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Sida 1 från 518 resultat
Effect of inflammatory factor-induced cyclo-oxygenase expression on the development of reperfusion-related no-reflow phenomenon in acute myocardial infarction.
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No reflow after reperfusion therapy for myocardial infarction is a strong predictor of clinical outcome. Increased levels of inflammatory factors, including C-reactive protein (CRP), in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) may
Gene transfer as a strategy to achieve permanent cardioprotection II: rAAV-mediated gene therapy with heme oxygenase-1 limits infarct size 1 year later without adverse functional consequences.
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Extensive evidence indicates that heme oxygenase-1 (HO-1) exerts potent cytoprotective effects in response to stress. Previous studies have shown that gene therapy with HO-1 protects against myocardial ischemia/reperfusion injury for up to 8 weeks after gene transfer. However, the long-term effects
[The significance of the changes in expressions of heat shock protein 70 and heme oxygenase-1 in the myocardium in patients died suddenly due to acute myocardial infarction].
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OBJECTIVE
To investigate the changes and its clinical significance of the expressions of the mRNA and protein of heat shock protein 70 (HSP70) and heme oxygenase-1 (HO-1) genes in the myocardium of acute myocardial infarction (AMI) areas in patients who died suddenly due to AMI.
METHODS
Specimens of
[Clinical study on changes of heme oxygenase-1 expression in patients with acute myocardial infarction].
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OBJECTIVE
To investigate changes in heme oxygenase-1(HO-1) in patients with acute myocardial infarction.
METHODS
Forty-five patients with acute myocardial infarction and 50 with coronary heart disease (diagnosed by coronary angiography) but without acute myocardial infarction were included in this
Are NSAIDs and selective cyclo-oxygenase 2 inhibitors associated with increased risk of myocardial infarction?
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Scott et al. conducted a systematic review to evaluate the risk of myocardial infarction (MI) associated with cyclo-oxygenase-2 (COX2) inhibitors and traditional NSAIDs. The review found a small increased risk of MI associated with COX2 inhibitors, particularly rofecoxib. Although a fixed-effects
Reduction of reperfusion-induced ventricular fibrillation and infarct size via heme oxygenase-1 overexpression in isolated mouse hearts.
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Heme oxygenase-1 (HO-1), also known as heat shock protein 32 (hsp-32) is a stress induced cytoprotective protein. The present investigation evaluated the capacity of HO-1 to reduce the incidence of reperfusion-induced ventricular fibrillation (VF) and infarct size. HO-1 transgenic (Tg) mice were
The coronary risk of cyclo-oxygenase-2 inhibitors in patients with a previous myocardial infarction.
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BACKGROUND
Cyclo-oxygenase-2 selective inhibitors have been associated with cardiovascular side effects, but previous studies have generally excluded people with previous myocardial infarction, thereby limiting our knowledge of their cardiotoxicity in this population.
OBJECTIVE
To determine whether
Expression of heme oxygenase-1 in response to myocardial infarction in rats.
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Heme oxygenase-1 (HO-1) is a heat shock protein catalysing the degradation of heme to yield biliverdin, carbon monoxide and iron. Several recent studies have proposed the stress-inducible HO-1 to participate in cellular protection also in the heart. We, therefore, examined the expression and
Acute myocardial infarction: measurement of arachidonate end-products in whole blood as an index of platelet cyclo-oxygenase activity in vivo.
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The endogenous arachidonic acid metabolism was investigated ex vivo, in separated serum from clotted whole blood, soon after the onset of acute myocardial infarction (3.3 +/- 0.7 hr). A group of eight consecutive male patients was selected, since no evidence was obtained of any associated disease
Selective cyclo-oxygenase-2 inhibitors and myocardial infarction: how strong is the link?
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There are concerns that selective cyclo-oxygenase (COX)-2 inhibitors may be prothrombotic and increase the risk of myocardial infarction. This has largely arisen because of an unexpected finding of a higher rate of myocardial infarction in patients receiving rofecoxib compared with patients
[Long-term effects of heme oxygenase 1 overexpression on post-infarction heart function in diabetic rats].
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OBJECTIVE
To clarify the impact of increased heme oxygenase-1 (HO-1) expression on cardiac function of diabetic rats with myocardial infarction and its mechanism.
METHODS
Sixty adult male Wistar rats were randomly divided into five groups (n = 12): sham operation group (sham), diabetes + sham
Long-term expression of heme oxygenase-1 (HO-1, HSP-32) following focal cerebral infarctions and traumatic brain injury in humans.
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Extracellular heme derived from hemoglobin following hemorrhage or released from dying cells induces the expression of heme oxygenase-1 (HO-1, HSP-32) which metabolizes heme to the gaseous mediator carbon monoxide (CO), iron (Fe) and biliverdin. Biliverdin and its product bilirubin are powerful
Hsp60 and heme oxygenase-1 (Hsp32) in acute myocardial infarction.
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Heat shock proteins (Hsps) are produced in response to various stressors, including ischemia-reperfusion, and they can exit cells and reach the blood. In this pilot study, we determined serum levels of Hsp60 and heme-oxygenase-1 (HO-1; also named Hsp32) in subjects with acute myocardial infarction
Heme oxygenase-1 induction protects the heart and modulates cellular and extracellular remodelling after myocardial infarction in rats.
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Heme oxygenase-1 (HO-1) is a cytoprotective enzyme, which regulates cell proliferation and has potential antifibrogenic properties. In the present study, we investigated the effects of pre-emptive HO-1 induction by cobalt protoporphyrin IX on the healing of myocardial infarction in rats. The
Heme oxygenase-1 (HO-1) inhibits postmyocardial infarct remodeling and restores ventricular function.
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We reported previously that predelivery of the anti-oxidant gene heme oxygenase-1 (HO-1) to the heart by adeno associated virus (AAV) markedly reduces injury after acute myocardial infarction (MI). However, the effect of HO-1 gene delivery on postinfarction recovery has not been investigated. In the
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