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glycolipid/диария

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Страница 1 от 38 резултата

Pathogenesis of Shigella diarrhea: XVII. A mammalian cell membrane glycolipid, Gb3, is required but not sufficient to confer sensitivity to Shiga toxin.

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Shiga toxin recognizes a galactose-alpha 1-->4-galactose terminal glycolipid, globotriaosylceramide (Gb3), in sensitive mammalian cells and is translocated by endocytosis to the cytoplasm, where it blocks protein synthesis. To determine if Gb3 is both required and sufficient for toxicity, Gb3

Pathogenesis of shigella diarrhea: evidence for a developmentally regulated glycolipid receptor for shigella toxin involved in the fluid secretory response of rabbit small intestine.

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Shigella toxin reproduces the major manifestations of shigellosis in ligated intestinal loops from adult rabbits and binds to a microvillus membrane (MVM) glycolipid receptor, globotriaosylceramide (Gb3). Because neonatal human shigellosis is uncommon, we used the animal model for obtaining MVMs

Pathogenesis of shigella diarrhea. XI. Isolation of a shigella toxin-binding glycolipid from rabbit jejunum and HeLa cells and its identification as globotriaosylceramide.

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A glycolipid that specifically binds shigella toxin was isolated from both HeLa cells and rabbit jejunal mucosa and identified as globotriaosylceramide (Gb3) by its identical mobility on HPTLC to authentic erythrocyte Gb3. Toxin also bound to a band tentatively identified as alpha-hydroxylated Gb3.

Production of a heat-labile enterotoxin B subunit-porcine epidemic diarrhea virus-neutralizing epitope fusion protein in transgenic lettuce (Lactuca sativa).

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Plant-based vaccines have been produced in transgenic plants including tobacco, potatoes, corn, and rice. However, these plants are not suitable for administration without cooking. To overcome this obstacle, a fusion gene encoding the synthetic enterotoxigenic Escherichia coli heat-labile

Cryptosporidium parvum sporozoite pellicle antigen recognized by a neutralizing monoclonal antibody is a beta-mannosylated glycolipid.

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The protozoan parasite Cryptosporidium parvum is an important cause of diarrhea in humans, calves, and other mammals worldwide. No approved vaccines or parasite-specific drugs are currently available for the control of cryptosporidiosis. To effectively immunize against C. parvum, identification and

Tumor necrosis factor concentrations in hemolytic uremic syndrome patients and children with bloody diarrhea in Argentina.

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Hemolytic uremic syndrome (HUS) is thought to be a vascular endothelial injury disease. The mechanism of injury is unknown although verocytotoxins (Shiga-like toxins (SLTs)) are known to be associated with it. Recent evidence suggests that in vitro treatment of some endothelial cells with tumor

Human milk contains the Shiga toxin and Shiga-like toxin receptor glycolipid Gb3.

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Human milk antibody and nonantibody factors are thought to be important in protecting infants from diarrheal diseases. The nonantibody factors include host receptor analogues that bind to specific pathogen virulence factors, thereby inhibiting these bacterial products from binding to their

Clostridium difficile contains plasmalogen species of phospholipids and glycolipids.

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Analysis of the polar lipids of many pathogenic and non-pathogenic clostridia has revealed the presence of plasmalogens, alk-1'-enyl ether-containing phospholipids and glycolipids. An exception to this finding so far has been Clostridium difficile, an important human pathogen which is the cause of

Age-related resistance to 987P fimbria-mediated colonization correlates with specific glycolipid receptors in intestinal mucus in swine.

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Strains of enterotoxigenic Escherichia coli that produce 987P fimbriae (987P+ strains) colonize the small intestines and cause diarrhea in neonatal (< 6-day-old) pigs but not in weaned pigs. However, 987P+ E. coli strains adhere in vitro to intestinal epithelial cells from pigs of both ages. Two

Rotavirus toxin NSP4 induces diarrhea by activation of TMEM16A and inhibition of Na+ absorption.

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Rotavirus infection is the most frequent cause for severe diarrhea in infants, killing more than 600,000 every year. The nonstructural protein NSP4 acts as a rotavirus enterotoxin, inducing secretory diarrhea without any structural organ damage. Electrolyte transport was assessed in the colonic

Changes in bacterial glycolipids as an index of intestinal lactobacilli and epithelial glycolipids in the digestive tracts of mice after administration of penicillin and streptomycin.

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The major lipid constituent of symbiotic gram-positive bacteria in animals are phosphatidylglycerol, cardiolipin and dihexaosyl diglycerides (DH-DG), whose hydrophobic structures are characteristic of the environments, and the carbohydrate structures of DH-DGs are bacterial species-characteristic.

Pathogenesis of Shigella diarrhea. XIV. Analysis of Shiga toxin receptors on cloned HeLa cells.

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Binding kinetics of Shiga toxin to HeLa CCL-2 cells and to cell lines cloned by limiting dilutions were determined. Lines with a wide range of sensitivity to Shiga toxin were obtained. Binding data, analyzed by a computer-based Scatchard model program, revealed two classes of binding sites, one of

Pathogenesis of Shigella diarrhea. XVI. Selective targetting of Shiga toxin to villus cells of rabbit jejunum explains the effect of the toxin on intestinal electrolyte transport.

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To examine the mechanism by which Shiga toxin alters intestinal water and electrolyte transport, ligated loops of rabbit jejunum were incubated in vivo with purified toxin and then studied in vivo by single pass perfusion and in vitro by the Ussing chamber voltage-clamp technique. Toxin exposure led

Activation of natural killer T cells by alpha-galactosylceramide in the presence of CD1d provides protection against colitis in mice.

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OBJECTIVE CD1d is a major histocompatibility complex class I-like molecule that presents glycolipid antigens to a subset of natural killer (NK)1.1(+) T cells. These NK T cells exhibit important immunoregulatory functions in several autoimmune disease models. METHODS To investigate whether CD1d and

[An acute axonal form of Guillain-Barré syndrome with antibodies against gangliosides GM1 and GD1b--a case report].

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We reported a case of Guillain-Barré syndrome with autoantibodies against gangliosides GM1 and GD1b, which has not been reported yet. A 25-year-old man was admitted with a 7-day history of acute progressive weakness in the extremities. Two weeks before admission he had suffered from an episode of
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