Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.26 (invertase)
 4,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium transport, mucosal structure, and epithelial enzymes were studied in piglets killed 10, 25, 40, 72, or 144 hr after infection with a standard dose of transmissible gastroenteritis virus. Glucose-stimulated Na transport measured in short-circuited jejunal epithelium and suspensions of villous enterocytes became progressively more abnormal during the first 40 hr, but recovered completely by 144 hr. As Na transport deteriorated, jejunal mucosal villi shortened and crypts deepened; cells isolated from the villi became more crypt-like in their enzyme profile, with high levels of thymidine kinase and low levels of sucrase activity 40 hr after infection. At 40 hr, when diarrhea is severe, little if any virus has been found in the epithelium. Our data suggest that the relatively undifferentiated crypt type enterocytes on the villi constitute an important determinant of altered Na transport and diarrhea in this invasive viral enteritis.
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PMID:Transmissible gastroenteritis: sodium transport and the intestinal epithelium during the course of viral enteritis. 83 94

Infants and young children are particularly susceptible to a recently identified viral enteritis which is highly contagious and seems both common and universal. In this disease, virus invades the upper intestinal epithelium, causing acute diarrhoea with early fever and vomiting. We studied a similar disease in pigs, infecting three-week-old animals with transmissible gastroenteritis virus (TGE), which also invades the upper intestinal epithelium. In this model, diarrhoea is massive 16-40 hours after infection, when stools contain increased electrolytes but no excess of sugar. In the jejunum of intact pigs at the 40-hour stage we found altered Na+ and water flux, decreased mucosal activities of disaccharidases and Na+, K+-ATPase, but normal adenylate cyclase activity. At the same stage the response of Na+ flux to glucose was blunted in jejunal epithelium studied in Ussing short-circuit chambers and in suspensions of villous cells; Cl- flux responded normally to theophylline, and thymidine kinase and sucrase activities of cells isolated from jejunal villi were similar to those found in crypt cells. Probably by 40 hours after infection most virus has been shed from the mucosa. Viral diarrhoea clearly differs from enterotoxigenic diarrhoea. Consideration of its pathogenesis must take into account the dynamic nature of the mucosal epithelium and the factors governing differentiation of enterocytes as they migrate from crypt to villus. Sufficient information is available now to characterize one specific and apparently prevalent viral enteritis in man and to identify additional viral enteritides. There is hope that preventative therapy can be developed. Our understanding of the mechanisms of viral diarrhoea is limited, but the availability of an animal model and the promise of others makes us optimistic that these deficiencies can be remedied. Greater understanding of the pathogenesis of viral diarrhoea should better the active therapy of affected infants and children.
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PMID:Viral gastroenteritis: recent progress, remaining problems. 104 55

In the relatively undifferentiated jejunal mucosa occurring in piglet viral enteritis, we measured the response of transepithelial Na+ and Cl- fluxes in vitro to raised intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels. At the acute 40-h stage of transmissible gastroenteritis (TGE), luminal membrane markers, sucrase and lactase, and a basolateral jejunal epithelial membrane marker Na+-K+-ATPase, were significantly decreased in activity, while a proliferative marker, thymidine kinase, was significantly enriched; these enzyme characteristics are typical of enterocytes isolated from crypts of other species. As expected, control piglet jejunum in short-circuited Ussing chambers after theophylline (10 mM) developed significant net secretory Na and Cl fluxes primarily due to significant antiabsorptive effects (delta JNa m----s = 3.48 +/- 0.52, delta JCl m----s = 2.59 +/- 0.28). Furosemide (10(-4) M), an inhibitor of electroneutral NaCl cotransport, produced antiabsorptive effects (delta JNa m----s = 2.53 +/- 0.31, delta JCl m----s = 2.58 +/- 0.28) in control jejunum that were not significantly different from those seen in response to theophylline. TGE jejunum, however, responded to theophylline not by an antiabsorptive effect but by significant electrogenic Cl- secretion (delta JCl s----m = 1.59 +/- 0.48); furosemide had no effect on ion fluxes in TGE tissue. Control and TGE jejunal mucosal homogenates did not differ in their basal or theophylline-stimulated levels of cAMP. We conclude that the relatively undifferentiated small intestine occurring in acute TGE does not generate either a cAMP-mediated antiabsorptive effect or a furosemide-mediated antiabsorptive effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absence of a cAMP-mediated antiabsorptive effect in an undifferentiated jejunal epithelium. 303 40

The effect of soy protein on the small bowel mucosa of 18 infants with acute gastroenteritis was studied. The infants were maintained on a protein hydrolysate formula for 6-8 weeks, following which they were readmitted for soy protein challenge studies. Jejunal biopsy was performed before and 24 h after challenge. On the basis of the clinical and histological reaction to soy protein challenge, three groups were identified. Group 1 consisted of three infants who had clinical and histological reaction. There was associated depletion of mucosal enzymes, lactase, sucrase, malatase, alkaline phosphatase, and blood xylose levels. Group 2 consisted of seven infants who had histological reaction but no clinical symptoms. Two of these seven infants, however, developed clinical reaction when rechallenged with soy protein 2 and 90 days later. Following challenge, mucosal enzymes and blood xylose levels were depressed in five of the seven infants tested. Group 3 consisted of eight infants who did not have either a clinical or a histological reaction. The mucosal enzymes and blood xylose levels were not depressed in four infants tested. The present study shows that the small bowel mucosa of some young infants recovering from acute gastroenteritis remains sensitive to soy protein for a variable period of time. The feeding of soy protein to these infants may result in the persistence of mucosal damage and perpetuation of diarrhea.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of soy protein on the small bowel mucosa of young infants recovering from acute gastroenteritis. 333 89

To investigate the effect of chronic protein-calorie malnutrition on intestinal repair after an enteric infection, we examined small intestinal structure, enzyme activity, and sodium transport in undernourished piglets during the acute and convalescent phases of a viral enteritis, transmissible gastroenteritis (TGE). Gnotobiotic pigs, nutritionally deprived from the age of 7 days, gained less weight than dietary controls from 14 days of age until the end of the study. Animals from malnourished and control diet groups were inoculated with TGE virus at 22-23 days and studied during the acute (40 h) and convalescent (4, 10, and 15 days) stages of this experimental enteritis along with noninfected dietary controls. After TGE infection, we observed a further decrease in weight gain and an increased mortality only in undernourished pigs. In jejunum and ileum of both dietary groups at 40 h after TGE infection, we observed comparable structural lesions, similar decreased activities of mucosal enzymes (sucrase, lactase, sodium-potassium-dependent ATPase), and increased thymidine kinase activities. Also we noted comparable diminution of glucose-stimulated jejunal sodium absorption in both dietary groups at 40 h. In control diet pigs, transport abnormalities recovered by 4 days after TGE infection and normal mucosal structure and enzyme activity returned over 4-15 days. In undernourished piglets, structural repair and enzyme abnormalities were prolonged when compared with the control diet group; glucose-stimulated sodium transport did not recover until 10 days after infection and never regained the enhanced activity seen in noninfected undernourished controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of chronic protein-calorie malnutrition on small intestinal repair after acute viral enteritis: a study in gnotobiotic piglets. 392 24

The use of probiotics to enhance intestinal health has been proposed for many years. Probiotics are traditionally defined as viable microorganisms that have a beneficial effect in the prevention and treatment of specific pathologic conditions when they are ingested. There is a relatively large volume of literature that supports the use of probiotics to prevent or treat intestinal disorders. However, the scientific basis of probiotic use has been firmly established only recently, and sound clinical studies have begun to be published. Currently, the best-studied probiotics are the lactic acid bacteria, particularly Lactobacillus sp. and Bifidobacterium sp. However, other organisms used as probiotics in humans include Escherichia coli, Streptococcus sp., Enterococcus sp., Bacteroides sp., Bacillus sp., Propionibacterium sp. and various fungi. Some probiotic preparations contain mixtures of more than one bacterial strain. Probiotics have been examined for their effectiveness in the prevention and treatment of a diverse spectrum of gastrointestinal disorders such as antibiotic-associated diarrhea (including Clostridium difficile-associated intestinal disease), infectious bacterial and viral diarrhea (including diarrhea caused by rotavirus, Shigella, Salmonella, enterotoxigenic E. coli, Vibrio cholerae and human immunodeficiency virus/acquired immunodeficiency disorder, enteral feeding diarrhea, Helicobacter pylori gastroenteritis, sucrase maltase deficiency, inflammatory bowel disease, irritable bowel syndrome, small bowel bacterial overgrowth and lactose intolerance. Probiotics have been found to inhibit intestinal bacterial enzymes involved in the synthesis of colonic carcinogens. There are many mechanisms by which probiotics enhance intestinal health, including stimulation of immunity, competition for limited nutrients, inhibition of epithelial and mucosal adherence, inhibition of epithelial invasion and production of antimicrobial substances. Probiotics represent an exciting prophylactic and therapeutic advance, although additional investigations must be undertaken before their role in intestinal health can be delineated clearly.
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PMID:The role of probiotic cultures in the control of gastrointestinal health. 1072 14

We report the complete nucleotide sequence and characterization of a cryptic plasmid, pHLHK26, recovered from a strain of Laribacter hongkongensis isolated from a patient with community acquired gastroenteritis. pHLHK26 consists of 8700 bp, with G + C content 51.3%. The copy number (mean +/- SD) is 0.57 +/- 0.07 and it is stable after four passages (about 240 generations) in the absence of selection. There is a predicted origin of replication that consists of a DnaA box and five 22-bp direct repeats. pHLHK26 has four ORFs with two genes encoded in the sense direction and the other two in antisense direction. These four ORFs encode a putative plasmid partitioning protein of the ParA family, a putative protein that contains putative ADP-ribose 1"-phosphatase activity belonging to the Appr-1-p processing enzyme family, a putative recombinase (TniR) of the resolvase/invertase family, and a putative replication protein, respectively. We speculate that pHLHK26 is a theta, possibly Class A, replicative plasmid, as it contains an origin of replication with AT-rich region, a number of iterons and a DnaA box and a gene that encodes a replicative protein most homologous to those of other theta replicative plasmids and it shares eight of the nine positions of the consensus sequence TTAT(C/A)CA(C/A)A (TTTTCCACA in pHLHK26) in the DnaA boxes observed in other classical examples of Class A plasmids of this group.
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PMID:Characterization of a novel cryptic plasmid, pHLHK26, in Laribacter hongkongensis. 1761 58