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chymotrypsin/infarktus
A hivatkozás a vágólapra kerül
Oldal 1 tól től 21 eredmények
[Intra-arterial infusion of alpha-chymotrypsin in the treatment of vascular infarcts during the course of arteriosclerosis].
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Proteomic profiling of extracellular vesicles reveals additional diagnostic biomarkers for myocardial infarction compared to plasma alone.
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Extracellular vesicles (EVs) are submicron, membrane-enclosed particles that are released from cells in various pathophysiological states. The molecular cargo of these vesicles is considered to reflect the composition of the cell of origin, and the EV proteome is therefore a potential source of
A homogeneous assay system of aspartate aminotransferase iso-enzymes using proteases and application for clinical evaluation of myocardial infarction.
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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
Elastase-2, an angiotensin II-generating enzyme, contributes to increased angiotensin II in resistance arteries of mice with myocardial infarction.
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Angiotensin II (Ang II), whose generation largely depends on angiotensin-converting enzyme (ACE) activity, mediates most of the renin-angiotensin-system (RAS) effects. Elastase-2 (ELA-2), a chymotrypsin-serine protease elastase family member 2A, alternatively generates Ang II in rat arteries.
Peroxynitrite-mediated oxidative modifications of complex II: relevance in myocardial infarction.
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Increased O(2)(*-) and NO production is a key mechanism of mitochondrial dysfunction in myocardial ischemia/reperfusion injury. In complex II, oxidative impairment and enhanced tyrosine nitration of the 70 kDa FAD-binding protein occur in the post-ischemic myocardium and are thought to be mediated
Inhibition of immunoproteasome reduces infarction volume and attenuates inflammatory reaction in a rat model of ischemic stroke.
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The detailed knowledge about the contribution of immunoproteasome to the neuroinflammation in ischemic stroke is still not available. The immunoreactivity of low molecular mass peptide 2 (LMP2) and low molecular mass peptide 7 (LMP7) was evident in the ipsilateral ischemic cerebral cortex and
Activation of Chymotrypsin-Like Activity of the Proteasome during Ischemia Induces Myocardial Dysfunction and Death.
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Inhibitors of the ubiquitin-proteasome system improve hemodynamic parameters and decrease the infarct size after ischemia reperfusion. The molecular basis of this protection is not fully understood since most available data report inhibition of the 26 proteasome after ischemia reperfusion. The
Inhibition of chymotrypsin-like activity of the proteasome by ixazomib prevents mitochondrial dysfunction during myocardial ischemia
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The heart is critically dependent on mitochondrial respiration for energy supply. Ischemia decreases oxygen availability, with catastrophic consequences for cellular energy systems. After a few minutes of ischemia, the mitochondrial respiratory chain halts, ATP levels drop and ion gradients across
The domain organization of streptokinase: nuclear magnetic resonance, circular dichroism, and functional characterization of proteolytic fragments.
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Streptococcus equisimilis streptokinase (SK) is a bacterial protein of unknown tertiary structure and domain organization that is used extensively to treat acute myocardial infarction following coronary thrombosis. Six fragments of SK were generated by limited proteolysis with chymotrypsin and
Proteasomal activity in brain tissue following ischemic stroke in Wistar rats.
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Functional as well as structural reorganization of brain tissues takes place in the surrounding and remotes brain areas after focal ischemic lesions. In particular, reactive or regenerative processes have been described to occur in the infarction areas and the contralateral hemisphere. Experiments
Lysine 156 promotes the anomalous proenzyme activity of tPA: X-ray crystal structure of single-chain human tPA.
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Tissue type plasminogen activator (tPA) is the physiological initiator of fibrinolysis, activating plasminogen via highly specific proteolysis; plasmin then degrades fibrin with relatively broad specificity. Unlike other chymotrypsin family serine proteinases, tPA is proteolytically active in a
Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig.
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Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemia-induced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of
Hereditary pancreatitis of 3 Chinese children: Case report and literature review.
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BACKGROUND
Hereditary pancreatitis (HP) is quite rare and is distinguished by incomplete penetrance presentation as early-onset relapsing pancreatitis, usually beginning in childhood. HP is now known to be commonly relevant to mutations in the PRSS1 (gene-encoding cationic trypsinogen), SPINK1
Chymase inhibition and cardiovascular protection.
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Human chymase, an angiotensin II-forming chymotrypsin-like serine proteinase, posses various biological actions mediating through local angiotensin II formation in the tissue level of many cardiovascular organs. Our previous experimental data have shown that chymase inhibitor increased a survival
Structural basis of specific inhibition of tissue-type plasminogen activator by plasminogen activators inhibitor-1.
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Thrombosis is a leading cause of death worldwide [1]. Recombinant tissue-type plasminogen activator (tPA) is the FDA-approved thrombolytic drug for ischemic strokes, myocardial infarction and pulmonary embolism. tPA is a multi-domain serine protease of the trypsin-family [2] and catalyses the
A legteljesebb gyógynövény-adatbázis, amelyet a tudomány támogat
- Működik 55 nyelven
- A tudomány által támogatott gyógynövényes kúrák
- Gyógynövények felismerése kép alapján
- Interaktív GPS térkép - jelölje meg a gyógynövényeket a helyszínen (hamarosan)
- Olvassa el a keresésével kapcsolatos tudományos publikációkat
- Keresse meg a gyógynövényeket hatásuk szerint
- Szervezze meg érdeklődését, és naprakész legyen a hírkutatással, a klinikai vizsgálatokkal és a szabadalmakkal
Írjon be egy tünetet vagy betegséget, és olvassa el azokat a gyógynövényeket, amelyek segíthetnek, beírhat egy gyógynövényt, és megtekintheti azokat a betegségeket és tüneteket, amelyek ellen használják.
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