infarction/protease

Platelet activation with subsequent aggregation is a complex process leading to thrombus formation, which remains a key component for atherothrombotic manifestations, in particular myocardial infarction. Therefore, antiplatelet therapies are pivotal for the treatment of these patients. Current oral

OBJECTIVE There are indications that acute myocardial infarction (AMI) may have an effect on the oral environment, which is reflected in the expression of salivary and gingival proteinases. According to our knowledge, no studies have been carried out to investigate the effect of AMI on the

Protease inhibitor (PI) therapy for patients infected with the human immunodeficiency virus has been associated with lipid disorders and insulin resistance. We compared the incidence of myocardial infarction (MI) among participants receiving treatment with PIs with or without nucleoside reverse

Ischaemic heart disease is one of the leading causes of death. Protease-activated receptor 2 (PAR2) is widely expressed within the cardiovascular system and is known to mediate inflammatory processes in various immunocytes, such as macrophages, mastocytes and neutrophils. Here, we investigated

We examined the efficacy of the combination of coronary reperfusion and calcium-activated neutral protease (CANP) inhibitor (E-64c) for the treatment of acute myocardial infarction in dogs. In 34 dogs, the left anterior descending artery (LAD) was occluded and reperfused after 1 hour (Groups A and

Calcium-activated neutral protease (CANP) might be involved in the irreversible degradation of myocardial proteins in the ischemic region, leading to the loss of contractility. The new compound, NCO-700, and its analogues were synthetized against CANP. Among these analogues, NCO-700 was the most

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

The purposes of this study were to investigate the sequential changes of PMN elastase during evolving myocardial infarction, and also to ascertain whether or not ulinastatin (UL), a clinically useful protease inhibitor, would affect the extent of ischemic myocardial injury. The levels of plasma PMN

Mouse mast cell protease-4 (mMCP4) is a chymase that has been implicated in cardiovascular diseases, including myocardial infarction (MI). This study tested a direct role of mMCP4 in mouse post-MI cardiac dysfunction and myocardial remodeling. Immunoblot and immunofluorescent double staining

Chymase, a mast cell serine protease involved in the generation of multiple cardiovascular factors, such as angiotensin II and endothelin-1 (ET-1), is elevated and participates in tissue degeneration after permanent myocardial infarction (PMI). Anesthetized 4-month old male wild-type (WT) C57BL/6J

We designed a rapid, homogeneous assay for human aspartate aminotransferase (AST) isoenzymes, by a selective proteolysis of soluble AST (s-AST), using chymotrypsin and protease 401. The linearity of mitochondrial (m-AST) was elongated up to 4000 U/l. m-AST values from the human liver, and determined

The paper reports on the efficacy of the protease inhibitors Contrycal and Hordox in acute myocardial infarction. The authors observed 154 patients, of whom 50 constituted the control group. They used to watch the process in the myocardium with biochemical, radioimmune and electrocardiographic

Some infarcted myocytes undergo caspase-dependent DNA fragmentation, but serine protease-dependent DNA fragmentation may also be involved. There is controversy regarding whether caspase inhibitors can reduce infarct size, so the present study investigated whether serine protease inhibitor can reduce

One hundred and forty-nine of 199 patients with myocardial infarction (MI) were treated with varying doses of kallikrein-protease inhibitors (KPI), contrical or gordox, for 4 to 5 days as part of combined treatment. KPI added to combined treatment at early dates of MI contributed significantly to

OBJECTIVE To determine the relation between Marburg I polymorphism of Factor VII-activating protease (FSAP) and cerebral infarction,and to analyze whether it is one of the risk factors of cerebral infarction. METHODS Single strand conformation polymorphism-polymerase chain reaction (SSCP-PCR) was