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EN
Matrix metalloproteases (MMPs) are synthesized in the form proenzymes. They are activated in the process of limited proteolysis and non-enzymatically by active forms of oxygen. Activity of these enzymes is controlled by tissue inhibitors of metalloproteases (TIMPs).
EN
Experimental aortic aneurysm may be evoked in animals by application of chemical compounds disturbing biosynthesis, posttranlating modifications and degradation of elastin and collagen, local damage of the aortic wall by chemical, thermal and mechanical factors and by increased blood preasure. Administration of protease inhibitors, anti-inflammatory drugs, agents enhancing synthesis and formation of elastic and collagen fibers and hypotensive drugs prevent formation enlargment and rupture of aneurysm.
EN
Prometalloproteases are activated by serine proteases, MMP-3, leucocytic elastase, furin, furin-like proteases and by membrane-type metalloproteases as well. They form complex with some proMMPs and thus they modify their activation.
EN
The literature referring to proteolytic enzymes of neutrophilic granulocytes was surveyed. Biosynthesis, subcellular distribution, division according to the catalytic site structure, inhibitors and methods used to determine the activity of these enzymes were discussed. The survey included metaloproteases (granulocytic collagenese, gelatinase B), serine proteases (granulocytic elastase, cathepsin G, protease-3), membraneous proteases (aminopeptidase N, aminopeptidase P, neprilisine), cysteine and aspartic cathepsins. The role of these proteases in the pathology and diagnostics of certain diseases was
EN
This review describe the oxidative modification of proteins and its effect on the proteases and antiproteases activity. The changes in the proteolytic- -antyproteolytic balance and the susceptibility of the protein substrates on proteolysis are also presented.
EN
Surgical trauma is associated with depression of the immune system, which results in a high complication rate following abdominal aortic aneurysm (AAA) repair. Monocyte chemotactic protein-1 (MCP-1) and regulated-on-activation normal T cell expressed and secreted (RANTES) protein are important mediators of the immune and inflammatory response. The aim of this study was to determine whether there is any relationship between MCP-1 or RANTES and operative injury and ischemia-reperfusion during AAA surgery in human. Peripheral blood samples were taken from 12 patients before surgery, after anesthesia induction, before unclamping of aorta (PreXoff), 90 min after unclamping (90minXoff), and at 24 and 48 h after surgery. The MCP-1 and RANTES serum concentrations were measured with the ELISA technique. MCP-1 concentration significantly increased after reperfusion (90minXoff) in comparison with the PreXoff level (p=0.001). Twenty-four hours after AAA repair, MCP-1 significantly decreased 269?225 pg/ml (p=0.005) and reached preoperative value. RANTES level was higher in AAA patients before surgery than in controls (p=0.025) and decreased significantly after ischemia-reperfusion to 13 ng/ml (p< 0.001) at 90minXoff. We showed increases in RANTES concentration to 26 ng/ml on the 1st and to 31 ng/ml on the 2nd day after surgery (p=0.020, p=0.012, respectively) compared with the 90minXoff level. Ischemia-reperfusion during AAA repair results in an increase in MCP-1 and decrease in RANTES concentrations in serum. The changes in chemokine concentrations may influence the development of immunosuppression after AAA repair, contributing to the postoperative course.
EN
In this review we try to summarize some of the new informations about the genetic base of bronchial asthma. We also mention apoptosis (programmed cell death) as the process modulating cell proliferation, differentiation and death. According to the latest reports, the disorders of the regulation of apoptosis may play an important role an the pathogenesis of autoimmunologic and atopic diseases (including bronchial asthma), AIDS and neoplasmatic diseases. There is a linkage between the induction of apoptosis and signal transduction disorders. We describe the Raf/MECK/ERK/MAP signal transduction pathway and 14-3-3 protein - the peptide which possibly might participate in the initiation of the programmed cell death.
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