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oligosaccharide/œdème
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[Anomaly of the polypeptide and oligosaccharide chains of alpha-2-neuraminoglycoprotein in various types of hereditary angioneurotic edema].
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Using two-dimensional immuno-electrophoresis to study a morphological abnormality of the alpha 2-neuramino-glycoprotein (alpha 2-NGP) we have been able to observe allelic exclusion in patients afflicted by hereditary angioneurotic oedema [1]. With the aid of two-dimensional
Anti-tumor-promoting activities of agaro-oligosaccharides on two-stage mouse skin carcinogenesis.
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We have previously reported that agaro-oligosaccharides (AGOs) suppressed the elevated levels of nitric oxide (NO), prostaglandin E₂(PGE₂), and pro-inflammatory cytokines in activated monocytes/macrophages, via heme oxygenase-1 induction. In this report, we initially demonstrated that AGOs intake
Phase IB clinical trial of the oligosaccharide processing inhibitor swainsonine in patients with advanced malignancies.
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The indolizidine alkaloid swainsonine, a potent inhibitor of Golgi alpha-mannosidase II, has been shown to reduce tumor cell metastasis, enhance cellular immune responses, and reduce solid tumor growth in mice. In our previous Phase I study, swainsonine administered by 5-day continuous infusion
In vitro and in vivo anti-inflammatory activity of digested peptides derived from salmon myofibrillar protein conjugated with a small quantity of alginate oligosaccharide.
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Salmon myofibrillar protein (Mf) was investigated as a source of edible anti-inflammatory products. Peptides produced by stepwise digestion of Mf (without carbohydrate) with pepsin and trypsin had little effect on the secretion of inflammation-related compounds from lipopolysaccharide-stimulated RAW
Sialyl Lewis(x) oligosaccharide reduces ischemia-reperfusion injury in the rabbit ear.
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Ischemia-reperfusion injury in the rabbit ear is neutrophil (PMN)-mediated, and is significantly reduced by anti-adhesion agents directed against beta 2 integrins, P-selectin, or L-selectin. We further examined selectin-mediated adherence in this setting following the administration of soluble
Determination of oligosaccharides and glycolipids in amniotic fluid by electrospray ionisation tandem mass spectrometry: in utero indicators of lysosomal storage diseases.
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Prenatal diagnosis is available for many lysosomal storage disorders (LSD) using chorionic villus samples or amniocytes. Such diagnoses can be problematical if sample transport and culture are required prior to analysis. The purpose of this study was to identify useful biochemical markers for the
Lysosomal storage diseases in non-immune hydrops fetalis pregnancies.
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BACKGROUND
At least 20 inborn errors of metabolism may cause hydrops fetalis. Most of these are lysosomal storage diseases. The study proposes a diagnostic flowchart for prenatal diagnosis of non-immune hydrops fetalis.
METHODS
This study contains a series of 75 non-immune hydrops fetalis
Merozoite surface protein-1 of Plasmodium yoelii fused via an oligosaccharide moiety of cholera toxin B subunit glycoprotein expressed in yeast induced protective immunity against lethal malaria infection in mice.
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Methylotrophic yeast (Pichia pastoris) secreted cholera toxin B subunit (CTB) predominantly as a biologically active pentamer (PpCTB) with identical ganglioside binding affinity profiles to that of choleragenoid. Unlike choleragenoid, however, the PpCTB did not induce a footpad edema response in
Fetal hydrops in GM(1) gangliosidosis: a case report.
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GM(1) gangliosidosis is a rare disorder characterized by deficiency of the ss-galactosidase enzyme, with the resulting accumulation of glycolipids, oligosaccharides and especially GM(1) ganglioside. It can be classified into three clinical types according to the time of onset: infantile, juvenile
Amniotic fluid for screening of lysosomal storage diseases presenting in utero (mainly as non-immune hydrops fetalis).
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Seventy amniotic fluids (AF) were sampled because of abnormal ultrasound findings (mainly non-immune hydrops fetalis (54 cases) or of the presence of vacuolated lymphocytes in fetal blood (3 cases)). They were analysed by a procedure involving AF supernatant analysis (glycosaminoglycans,
Nonimmune hydrops fetalis with galactosialidosis: consequences for family planning.
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At the 28th week of gestation a hydrops fetalis was first detected by ultrasound. At birth a generalized hydrops with Hurler-like craniofacial dysmorphism, hepatosplenomegaly and a moderate dystostosis multiplex was noted. High urinary excretion of oligosaccharides and a severe deficiency of
Neuraminidase deficiency presenting as non-immune hydrops fetalis.
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A newborn infant with oedema, ascites and hepatosplenomegaly is described. In ascites fluid foamy macrophages were found, in a liver biopsy cytoplasmic inclusions and membrane-bound vacuoles were seen. Furthermore the child excreted excessive amounts of sialic acid-rich oligosaccharides in the
Sialidosis presenting as severe nonimmune fetal hydrops is associated with two novel mutations in lysosomal alpha-neuraminidase.
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Sialidosis is a lysosomal storage disease characterized by accumulation of sialylated oligosaccharides in tissues, blood and urine and is caused by mutations in the gene for lysosomal alpha-neuraminidase (NEU1). There is wide variability in the age of onset and severity of symptoms in sialidosis. We
[Fetal ascites as a manifestation of infantile sialidosis. Significance of a study of oligosaccharides in amniotic fluid].
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Non immune hydramnios and fetal ascite are demonstrated at 31 weeks gestation. There is no familial story. All etiologic investigations (repeated ultrasonographic examinations, amniocentesis) are negative. The delivered girl has a normal development. She presents a congenital ascite and edema. The
A computational study of the oligosaccharide binding sites in the lectin-like domain of Tumor Necrosis Factor and the TNF-derived TIP peptide.
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The lectin-like domain of Tumor Necrosis Factor (TNF), mimicked by the TIP peptide, activates amiloride-sensitive sodium uptake in type II alveolar epithelial cells and as such increases alveolar liquid clearance in dysfunctional lungs. This protective effect is blunted upon mutation of residues
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