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Σελίδα 1 από 1868 Αποτελέσματα
Mechanisms for the deterioration in glucose tolerance associated with HIV protease inhibitor regimens.
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The mechanisms responsible for the deterioration in glucose tolerance associated with protease inhibitor-containing regimens in HIV infection are unclear. Insulin resistance has been implicated as a major factor, but the affected tissues have not been identified. Furthermore, beta-cell function has
Loss of Drosophila i-AAA protease, dYME1L, causes abnormal mitochondria and apoptotic degeneration.
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Mitochondrial AAA (ATPases Associated with diverse cellular Activities) proteases i-AAA (intermembrane space-AAA) and m-AAA (matrix-AAA) are closely related and have major roles in inner membrane protein homeostasis. Mutations of m-AAA proteases are associated with neuromuscular disorders in humans.
Decreased expression of protease inhibitor 9, a granzyme B inhibitor, in celiac disease: a potential mechanism in enterocyte destruction and villous atrophy.
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The objective of this study was to assess the expression of protease inhibitor 9, a granzyme B inhibitor, in human small intestine, and to evaluate its cytoprotective role in the celiac disease of children. Twelve subjects with untreated celiac disease and thirteen healthy controls were examined by
Cathepsin proteases mediate photoreceptor cell degeneration in Drosophila.
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Endocytosis-mediated cell death is a form of degeneration displayed in several Drosophila mutants. This form of degeneration is displayed in several Drosophila mutant lines including flies lacking the eye-specific PLC (norpA). The cell death pathway is initiated by the stabilization of complexes
Exocellular proteases of Malbranchea gypsea and their role in keratin deterioration.
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Malbranchea gypsea IMI 338,168 isolated from the soils of Keoladeo National Park, Bharatpur was studied for its ability to produce exocellular proteases on glucose-gelatin medium at pH 7; 28 degrees C. The fungus was observed to be a potent producer of such enzymes. Protease production was optimal
Interrelation of intracellular proteases with total parenteral nutrition-induced gut mucosal atrophy and increase of mucosal macromolecular transmission in rats.
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Total parenteral nutrition (TPN) is known to induce mucosal atrophy and to increase macromolecular transmission of the small intestine. The potential participation of various proteases in that process was investigated. Male Wistar rats were randomly divided into two groups: the TPN group (n = 11)
Degeneration of neuronal processes in rats induced by a protease inhibitor, leupeptin.
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Severe degeneration of neuronal processes, including axons and dendrites, as well as accumulation of lipofuscin-like dense bodies have been induced in rats by continuous intraventricular administration by infusion of a protase inhibitor, leupeptin. The aggregation of degenerated processes in
Down-regulation of the mitochondrial i-AAA protease Yme1L induces muscle atrophy via FoxO3a and myostatin activation.
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Muscle atrophy is closely associated with many diseases, including diabetes and cardiac failure. Growing evidence has shown that mitochondrial dysfunction is related to muscle atrophy; however, the underlying mechanisms are still unclear. To elucidate how mitochondrial dysfunction causes muscle
Elevated levels of a calcium-activated muscle protease in rapidly atrophying muscles from vitamin E-deficient rabbits.
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A Ca2+-activated proteolytic enzyme that partially degrades myofibrils was isolated from hind limb muscles of normal rabbits and rabbits undergoing rapid muscle atrophy as a result of vitamin E deficiency. Extractable Ca2+-activated protease activity was 3.6 times higher in muscle tissue from
Memory disturbance and hippocampal degeneration induced by continuous intraventricular infusion of a protease inhibitor, leupeptin.
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Effects of a protease inhibitor, leupeptin, on the memory function and the morphological changes in the hippocampus were examined in rats. The leupeptin was infused by an implanted-osmotic minipump into the lateral ventricle of the rats for 14 days. The acquisition and the maintenance of memory were
Treatment of facial fat atrophy related to treatment with protease inhibitors by autologous fat injection in patients with human immunodeficiency virus infection.
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A parallel effect of the use of protease inhibitors in human immunodeficiency virus-positive patients is the appearance of facial fat atrophy. To correct this, the authors propose lipoinjection of autologous fat into the areas of facial atrophy by a technique based on the atraumatic procurement of
Correlation between the Expression of High Temperature Requirement Serine Protease A1 in Nucleus Pulposus Tissue and the Degree of Intervertebral Disc Degeneration.
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Objective To investigate the correlation between the expression level of high temperature requirement serine protease A1 (HtrA1) in nucleus pulposus and the degree of intervertebral disc degeneration (Pfirrmann grade).Methods Thirty-six patients who underwent excision of nucleus pulposus were
Proteomics-based identification and validation of novel plasma biomarkers phospholipid transfer protein and mannan-binding lectin serine protease-1 in age-related macular degeneration.
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Age-related macular degeneration (AMD) is a major cause of severe, progressive visual loss among the elderly. There are currently no established serological markers for the diagnosis of AMD. In this study, we carried out a large-scale quantitative proteomics analysis to identify plasma proteins that
Structural basis of inactivation of human counterpart of mouse motor neuron degeneration 2 mutant in serine protease HtrA2.
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Serine protease high temperature requirement protease A2 (HtrA2) is involved in apoptosis and protein quality control. However, one of its murine inactive mutants (S276C aka mnd2) is associated with motor neuron degeneration 2. Similarly, this conserved mutation in human HtrA2 (hHtrA2) also renders
c-Cbl ubiquitin ligase regulates focal adhesion protein turnover and myofibril degeneration induced by neutrophil protease cathepsin G.
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The neutrophil-derived serine protease, cathepsin G (Cat.G), has been shown to induce myocyte detachment and apoptosis by anoikis through down-regulation of focal adhesion (FA) signaling. However, the mechanisms that control FA protein stability and turnover in myocytes are not well understood.
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