ribonuclease/infarction

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Serum ribonuclease activity in acute myocardial infarction.

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Ribonuclease (RNase) activity measured at pH 7.8 (the alkaline RNase) and pH 6.7 (the acid RNase) was estimated in serum of 54 patients with acute myocardial infarction (AMI). The estimations were performed on the first day of disease, then on the seven consecutive days and on the 14th day. A

[Ribonuclease (RNase) activity in blood serum of patients with myocardial infarction. I. The changes of activity during first three days of the disease].

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Serum ribonuclease activity in patients with myocardial infarction. I. Changes in the first three days of the disease.

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Heart function and molecular biological parameters are comparable in young adult and aged rats after chronic myocardial infarction.

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OBJECTIVE To test the hypothesis that IL-1beta and IL-6 play a pivotal role after myocardial infarction (MI) particularly in aged rats. METHODS Chronic MI was induced in young adult (3.5 months) and aged (18 months) female Sprague-Dawley rats by ligation of the left coronary artery. Sham-operated

Targeting of Extracellular RNA Reduces Edema Formation and Infarct Size and Improves Survival After Myocardial Infarction in Mice.

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BACKGROUND Following myocardial infarction (MI), peri-infarct myocardial edema formation further impairs cardiac function. Extracellular RNA (eRNA) released from injured cells strongly increases vascular permeability. This study aimed to assess the role of eRNA in MI-induced cardiac edema formation,

FR167653 diminishes infarct size in a murine model of myocardial ischemia-reperfusion injury.

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OBJECTIVE During myocardial ischemia-reperfusion injury, p38 mitogen-activated protein kinase is activated. We examined the effect of a highly specific inhibitor of p38 mitogen-activated protein kinase, FR167653, in an experimental model of regional myocardial ischemia-reperfusion. METHODS CD-1 mice

Migration towards SDF-1 selects angiogenin-expressing bone marrow monocytes endowed with cardiac reparative activity in patients with previous myocardial infarction.

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BACKGROUND Chemokine-directed migration is crucial for homing of regenerative cells to the infarcted heart and correlates with outcomes of cell therapy trials. Hence, transplantation of chemokine-responsive bone marrow cells may be ideal for treatment of myocardial ischemia. To verify the

Gene expression of colony-stimulating factors and stem cell factor after myocardial infarction in the mouse.

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Recent studies have suggested that cytokines such as macrophage colony-stimulating factor (M-CSF) might be involved in the pathogenesis of ischaemic heart disease. Macrophage colony-stimulating factor, granulocyte-colony stimulating factor (G-CSF), granulocyte-macrophage-colony stimulating factor

Determining of actual activities of acid and alkaline ribonuclease in human serum and urine.

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Acid and alkaline ribonuclease (RNase) activities were measured in serum and urine using procedure based on assumption that all determined RNase activities, both at pH 6.5 and 7.8 represent values produced by overlapping of activities of acid leukocyte type RNase and alkaline pancreatic type RNase.

Rapid expression of fibronectin in the rabbit heart after myocardial infarction with and without reperfusion.

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The expression of fibronectin in the repair process after myocardial infarction was studied using two protocols of coronary occlusion in the rabbit: a permanent occlusion or 3 h of occlusion followed by reperfusion (too late for salvage). We found a rapid and progressive increase in cardiac

Discovery of potential plasma protein biomarkers for acute myocardial infarction via proteomics.

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Acute myocardial infarction (AMI) is an acute disease with high mortality and seriously threatens human health. The identification of new effective biological markers for AMI is a prerequisite for treatment. Most proteomic studies have focused on atherosclerotic plaques, vascular

Ribose treatment reduced the infarct size and improved heart function after myocardial infarction in rats.

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OBJECTIVE In this study the effect of ribose on heart function and infarct-size was analyzed 6 h after myocardial infarction (MI) in rats. METHODS Continuous i.v.-infusion of NaCl or ribose (200 mg/kg/h) was started one day prior to induction of MI in female Sprague-Dawley rats which was done by

Differential cytokine expression in myocytes and non-myocytes after myocardial infarction in rats.

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The proinflammatory cytokines interleukin (IL)-1beta and IL-6 are increased after acute myocardial infarction (MI). Moreover, serum IL-6 level is elevated after MI, but has also been associated with heart failure. In the present study, heart function was monitored in a rat model of chronic MI.

RNase therapy assessed by magnetic resonance imaging reduces cerebral edema and infarction size in acute stroke.

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Ischemic stroke causes cell necrosis with the exposure of extracellular ribonucleic acid (RNA) and other intracellular material. As shown recently, extracellular RNA impaired the blood-brain-barrier and contributed to vasogenic edema-formation. Application of ribonuclease 1 (RNase 1) diminished

[1 of the possible causes of an increase in acid hydrolase activity in homogenates of heart muscle following myocardial infarct].

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A "free" activity of acidic hydrolases (acidic phosphatase, acidic ribonuclease and cathepsin D) was increased in homogenates of dog heart muscle with simultaneous decrease of the enzymes activity in the fraction enriched by lysosomes, within 4-5 hrs after ligation of the descending ramus of

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