor tone activity that

Effect of fucoidan treatment on collagenase-induced intracerebral hemorrhage in rats.

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Inflammatory cells are postulated to mediate some of the brain damage following ischemic stroke. Intracerebral hemorrhage is associated with more inflammation than ischemic stroke. We tested the sulfated polysaccharide fucoidan, which has been reported to reduce inflammatory brain damage, in a rat

Leukocyte-platelet aggregates in rat peripheral blood after ischemic stroke and reperfusion.

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Ischemic stroke and reperfusion (ISR) is associated with an inflammatory response characterized, in part, by the formation of leukocyte-platelet aggregates (LPA). Aggregate formation may amplify the immunologic and hemostatic functions of both cell types and thus exacerbate reperfusion injury after
Atherosclerosis has been implicated in myocardial infarction, stroke and a host of cardiovascular diseases. The presence of activated T lymphocytes and macrophages, and the increased expression of HLA-DR antigen are consistent with the notion of immune activity in the atherosclerotic plaque. The

Whole blood aggregation and coagulation in db/db and ob/ob mouse models of type 2 diabetes.

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Type 2 diabetes in humans is associated with a significant hypercoagulable state; however, the effects of this on stroke and cardiovascular disease are not completely understood. The genetic mutations in db/db and ob/ob mice produce metabolic abnormalities similar to type 2 diabetes, but little is
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