mannose/heilablóðfall

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Prognostic value of mannose-binding lectin: 90-day outcome in patients with acute ischemic stroke.

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Complement activation and inflammation have been suggested in the pathogenesis of stroke; mannose-binding lectin (MBL) was found to have roles during the process. We therefore evaluated the short-term prognostic value of serum MBL in Chinese patients with an acute ischemic stroke (AIS). Consecutive

Elevated Serum Mannose-Binding Lectin Levels Are Associated with Poor Outcome After Acute Ischemic Stroke in Patients with Type 2 Diabetes.

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The activation of the complement system may be involved in the pathology of stroke and type 2 diabetes (T2DM). We therefore evaluated the long-term prognostic value of early measurement of serum mannose-binding lectin (MBL) levels, an activator of the complement system, in Chinese T2DM with acute

Genetically-defined deficiency of mannose-binding lectin is associated with protection after experimental stroke in mice and outcome in human stroke.

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BACKGROUND The complement system is a major effector of innate immunity that has been involved in stroke brain damage. Complement activation occurs through the classical, alternative and lectin pathways. The latter is initiated by mannose-binding lectin (MBL) and MBL-associated serine proteases

Mannose-binding lectin deficiency is associated with smaller infarction size and favorable outcome in ischemic stroke patients.

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BACKGROUND The Mannose-binding lectin (MBL) pathway of complement plays a pivotal role in the pathogenesis of ischemia/reperfusion (I/R) injury after experimental ischemic stroke. As comparable data in human ischemic stroke are limited, we investigated in more detail the association of MBL

The Neuroprotective Effect of Genetic Mannose-binding Lectin Deficiency is not Sustained in the Sub-acute Phase of Stroke.

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BACKGROUND The complement cascade is a critical mediator of the inflammatory response following cerebral ischemia. Recent work has demonstrated that genetic-deficiency of Mannose-binding lectin(MBL) ameliorates reperfusion injury and improves outcome in the acute phase of stroke. The present study

The contribution of mannose binding lectin to reperfusion injury after ischemic stroke.

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After complement system (CS) activation, the sequential production of complement products increases cell injury and death through opsonophagocytosis, cytolysis, adaptive, and inflammatory cell responses. These responses potentiate cerebral ischemia-reperfusion (IR) injury after ischemic stroke and

The relationship between serum mannose-binding lectin levels and acute ischemic stroke risk.

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Complement activation and inflammation have been suggested in the pathogenesis of stroke, mannose-binding lectin (MBL) were found to have roles during the process. The aim of this study was to investigate the relationship between acute ischemic stroke (AIS) and serum MBL levels in Chinese

Low ficolin-3 levels in early follow-up serum samples are associated with the severity and unfavorable outcome of acute ischemic stroke.

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BACKGROUND A number of data indicate that the lectin pathway of complement activation contributes to the pathophysiology of ischemic stroke. The lectin pathway may be triggered by the binding of mannose-binding lectin (MBL), ficolin-2 or ficolin-3 to different ligands. Although several papers

Specific contribution of mannose-binding lectin murine isoforms to brain ischemia/reperfusion injury.

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Mannose-binding lectin (MBL), an initiator of the lectin pathway (LP) of complement activation, is detrimental in ischemic stroke, as shown in clinical studies and rodent models. Whereas humans have one functional MBL protein, rodents have two isoforms, MBL-A and MBL-C, whose functions relative to

Scaffold Optimisation of Tetravalent Antagonists of the Mannose Binding Lectin.

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Antagonists of mannose binding lectin (MBL) have shown a protective role against brain reperfusion damage after acute ischemic stroke. Here we describe the design and streamlined synthesis of glycomimetic MBL antagonists based on a new tetravalent dendron scaffold. The dendron was developed by

Serum protein biomarkers screening in patients with ischemic stroke by LC-MS/MS.

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BACKGROUND The purpose of this study was to investigate the serum proteins biomarkers by label-free liquid chromatography coupled to tandem mass spectrometry quantification methods in the Chinese patients with acute ischemic stroke (AIS). METHODS In the study period, sera from 40 AIS patients and 40

Mannose-Binding Lectin and Risk of Cardiovascular Events and Mortality in Type 2 Diabetes: A Danish Cohort Study

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Objective: Mannose-binding lectin (MBL) is linked to risk of cardiovascular disease (CVD) in diabetes, but the nature of the association is unclear. We investigated the association between MBL and the risk of cardiovascular events (CVE)

Systemic lupus erythematosus in a multiethnic US cohort: XXXIV. Deficient mannose-binding lectin exon 1 polymorphisms are associated with cerebrovascular but not with other arterial thrombotic events.

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OBJECTIVE To study the association between deficient mannose-binding lectin (MBL) genotypes and arterial thrombotic events in systemic lupus erythematosus (SLE). METHODS Patients with SLE of Hispanic, African American, and Caucasian ethnicity from LUMINA (LUpus in MInorities, NAture versus nurture),

Mannose 6-phosphate receptor and sortilin mediated endocytosis of α-galactosidase A in kidney endothelial cells.

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Prominent vasculopathy in Fabry disease patients is caused by excessive intracellular accumulation of globotriaosylceramide (GL-3) throughout the vascular endothelial cells causing progressive cerebrovascular, cardiac and renal impairments. The vascular lesions lead to myocardial ischemia,

Mannose-binding lectin genotype and phenotype in patients with type 2 diabetes and myocardial infarction: a report from the DIGAMI 2 trial.

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OBJECTIVE The present study characterizes mannose-binding lectin (MBL), an activator of the complement system and thereby important for inflammatory activation, in patients with diabetes and myocardial infarction. METHODS Serum (S)-MBL was determined at hospital admission in 387 patients with type 2

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