Rye bread improves bowel function and decreases the concentrations of some compounds that are putative colon cancer risk markers in middle-aged women and men.
(65/970)
Cereal fiber may reduce the risk of colorectal cancer by diluting colonic contents due to increased fecal output, by accelerating intestinal transit, by increasing fecal frequency and by altering bacterial metabolism. The effects of whole-meal rye bread on some putative colon cancer risk markers were investigated in 17 healthy Finnish subjects using a randomized crossover trial with two 4-wk bread consumption periods and a 4-wk washout period between the bread periods. White wheat bread was used as a control. Test breads covered a minimum of 20% of the daily energy intake (range, 4330-14, 033 kJ/d). Intestinal transit time, stool weight, fecal bacterial enzyme activities and short-chain fatty acid, ammonia, diacylglycerol (DAG) and bile acid concentrations in feces (expressed per gram wet feces) were measured. Whole-meal rye bread significantly increased fecal output and fecal frequency and shortened mean intestinal transit time compared with wheat bread in both women and men. Activities of beta-glucuronidase and beta-glucosidase (expressed per gram wet feces) were significantly lower in men and urease activity significantly higher in women during the rye bread period (RBP). Fecal butyrate concentration was higher during the RBP in men. Fecal ammonia and DAG concentrations did not differ between bread periods. Fecal total and secondary bile acid concentrations were significantly lower during RBP in both women and men. This study shows that whole-meal rye bread significantly improves bowel function in healthy adults and may decrease the concentration of some compounds that are putative colon cancer risk markers. (+info)
Parkinsonism: differential age-trend in Helicobacter pylori antibody.
(66/970)
BACKGROUND: Parkinsonism is associated with prodromal peptic ulceration. Dopamine antagonists provoke experimental ulcer, dopaminergic agents protect, and might inhibit growth of Helicobacter pylori. OBJECTIVE: To describe the relationship between H. pylori serology and parkinsonism. METHODS: Serum H. pylori anti-urease-IgG antibody was measured in 105 people with (idiopathic) parkinsonism, 210 without, from same locality. None had received specific eradication therapy. RESULTS: Controls showed a birth-cohort effect: antibody titre rose from 30 to 90 years (P < 0. 001). Parkinsonism obliterated this (disease status. age interaction, P < 0.05), the differential age trend not being attributable to social class. Those with diagnosed parkinsonism were more likely to be seropositive (odds ratio 2.04 (95% CI: 1.04, 4.22) P < 0.04) before 72.5 years. Overall, titre fell (P=0.01) by 5 (1, 9)% per unit increase in a global, 30-point rating (median 14 (interquartile range 10.5, 17)) of disease severity. No individual category of anti-parkinsonian medication (92% taking) had a differential lowering effect. CONCLUSIONS: Higher prevalence of seropositivity in parkinsonism, before 8th decade, may be due to host susceptibility/reaction, or, conversely, infection with particular H. pylori strain(s) lowering dopaminergic status. Absence of a birth cohort effect in parkinsonism, despite similar social class representation, may be consequent on eradication, spontaneous (gastric atrophy) or by anti-parkinsonian medication. (+info)
Genetic characterization of DNA region containing the trh and ure genes of Vibrio parahaemolyticus.
(67/970)
We have demonstrated that possession of the gene for thermostable direct hemolysin-related hemolysin (trh) coincides with the presence of the urease gene among clinical Vibrio parahaemolyticus strains and that the location of the two genes are in close proximity on the chromosome. Here, we cloned and sequenced the 15,754-bp DNA region containing the trh gene and the gene cluster for urease production from the chromosome of clinical V. parahaemolyticus (TH3996). We found 16 open reading frames (ORFs) and a lower G+C content (41%) compared with the total genome of this bacterium (46 to 47%). The ure cluster consisted of eight genes, namely, ureDABCEFG and ureR. ureR was located 5.2 kb upstream of the other seven genes in the opposite direction. The genetic organization and sequences of the ure genes resembled those found in Proteus mirabilis. Between ureR and the other ure genes, there were five ORFs, which are homologous with the nickel transport operon (nik) of Escherichia coli. We disrupted each of the ureR, ureC, and nikD genes in TH3996 by homologous recombination and analyzed the phenotype of the mutants. In the presence of urea these mutant strains had dramatically less urease activity than the strain they were derived from. Disruption of ureR, nikD, or ureC, however, had no effect on TRH production. The DNA region containing the trh, nik, and ure genes was found in only trh-positive strains and not in Kanagawa phenomenon-positive and environmental V. parahaemolyticus strains. At the end of the region, an insertion sequence-like element existed. These results suggest that the DNA region was introduced into V. parahaemolyticus in the past through a mechanism mediated by insertion sequences. This is the first reported case that the genes for an ATP-binding cassette-type nickel transport system, which may play a role in nickel transport through bacterial cytoplasmic membrane, are located adjacent to the ure cluster on the genome of an organism. (+info)
Unusual Enterobacteriaceae: a Salmonella cubana that is urease positive.
(68/970)
This is the first report of a naturally occurring Salmonella that is urea positive. The strain was identified as Salmonella cubana and it was typical in all biochemical, serological, and bacteriophage reactions, except that is produced urease strongly. (+info)
Effects of supplemental zinc and manganese on ruminal fermentation, forage intake, and digestion by cattle fed prairie hay and urea.
(69/970)
One in vitro and one in vivo metabolism experiment were conducted to examine the effects of supplemental Zn on ruminal parameters, digestion, and DMI by heifers fed low-quality prairie hay supplemented with urea. In Exp. 1, prairie hay was incubated in vitro for 24 h with five different concentrations of supplemental Zn (0, 5, 10, 15, and 20 ppm) and two concentrations of supplemental Mn (0 and 100 ppm), both provided as chloride salts. Added Mn increased (P < 0.02) IVDMD, but added Zn linearly decreased (P < 0.03) IVDMD. Added Zn tended to increase the amount of residual urea linearly (P < 0.06) at 120 min and quadratically (P < 0.02) at 180 min of incubation, although added Mn counteracted these effects of added Zn. Six 363-kg heifers in two simultaneous 3 x 3 Latin squares were fed prairie hay and dosed once daily via ruminal cannulas with urea (45 or 90 g/d) and with Zn chloride to provide the equivalent of an additional 30 (the dietary requirement), 250, or 470 ppm of dietary Zn. After a 7-d adaptation period, ruminal contents were sampled 2, 4, 6, 12, 18, 21, and 24 h after the supplement was dosed. Supplemental Zn did not alter prairie hay DMI (mean = 4.9 kg/d) or digestibility, although 470 ppm added Zn tended to decrease (P < 0.06) intake of digestible DM, primarily due to a trend for reduced digestibility with 470 ppm supplemental Zn. Zinc x time interactions were detected for both pH (P = 0.06) and NH3 (P = 0.06). At 2 h after dosing, ruminal pH and ruminal ammonia were linearly decreased (P < 0.05; P < 0.01) by added Zn. At 5 h after feeding, ruminal pH was linearly increased (P < 0.05) by added Zn, suggesting that added Zn delayed ammonia release from urea. The molar proportion of propionate in ruminal fluid was linearly and quadratically increased (P < 0.02; P < 0.01) whereas the acetate:propionate ratio was linearly and quadratically decreased (P = 0.02; P < 0.05) by added Zn. Through retarding ammonia release from urea and increasing the proportion of propionate in ruminal VFA, Zn supplementation at a concentration of 250 ppm may decrease the likelihood of urea toxicity and increase energetic efficiency of ruminal fermentation. (+info)
Review article: the control of gastric acid and Helicobacter pylori eradication.
(70/970)
This review focuses on the gastric acid pump as a therapeutic target for the control of acid secretion in peptic ulcer and gastro-oesophageal reflux disease. The mechanism of the proton pump inhibitors is discussed as well as their clinical use. The biology of Helicobacter pylori as a gastric denizen is then discussed, with special regard to its mechanisms of acid resistance. Here the properties of the products of the urease gene clusters, ureA, B and ureI, E, F, G and H are explored in order to explain the unique location of this pathogen. The dominant requirement for acid resistance is the presence of a proton gated urea transporter, UreI, which increases access of gastric juice urea to the intrabacterial urease 300-fold. This enables rapid and continuous buffering of the bacterial periplasm to approximately pH 6.0, allowing acid resistance and growth at acidic pH in the presence of 1 mM urea. A hypothesis for the basis of combination therapy for eradication is also presented. (+info)
The elimination of urease activity in Streptococcus faecium as evidence for plasmid-coded urease.
(71/970)
A strain of Streptococcus faecium from the sheep rumen showed spontaneous loss of urease activity when subcultured at the normal rumen temperature of 38 degrees C, although in mixed cultures in vivo or in vitro loss of urease was not apparent. The rate of loss of urease in pure cultures was increased at incubation temperatures above 38 degrees C, but loss was never complete. However, at temperatures below 38 degrees C loss was greater, and at 22 or 18 degrees C the urease was completely eliminated. Incubation with sodium dodecyl sulphate (0-002%) or ethidium bromide (2-5 X 10(-5)M) caused complete loss of urease activity. The urease activity was also eliminated when the streptococcus was grown aerobically, and this loss of activity was irreversible. It is suggested that the urease activity is controlled by a plasmid gene and that aeration, low growth temperature and chemical agents 'cure' the streptococcus of the plasmid. Attempts to demonstrate the presence of covalently closed circular extrachromosomal DNA by caesium chloride-ethidium bromide equilibrium density-gradient centrifugation were unsuccessful. (+info)
Analysis of urease expression in Actinomyces naeslundii WVU45.
(72/970)
The hydrolysis of urea by ureases of oral bacteria in dental plaque can cause a considerable increase in plaque pH, which can inhibit the development of dental caries. There is also indirect evidence that urea metabolism may promote the formation of calculus and that ammonia release from urea could exacerbate periodontal diseases. Actinomyces naeslundii, an early colonizer of the oral cavity and a numerically significant plaque constituent, demonstrates comparatively low levels of urease activity on isolation, so this organism has not been considered a major contributor to total oral urease activity. In this study it was observed that urease activity and urease-specific mRNA levels in A. naeslundii WVU45 can increase up to 50-fold during growth under nitrogen-limiting conditions. Using primer extension analysis, a putative, proximal, nitrogen-regulated promoter of the A. naeslundii urease gene cluster was identified. The functionality and nitrogen responsiveness of this promoter were confirmed using reporter gene fusions and 5' deletion analysis. The data indicated that regulation of urease expression by nitrogen availability in A. naeslundii may require a positive transcriptional activator. Plaque bacteria may experience nitrogen limitation when carbohydrates are present in excess. Therefore, based on the results of this study and in contrast to previous beliefs, strains of A. naeslundii may have the potential to be significant contributors to total plaque ureolysis, particularly during periods when there is an increased risk for caries development. (+info)