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lectin/infarkti

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Sivu 1 alkaen 224 tuloksia

Mannan binding lectin as an adjunct to risk assessment for myocardial infarction in individuals with enhanced risk.

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Inflammation can predispose to myocardial infarction (MI), and mannan binding lectin (MBL) promotes phagocytic clearance of inflammatory agents, but the predictive value of MBL levels for MI is not known. MBL was analyzed in subgroups of the population-based Reykjavik study, a cohort of 19,381
This case illustrates the benefits of using plasma levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) to distinguish between myocardial injuries caused by coronary vasospasm or coronary plaque rupture. A 62-year-old woman with a history of dyslipidemia was admitted

Association between lectin complement pathway initiators, C-reactive protein and left ventricular remodeling in myocardial infarction-a magnetic resonance study.

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BACKGROUND Lectin complement pathway (LP) activation is an important mechanism in myocardial ischemia reperfusion injury (IRI). LP is activated via the recognition molecules mannose-binding lectin (MBL), ficolins-2 and-3 and is regulated by MBL/Ficolin-associated Protein-1 (MAP-1). Also, C-reactive
OBJECTIVE Experimental data point towards a favourable effect of low serum concentrations of complement mannose-binding lectin (MBL) on myocardial ischaemia/reperfusion (I/R) injury. As comparable data on the role of MBL in human I/R injury is lacking, we investigated the influence of low serum MBL

Mannose binding lectin and soluble Toll-like receptor 2 in heart failure following acute myocardial infarction.

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BACKGROUND To determine the relationship between markers of innate immunity and clinical outcomes in patients with heart failure (HF) after acute myocardial infarction (AMI). Atherogenesis and HF is associated with the altered control of inflammation by innate immune defenses that include

Mannose-binding lectin deficiency is associated with myocardial infarction: the HUNT2 study in Norway.

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OBJECTIVE Mannose-binding lectin (MBL) and ficolins activate the complement cascade, which is involved in atherogenesis. Based on a pilot study, we hypothesized that functional polymorphisms in the MBL gene (MBL2) leading to dysfunctional protein are related to development of myocardial infarction

Circulating lectin pathway proteins do not predict short-term cardiac outcomes after myocardial infarction.

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Despite improvements in treatment, coronary artery disease is still responsible for one-third of all deaths globally, due predominantly to myocardial infarction (MI) and stroke. There is an important potential in developing new strategies for treatment of patients with these conditions.
BACKGROUND Soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) level is a reliable prognostic biomarker in acute coronary syndrome. However, it is unclear whether its plasma level at acute phase is related to the long-term prognosis in patients with ST-segment elevation acute

Pentraxin 3, ficolin-2 and lectin pathway associated serine protease MASP-3 as early predictors of myocardial infarction - the HUNT2 study.

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The lectin complement pathway is suggested to play a role in atherogenesis. Pentraxin-3 (PTX3), ficolin-1, ficolin-2, ficolin-3, MBL/ficolin/collectin-associated serine protease-3 (MASP-3) and MBL/ficolin/collectin-associated protein-1 (MAP-1) are molecules related to activation of the lectin

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

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
Percutaneous coronary intervention-related periprocedural myocardial infarction (PCI-RPMI) has now been definitively linked in large data sets to long-term adverse outcomes. It is more likely that the relationship is caused by the underlying predisposing factors that led to the PCI-RPMI, such as
BACKGROUND The diagnostic sensitivity of myocardial necrosis markers, such as creatine kinase-MB (CK-MB), cardiac troponins, myoglobin and heart-type fatty acid-binding protein (H-FABP) for the earliest stage of ST-elevation myocardial infarction (STEMI), remains insufficient. We compared a new

Lectin (UEA-1) reaction of capillary endothelium with reference to permeability in autopsied cases of cerebral infarction.

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The relationship between endothelial reactivity to Ulex europaeus agglutinin-1 (UEA-1) and the permeability of the vascular wall in human autopsied cases of cerebral infarction was studied. Sections from the cerebral cortex were reacted with horseradish peroxidase UEA-1 to demonstrate the surface
Villorita cyprinoides (black clam) is a fresh water clam that belongs as a bivalve to the group of mollusc. The saline extracts from the muscle reveal high titers of agglutination potency on trypsin-treated rabbit erythrocytes. With the help of affinity chromatography a hemolytic protein with lectin
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