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S M Burridge

Publications and source records attributed to S M Burridge.

8 recordsLinked to original sources
PubMed1995

New members of the 3 beta-hydroxysteroid dehydrogenase gene family.

Several bands of hydridization are detected when southern blots of human genomic DNA are proved with cDNA of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) type I. Two experimental approaches were adopted to estimate the size of the 3 beta-HSD gene family. Firstly, primer designed to amplify 3 beta-HSD type I and II genes were found on occasion to amplify DNA products of appropriate length but which were resolved as distinct sequences by denaturing gradient gel electrophoresis (DGGE). Five of these novel bands were cloned and their sequences were found to be closely related to 3 beta-HSD types I and II. Secondly, 57 genomic clones were selected from two lambda genomic libraries by hybridization with exonic probes of 3 beta -HSD type I. These were screened for novel members of the gene family by pcr amplification using various combinations of PCR primers to the type I and II genes, particularly those primers that previously amplified novel PCR products from genomic DNA. Amplification products from (lambda) clones were screened for novel sequences by DGGE. As a result of these approaches, at least five new members of the 3 beta-HSD gene family were found, one of which locates to the 3 beta -HSD type I and II gene cluster on 1p13. The existence of additional closely related but distinct members of the gene family should be recognized as a potential complication when screening PCR fragments for mutations in the type I and II genes. DGGE was found to be an exceedingly rapid means of screening amplification products from (lambda) clones to search for novel members of the gene family.

3-Hydroxysteroid Dehydrogenases↗
PubMed1992

Does a previous course of tripotassium dicitrato bismuthate affect the subsequent chances of successful Helicobacter pylori eradication?

We have performed a retrospective study of 103 patients with either peptic ulcer or non-ulcer dyspepsia, infected with metronidazole-sensitive strains of Helicobacter pylori (H. pylori), who were treated with a combination of tripotassium dicitrato bismuthate and metronidazole for a period of at least two weeks. Dual therapy with tripotassium dicitrato bismuthate plus metronidazole showed similarly high eradication rates (greater than or equal to 80%) of H. pylori from patients irrespective of age, gender or clinical diagnosis. Most importantly, dual therapy achieved a similar eradication rate of H. pylori infection in 41 patients who had previously been treated with tripotassium dicitrato bismuthate alone or in combination with an antibiotic other than metronidazole. It therefore appears that H. pylori does not become resistant to treatment with tripotassium dicitrato bismuthate.

Adult↗
PubMed1992

Experience with 'triple' anti-Helicobacter pylori eradication therapy: side effects and the importance of testing the pre-treatment bacterial isolate for metronidazole resistance.

At the 1990 World Congresses of Gastroenterology, the Working Party on Helicobacter pylori (H. pylori) recommended that, in suitable patients, the bacterium should be eradicated using a therapeutic regimen comprising a bismuth salt, tetracycline and metronidazole for two weeks. We have treated 40 patients infected with H. pylori with 'triple' therapy consisting of 120 mg tripotassium dicitrato bismuthate q.d.s., 500 mg tetracycline q.d.s. and 400 mg metronidazole t.d.s. for two weeks. The success rate, in terms of bacterial eradication, was 19/21 (90.5%) in patients with metronidazole-sensitive organisms, compared with only 6/19 (31.6%) in patients whose H. pylori were resistant to metronidazole (P less than 0.01). Side effects, particularly diarrhoea and vomiting/nausea, were common: 23/40 patients reported such symptoms during the 14-day course of therapy. Fifteen of these 23 patients completed the entire 14-day course, although suffering from significant side effects, while the remaining eight patients had to discontinue the treatment because side effects became intolerable. If a form of triple therapy is going to be widely used to eradicate H. pylori infection, the regimen will have to be simpler, shorter, produce fewer side effects and be more effective in patients with metronidazole-resistant bacteria.

Adult↗
PubMed1992

Short report: omeprazole plus antibiotic combinations for the eradication of metronidazole-resistant Helicobacter pylori.

Twenty-eight Helicobacter pylori-positive patients with metronidazole-resistant isolates and 25 with metronidazole-sensitive isolates were treated for 14 days with 40 mg omeprazole nocte plus 500 mg amoxycillin t.d.s. Eradication of H. pylori, defined as absence of the organism one month after cessation of treatment, was assessed using the [14C]urea breath test. The eradication rate in patients with metronidazole-resistant isolates was 14/28 (50%) while that in patients was metronidazole-sensitive isolates was 12/25 (48%). In contrast to these encouraging eradication rates, very poor results were obtained with a 7-day course of omeprazole (40 mg nocte) in combination with erythromycin ethylsuccinate (500 mg q.d.s.) and tripotassium dicitrato bismuthate tablets (120 mg q.d.s.). The latter eradication rates were 3/20 (15%) in patients taking erythromycin tablets and 3/19 (16%) in those taking a liquid formulation of erythromycin. All treatment regimens were well tolerated and all patients completed the prescribed course of therapy.

Adult↗
PubMed1980

Ammonia production by intestinal bacteria: the effects of lactose, lactulose and glucose.

Ammonia production by eight groups of intestinal bacteria was measured, and the effect on ammonia production of lowered pH and ambient ammonia concentration was determined. Endogenous ammonia production from bacterial protoplasm was also examined. To examine the mechanisms by which fermentable substrates reduce ammonia formation in a faecal incubation system, the effect of lactose, lactulose or glucose on ammonia release by pure cultures of intestinal bacteria was studied. The largest amounts of ammonia were generated by gram-negative anaerobes, clostridia, enterobacteria, and Bacillus spp. Gram-positive non-sporing anaerobes, streptococci and micrococci formed modest amounts, and lactobacilli and yeasts formed very little ammonia. All groups of bacteria formed less ammonia at pH 5.0 than at pH 7.0 and production of ammonia was not inhibited when 30 mmol ammonia/litre was included in the medium. Small amounts of ammonia were formed due to endogenous metabolism of bacterial cells. Washed cell suspensions of four isolates of Bacteroides, one clostridial isolate and two streptococcal isolates formed less ammonia from alanine, methionine or histidine after growth in the presence of either lactose or lactulose. In contrast, the Bacteroides isolates formed more ammonia from aspartate than from either lactose or lactulose. Also, cultures of gram-negative anaerobes and enterobacteria, and to a lesser extent clostridia and streptococci, formed significantly less ammonia in nutrient broth when lactose, lactulose or glucose was included in the medium. This decrease in ammonia formation was not due to a fall in pH of the medium. Ammonia production by gram-positive non-sporing anaerobes was not affected by carbohydrate fermentation. These results suggest that gram-negative anaerobic bacteria make a major contribution to ammonia generated from peptides and amino acids in vivo, and that ammonia may be formed from bacterial cells in the colon. Fermentation of lactose and lactulose may repress the formation and inhibit the activity of enzymes responsible for ammonia release. In the human colon these substrate effects may decrease the amount of ammonia available to exert a toxic effect on the host, and thus contribute to the beneficial effects of lactulose when it is used in the treatment of portosystemic encephalopathy.

Amino Acids↗
PubMedDate not supplied

Upper gastrointestinal endoscopy: a prospective randomized study comparing continuous supplemental oxygen via the nasal or oral route.

We have examined the efficacy of supplemental oxygen in preventing episodes of significant arterial desaturation (SpO2 less than 90%) during upper gastrointestinal endoscopy. We have compared the effects of 2 liters.min-1 of oxygen given orally via the bite-guard with the same flow rate via nasal cannulas and have also examined the effects of pre-oxygenation. Results of this study at a flow rate of 2 liters.min-1 have been compared with previously published results at a flow rate of 3 liters.min-1. Although in this study fewer episodes of desaturation were seen in the orally supplemented group compared with the nasal group, the difference observed was not statistically significant. Pre-oxygenation significantly reduced episodes of desaturation (SpO2 less than 90%, p less than 0.01) and prevented SpO2 falls below 85% in all patients studied. Supplemental oxygen given at a rate of 2 liters.min-1 was as effective as that given at a rate of 3 liters.min-1 in preventing significant desaturation, as previously defined, during the procedure. We therefore recommend the use of supplemental oxygen at a flow rate of 2 liters.min-1 in all high risk patients and conclude that the oral route has practical advantages and is at least as effective as nasal cannulas.

Endoscopy, Gastrointestinal↗
PubMedDate not supplied

Variation in the expression of human 3 beta-hydroxysteroid dehydrogenase.

Polymorphic genetic variation shows that the genes for human 3 beta-hydroxysteroid dehydrogenases (3 beta-HSD) types I and II are closely linked. The type II mutations A82T, S100N and L173R are associated with male pseudohermaphroditism and A82T is associated, with variable penetrance, with female premature puberty. When expressed in vitro A82T showed less than 5% of normal activity and L173R showed a 30-50% reduction in activity. PCR experiments and direct genomic cloning show that there is a larger family of 3 beta-HSD sequences which require to be tested for expression. The phenomenon of epitopic heterogeneity of 3 beta-HSD is discussed and is now shown to apply to testicular Leydig cells as well as extrauterine trophoblast. RT-PCR analyses indicate that the phenomenon is most likely to be due to post-translational modification affecting the carboxytermini 3 beta-HSD types I and II. This phenomenon may reflect a further level at which enzyme activity is regulated.

3-Hydroxysteroid Dehydrogenases↗