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OBJECTIVE
The mechanism(s) of preterm premature rupture of fetal membranes resulting in preterm birth remains unknown. Studies suggest that fetal membranes are susceptible to weakening by protease attack and that collagenases may be active at the site of rupture. In this study fetal membranes from
The effect of NCO-700 (1), a protease inhibitor, on subcellular distribution of lysosomal enzymes was studied in the ischemic perfused rat heart. Ischemia was induced by lowering the afterload pressure of the working heart preparation. The subcellular distribution of lysosomal enzymes was estimated
Ischemic cell death is a complex process and the initial distinction between apoptosis and necrosis appears to be an oversimplification. We previously reported that in ischemic neurons with disrupted plasmalemma, apoptotic mechanisms were also active. In the present study, we investigated cellular
Protease genes were identified that exhibited increased mRNA levels before and immediately after rupture of the naturally selected, dominant follicle of rhesus macaques at specific intervals after an ovulatory stimulus. Quantitative real-time PCR validation revealed increased mRNA levels for matrix
Background: Cardiac rupture is a major lethal complication of acute myocardial infarction (MI). Despite significant advances in reperfusion strategies, mortality from cardiac rupture remains high. Studies suggest that cardiac rupture can be accelerated by thrombolytic therapy, but the
The inbred Brown Norway (BN) rat develops spontaneous ruptures of the internal elastic lamina (RIEL) of the abdominal aorta (AA) and iliac arteries. Prior studies with crosses of the BN/Orl RJ (susceptible) and LOU/M (resistant) showed the presence of a significant QTL on chromosome 5 and the
OBJECTIVE
Neutrophil elastase (NE), a multifunctional serine protease stored in azurophilic granules of mature neutrophils, is capable of intracellular degradation of proteins during phagocytosis and extracellular degradation of connective tissue during an inflammatory process. Secretory leukocyte
Newly replicated Plasmodium falciparum parasites escape from host erythrocytes through a tightly regulated process that is mediated by multiple classes of proteolytic enzymes. However, the identification of specific proteases has been challenging. We describe here a forward chemical genetic screen
OBJECTIVE
To determine expression of collagenolytic genes and collagen degradation in stifle tissues of dogs with ruptured cranial cruciate ligament (CCL).
METHODS
Six dogs with CCL rupture and 11 dogs with intact CCL.
METHODS
Gene expression in CCL tissue and synovial fluid cells was studied using
The parameters half-life, z value, enthalpy, entropy, and free energy were evaluated in the temperature range of 40 to 55°C for a Bacillus sp. P45 protease present in a medium composed of ionic liquid (IL) and organic solvent. The protease was previously treated in IL [Emim][Tf2 N] and increased
Ultrastructural changes to the midgut epithelium of nymphs of the black field cricket (Teleogryllus commodus) after ingestion of potato protease inhibitor II (PPI-II) (0.6% (w/v) in artificial diet) were determined by light and electron microscopy. Crickets fed diet containing PPI-II grew more
Senescence is a tightly regulated process and both compartmentalisation and regulated activation of degradative enzymes is critical to avoid premature cellular destruction. Proteolysis is a key process in senescent tissues, linked to disassembly of cellular contents and nutrient remobilisation.
The fibrous cap of a lipid-containing atherosclerotic plaque consists of collagen produced by arterial smooth muscle cells (SMCs) of synthetic phenotype. A thick cap protects the lipid-rich core, whereas a thin cap predisposes it to rupture, with ensuing acute clinical complications, such as
Premature rupture of membranes and preterm delivery are associated with Ureaplasma infection. We hypothesized that Ureaplasma induced extracellular collagen fragmentation results in production of the tripeptide PGP (proline-glycine-proline), a neutrophil chemoattractant. PGP release from collagen
The malaria parasite Plasmodium falciparum invades human red blood cells. Before infecting new erythrocytes, the merozoites have to exit their host cell to get into the blood plasma. Knowledge about the mechanism of egress is scarce, but it is thought that proteases are basically involved in this