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mucin/дијареја

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Страна 1 од 151 резултати

Binding of E. coli isolates from pigs with postweaning diarrhea or edema disease to crude intestinal mucin of a weaned pig.

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The presence of the fedA (gene coding F18 fimbriae) and genes coding STa and LTI enterotoxins and verotoxin Stx2v was determined in 30 E. coli strains isolated from weaned pigs with postweaning diarrhea (PWD) and edema disease (ED). The fedA gene was detected in 22 strains (73.3%). It was mostly

Fecal metatranscriptomics of macaques with idiopathic chronic diarrhea reveals altered mucin degradation and fucose utilization.

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Idiopathic chronic diarrhea (ICD) is a common cause of morbidity and mortality among juvenile rhesus macaques. Characterized by chronic inflammation of the colon and repeated bouts of diarrhea, ICD is largely unresponsive to medical interventions, including corticosteroid,

Inhibition of adhesion of Escherichia coli k88ac fimbria to its receptor, intestinal mucin-type glycoproteins, by a monoclonal antibody directed against a variable domain of the fimbria.

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Strains of enterotoxigenic Escherichia coli that express K88 fimbriae are among the most common causes of diarrhea in young pigs. Adhesion of bacteria to receptors on intestinal epithelial cells, mediated by K88 fimbriae, is the initial step in the establishment of infection. Three antigenic

Expression of mucin-type glycoprotein K88 receptors strongly correlates with piglet susceptibility to K88(+) enterotoxigenic Escherichia coli, but adhesion of this bacterium to brush borders does not.

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Three antigenic variants of the K88 fimbrial adhesin exist in nature, K88ab, K88ac, and K88ad. Enterotoxigenic Escherichia coli (ETEC) strains that produce these fimbriae cause life-threatening diarrhea in some but not all young pigs. The susceptibility of pigs to these organisms has been correlated

Enteroendocrine and neuronal mechanisms in pathophysiology of acute infectious diarrhea.

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BACKGROUND While enterocyte secretion is the predominant mechanism considered responsible for secretory diarrhea in response to acute enteric infections, there are several lines of evidence that support alternative mechanisms controlling fluid and electrolyte secretion in diarrhea. OBJECTIVE To

Oral ingestion of egg yolk immunoglobulin from hens immunized with an enterotoxigenic Escherichia coli strain prevents diarrhea in rabbits challenged with the same strain.

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White Leghorn hens were immunized with enterotoxigenic Escherichia coli B16-4 with heat-labile enterotoxin and colonization factor antigen I in Freund's adjuvant. Specific antibodies were detected by an enzyme-linked immunosorbent assay in the serum after 8 days and in eggs after 10 days, with

Rectal histopathology in endemic Shigella and Salmonella diarrhea.

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Rectal histopathology was evaluated in 34 cases (2 months-12 yrs old) of endemic "invasive diarrhea" [> 20 WBCs per high-power field on stool microscopy with (RBC positive) or without (RBC negative) associated RBCs] where S. dysenteriae (n = 9), S. flexneri (n = 11), and nontyphoidal Salmonella were

Human ileal organoid model recapitulates clinical incidence of diarrhea associated with small molecule drugs

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Drug-induced gastrointestinal toxicity (GIT) is a common treatment-emergent adverse event that can negatively impact dosing, thereby limiting efficacy and treatment options for patients. An in vitro assay of GIT is needed to address patient variability, mimic the microphysiology of the gut, and

Role of Sialic Acid in Brachyspira hyodysenteriae Adhesion to Pig Colonic Mucins.

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Infection with Brachyspira hyodysenteriae results in mucoid hemorrhagic diarrhea. This pathogen is associated with the colonic mucus layer, mainly composed of mucins. Infection regulates mucin O-glycosylation in the colon and increases mucin secretion as well as B.

NanI Sialidase Can Support the Growth and Survival of Clostridium perfringens Strain F4969 in the Presence of Sialyated Host Macromolecules (Mucin) or Caco-2 Cells.

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Enterotoxin-producing Clostridium perfringens type A strains cause human gastrointestinal (GI) infections, including a very common food poisoning and 5 to 10% of all cases of antibiotic-associated diarrhea. This bacterium can utilize free sialic acid for growth, but most sialic acids in the GI tract

Pilus-mediated binding of bovine enterotoxigenic Escherichia coli to calf small intestinal mucins.

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In this study we show that the adhesion to mucus of the enterotoxigenic Escherichia coli strains responsible for diarrhea in calves involves a bacterium-mucin recognition phenomenon in which the bacterial pili and specific mucus receptors carried by the glycoproteins (2,000 to 400 kilodalton) play a

Effects of lactadherin on plasma D-lactic acid and small intestinal MUC2 and claudin-1 expression levels in rats with rotavirus-induced diarrhea.

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The aim of the present study was to investigate the effects of lactadherin on plasma D-lactic acid and small intestinal mucin (MUC) 2 and claudin-1 expression levels in rats with diarrhea induced by rotavirus (RV) infection. A total of 75 seven-day-old healthy Sprague-Dawley rats were randomly

A novel multi-domain mucin-like glycoprotein of Cryptosporidium parvum mediates invasion.

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Cryptosporidium parvum is a protozoan parasite which produces self-limited disease in immunocompetent hosts and devastating, persistent diarrhea in immunocompromised individuals. There is no effective treatment for cryptosporidiosis and little is known about the basic biology of the organism.

Wuji Wan Formula Ameliorates Diarrhea and Disordered Colonic Motility in Post-inflammation Irritable Bowel Syndrome Rats by Modulating the Gut Microbiota.

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Emerging evidence suggests that gut microbiota contribute to the treatment of post-inflammatory irritable bowel syndrome (PI-IBS). Our previous studies have demonstrated that a Chinese formula, Wuji Wan, has the ability to mitigate abdominal pain and diarrhea in PI-IBS rats. However, little is known

Cholera-induced mucin secretion from rat intestine: lack of effect of cAMP, cycloheximide, VIP, and colchicine.

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Purified cholera enterotoxin (20-50 micrograms) and dialyzed cholera filtrate (50-125 mg) increased net glycoprotein synthetic and secretory rates in rat intestinal epithelium. Specific goblet cell mucin secretion was increased 5- to 10-fold. However, other agents that increase intestinal cAMP and
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