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Seite 1 von 48 Ergebnisse
Hypoxia-enhanced expression of free deaminoneuraminic acid in human cancer cells.
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Hypoxia is a common characteristic of locally advanced tumors and cancer cells of high invasiveness and metastasis. We first demonstrate that hypoxic culture of human cancer HeLa, LS174T, and Caco-2 cells enhances the de novo synthesis of free sialic acids including deaminoneuraminic acid (Kdn), a
Cation-independent mannose 6-phosphate receptor inhibitor (PXS25) inhibits fibrosis in human proximal tubular cells by inhibiting conversion of latent to active TGF-beta1.
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Hyperglycemia and hypoxia have independent and convergent roles in the development of renal disease. Transforming growth factor-β(1) (TGF-β(1)) is a key cytokine promoting the production of extracellular matrix proteins. The cationic-independent mannose 6-phosphate receptor (CI-M6PR) is a membrane
Systemic mannose-binding lectin is not associated with Chronic Obstructive Pulmonary Disease.
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Mannose-binding lectin (MBL) deficiency is associated with increased susceptibility to airways infections and autoimmunity. We examined whether MBL deficiency was more common in COPD patients, and whether MBL deficiency was associated with COPD severity. 415 COPD patients and 231 healthy subjects,
Associations between complement pathways activity, mannose-binding lectin, and odds of unprovoked venous thromboembolism.
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Deep vein thrombosis (DVT) originates in the valvular sinuses of large veins in a local milieu characterized by stasis and severe hypoxia. This may induce complement- and coagulation activation, which potentially increases the risk of venous thromboembolism (VTE). The aim of the present study was to
Mannose Binding Lectin, S100 B Protein, and Brain Injuries in Neonates With Perinatal Asphyxia
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Perinatal asphyxia triggers an acute inflammatory response in the injured brain. Complement activation and neuroinflammation worsen brain damage after a systemic ischemia/reperfusion insult. The increase of mannose binding lectin (MBL) during asphyxia may contribute to the brain damage, via
Effect of glucose on recovery of energy metabolism following hypoxia-oligemia in mouse brain: dose-dependence and carbohydrate specificity.
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Unilateral cerebral hypoxia-oligemia was produced in anesthetized mice using carotid artery occlusion combined with systemic hypoxia (10% O2). In the cerebral cortex ipsilateral to the carotid occlusion, ATP levels were depleted during a 30-min insult, but were restored to 64% of control during 60
Polysaccharides from the Edible Mushroom Agaricus bitorquis (Quél.) Sacc. Chaidam Show Anti-hypoxia Activities in Pulmonary Artery Smooth Muscle Cells.
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Three kinds of new water-soluble polysaccharides (FA, FB and FC) were isolated from wild mushroom Agaricus bitorquis (Quél.) Sacc. Chaidam by the classical method "water extraction and alcohol precipitation" and purified by column chromatography. The Mw of FA, FB and FC ranged from
The paradox between resistance to hypoxia and liability to hypoxic damage in hyperglycemic peripheral nerves. Evidence for glycolysis involvement.
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Isolated ventral and dorsal rat spinal roots incubated in normal (2.5 mM) or high glucose (25 mM) concentrations or in high concentrations of other hexoses were exposed transiently to hypoxia (30 min) in a solution of low buffering power. Compound nerve action potentials, extracellular direct
Substrate supply and function of isolated venous smooth muscle under anoxia and metabolic inhibition.
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The contractile recoverability of isolated portal veins made hypodynamic by removal of glucose from the perfusion medium by diverse exogenous substrates was studied. It was found that glucose, mannose, pyruvate, lactate, acetate, and butyrate readily restored contraction. The effects of anoxia and
Hypoxia-elicited impairment of cell wall integrity, glycosylation precursor synthesis, and growth in scaled-up high-cell density fed-batch cultures of Saccharomyces cerevisiae.
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BACKGROUND
In this study we examine the integrity of the cell wall during scale up of a yeast fermentation process from laboratory scale (10 L) to industrial scale (10,000 L). In a previous study we observed a clear difference in the volume fraction occupied by yeast cells as revealed by wet cell
Role of hypoxia and EGF on expression, activity, localization and phosphorylation of carbonic anhydrase IX in MDA-MB-231 breast cancer cells.
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Carbonic anhydrase IX (CAIX) is a zinc metalloenzyme that catalyzes the reversible hydration of CO(2). CAIX is overexpressed in many types of cancer, including breast cancer, but is most frequently absent in corresponding normal tissues. CAIX expression is strongly induced by hypoxia and is
Transcriptome analysis reveals new insights into immune response to hypoxia challenge of large yellow croaker (Larimichthys crocea).
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Fish live in direct contact with aquatic environment, which exhibits much wider temporal and spatial variations in oxygen content. The molecular mechanisms underlying fish response to hypoxia have become a subject of great concern in recent years. In the present study, we performed transcriptome
Mannose-binding lectin has a direct deleterious effect on ischemic brain microvascular endothelial cells.
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Mannose-binding lectin (MBL), an initiator of the lectin pathway, is detrimental in ischemic stroke. MBL deposition on the ischemic endothelium indicates the beginning of its actions, but downstream mechanisms are not clear yet. We investigated MBL interactions with the ischemic endothelium by
Inhibition of Asparagine-linked Glycosylation Participates in Hypoxia-induced Down-regulation of Cell-surface MICA Expression.
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Hypoxia down-regulates the expression of cell surface major histocompatibility class I-related chain molecule A (MICA) without increasing its shedding. Recently, the inhibition of N-linked glycosylation was also shown to reduce the cell-surface expression of MICA. We investigated the participation
NFIL3 suppresses hypoxia-induced apoptotic cell death by targeting the insulin-like growth factor 2 receptor.
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The insulin-like growth factor-II/mannose 6-phosphate receptor (IGF2R) over-expression correlates with heart disease progression. The IGF2R is not only an IGF2 clearance receptor, but it also triggers signal transduction, resulting in cardiac hypertrophy, apoptosis and fibrosis. The present study
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