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13篇 您的检索式:作者名="Gearry R"
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1Probiotic effects on intestinal fermentation patterns in patients with irritable bowel syndrome显示文摘AIM: To determine whether Lactobacillus casei strain Shirota (Yakult ) can alter small intestinal bacterial overgrowth (SIBO), as tested by the lactulose breath test, and whether this is associated with changes in symptoms in irritable bowel syndrome (IBS). METHODS: 18 patients with IBS (Rome Ⅱ criteria), who showed an early rise in breath hydrogen with lactulose (ERBHAL), consumed 65 mL of Yakult daily for 6 wk. Lactulose breath test was repeated at the end of the treatment period. Symptoms were recorded daily using a 10 cm visual analogue scale. RESULTS: 14 patients completed the study, 9 (64%) had reversal of ERBHAL, with the median time of f irst rise in breath hydrogen increasing from 45 to 75 min (P = 0.03). There was no signifi cant improvement in the symptom score with probiotic therapy, except for wind (P=0.04). Patients commencing with at least moderate symptoms and who no longer had ERBHAL at the end of treatment, showed improvement in the overall symptoms scores [median fi nal score 5.3 (IQR3.9-5.9), 55% reduction; n=6] to a greater extent than those who had had persisting ERBHAL [final score 6.9 (5.0-7.0), 12% reduction; n = 5; P = 0.18]. CONCLUSION: Yakult is effective in altering fermentation patterns in the small bowel, consistent with reducing SIBO. The loss of ERBHAL was associated with reduced symptoms. The true interpretation of these fi ndings awaits a randomised, controlled trial.Jacqueline S Barrett Kim EK Canale Richard B Gearry Peter M Irving Peter R Gibson 2008World Journal of Gastroenterology2008,14,32:16
2Macrophage migration inhibitory factor gene polymorphisms in inflammatory bowel disease: An association study in New Zealand Caucasians and meta-analysis显示文摘AIM:To investigate the association of macrophage migration inhibitory factor(MIF)promoter polymorphisms with inflammatory bowel disease(IBD)risk.METHODS:One thousand and six New Zealand Caucasian cases and 540 Caucasian controls were genotyped for the MIF SNP-173G>C(rs755622)and the repeat polymorphism CATT5-8(rs5844572)using a predesigned TaqMan SNP assay and capillary electrophoresis,respectively.Data were analysed for single site and haplotype association with IBD risk and phenotype.Meta-analysis was employed,to assess cumulative evidence of association of MIF-173G>C with IBD.All published genotype data for MIF-173G>C in IBD were identified using PubMed and subsequently searching the references of all PubMed-identified studies.Imputed genotypes for MIF-173G>C were generated from the Wellcome Trust Case Control Consortium(and National Institute of Diabetes and Digestive and Kidney Diseases).Separate meta-analyses were performed on Caucasian Crohn’s disease(CD)(3863 patients,6031controls),Caucasian ulcerative colitis(UC)(1260 patients,1987 controls),and East Asian UC(416 patients and 789 controls)datasets using the Mantel-Haenszel method.The New Zealand dataset had 93%power,and the meta-analyses had 100%power to detect an effect size of OR=1.40 atα=0.05,respectively.RESULTS:In our New Zealand dataset,single-site analysis found no evidence of association of MIF polymorphisms with overall risk of CD,UC,and IBD or disease phenotype(all P values>0.05).Haplotype analysis found the CATT5/-173C haplotype occurred at a higher frequency in New Zealand controls compared to IBD patients(0.6 vs 0.01;P=0.03,OR=0.22;95%CI:0.05-0.99),but this association did not survive bonferroni correction.Meta-analysis of our New Zealand MIF-173G>C data with data from seven additional Caucasian datasets using a random effects model found no association of MIF polymorphisms with CD,UC,or overall IBD.Similarly,meta-analysis of all published MIF-173G>C data from East Asian datasets(416UC patients,789 controls)found no association of this promoter polymorphism with UC.James D Falvey Robert W Bentley Tony R Merriman Mark B Hampton Murray L Barclay Richard B Gearry Rebecca L Roberts 2013World Journal of Gastroenterology2013,19,39:9
3Single nucleotide polymorphism in the tumor necrosis factor-alpha gene affects inflammatory bowel diseases risk显示文摘AIM: To investigate the role that single nucleotide polymorphisms (SNPs) in the promoter of the tumour necrosis factor-alpha (TNF-α) gene play in the risk of inflammatory bowel diseases (IBDs) in a New Zealand population, in the context of international studies. METHODS: DNA samples from 388 patients with Crohn's disease (CD), 405 ulcerative colitis (UC), 27 indeterminate colitis (IC) and 201 randomly selected controls, from Canterbury, New Zealand were screened for 3 common polymorphisms in the TNF-α receptor: -238 G→A, -308 G→A and -857C→T, using a TaqmanR assay. A meta-analysis was performed on the data obtained on these polymorphisms combined with that from other published studies. RESULTS: Individuals carrying the -308 G/A allele had a significantly (OR = 1.91, χ2 = 17.36, P < 0.0001) increased risk of pancolitis, and a 1.57-fold increased risk (OR = 1.57, χ2 = 4.34, P = 0.037) of requiring a bowel resection in UC. Carrying the -857 C/T variant decreased the risk of ileocolonic CD (OR = 0.56, χ2 =4.32, P = 0.037), and the need for a bowel resection (OR = 0.59, χ2 = 4.85, P = 0.028). The risk of UC was reduced in individuals who were smokers at diagnosis, (OR = 0.48, χ2 = 4.86, P = 0.028). CONCLUSION: TNF-α is a key cytokine known to play a role in inflammatory response, and the locus for the gene is found in the IBD3 region on chromosome 6p21, known to be associated with an increased risk for IBD. The -308 G/A SNP in the TNF-α promoter is functional, and may account in part for the increased UC risk associated with the IBD3 genomic region. The -857 C/T SNP may decrease IBD risk in certain groups. Pharmaco- or nutrigenomic approaches may be desir- able for individuals with such affected genotypes.Lynnette R Ferguson Claudia Huebner Ivonne Petermann Richard B Gearry Murray L Barclay Pieter Demmers Alan McCulloch Dug Yeo Han 2008World Journal of Gastroenterology2008,14,29:7
4The role of S100A12 as a systemic marker of inflammation 显示文摘MEIJER B GEARRY R B DAY A S 2012Int J Inflam2012,3,:1
5Antibiotics associated with increased risk of new-onset Crohn's disease but not ulcerative colitis~ a meta-analysis显示文摘Ungaro R Bernstein CN Gearry R 2014Am J Gastroenterol2014,109,11:1
6Antibiotics associated with in- creased risk of new-onset Crohn's disease but not ulcerative colitis: a meta-analysis 显示文摘Ungaro R Bernstein CN Gearry R 2014Am J Gastroentero12014,109,11:1
7Thiopurine S-methyltransferase (TPMT) genotype does not predict adverse drug reactions to thiopurine drugs in patients with inflammatory bowel disease显示文摘Gearry R B Barclay M L Burt M J 2003Aliment Pharmacol Ther2003,18,4:1
8The role of SIOOA12 as a systemic marker of inflammation 显示文摘MEUER B GEARRY R B DAY A S 2012Int J Inflam2012,2012,90:1
9Preferences of inflammatory boweldisease patients for computerised versus face-to-face psychologicalinterventions显示文摘McCombie A Gearry R Mulder R 2014J Crohns Colitis2014,8,6:1
10The role of S100A12 as a sys- temic marker of inflammation 显示文摘Meijer B Gearry R B Day A S 2012Int J Inflam2012,2012,90:1
11Antibiotics associated with increased risk of new onset Crohn' s disease but not ulcerative colitis: a meta-analysis 显示文摘Ungaro R Bernstein CN Gearry R 2014Am J Gastroenterol2014,109,11:1
12Takayasu's arteritis and ulcerative colitis 显示文摘Gearry R Came P Frizelle F 2003NZ Med J2003,116,1170:1
13Thiopurine methyltransferase and 6-thioguanine nucleotide measurement:early experience of use in clinical practice显示文摘Gearry R Barclay M Roberts R 2005Int Med Jo2005,35,6:1
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