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4篇 您的检索式:作者名="Scott Merrell D"
    题名 作者 年代 出处 被引量
1Polymorphism in the interleukin-17A promoter contributes to gastric cancer显示文摘AIM:To evaluate the contribution of the G-197A polymorphism in the interleukin-17(IL-17)promoter region to gastric cancer risk in an Iranian population.METHODS:We performed a case control study using samples from 161 individuals with gastric cancer and171 healthy controls.For each individual,the G-197A genotype was determined by restriction fragment length polymorphism analysis of polymerase chain reaction-amplified fragments.Statistical analyses were performed to determine whether any demographic or behavioral factors,infection with Helicobacter pylori(H.pylori),or a particular G-197A genotype was associated with gastric cancer risk.RESULTS:We found that the G-197A genotype wassignificantly associated with increased gastric cancer risk(P=0.001).Patients who were homozygous(AA)at position-197 were 2.9 times more likely to develop disease(95%CI:1.56-5.4;P=0.001).Furthermore,logistic regression analysis revealed that the presence of a single A allele increased the risk of gastric cancer up to 1.7-fold(95%CI:1.26-2.369;P=0.001).This association was observed for early stage gastric adenocarcinomas only,and was not linked to H.pylori infection.CONCLUSION:These results suggest that carrying one or more G-197A polymorphisms at position-197 in the IL-17 promoter region significantly increases gastric cancer risk in this patient population.Alireza Rafiei Vahid Hosseini Ghasem Janbabai Abuzar Ghorbani Abulghasem Ajami Touraj Farzmandfar Maedeh Darzyani Azizi Jeremy J Gilbreath D Scott Merrell 2013World Journal of Gastroenterology2013,19,34:7
2Inducible nitric oxide synthetase genotype and Helicobacter pylori infection affect gastric cancer risk显示文摘AIM:To investigate the association of the inducible nitric oxide synthetase(iNOS) C150T polymorphism with Helicobacter pylori(H.pylori) infection and gastric cancer(GC) risk in Iran.METHODS:In order to determine whether there was a correlation between iNOS genotype and GC in Iran,we conducted a case-control study using samples from 329 individuals.For each sample,the C150T iNOS polymorphism was genotyped by polymerase chain reaction(PCR) and restriction digestion.Patients were grouped by cancer presence,demographic and behavior characteristics,and H.pylori infection status.Statistical tests were conducted to determine whether any behavioral factors or a particular iNOS genotype was associated with GC in the study population.RESULTS:In this population,we found that smoking,hot beverage consumption,a familial history of GC and H.pylori infection status were significantly associated with GC development(P = 0.015,P < 0.001,P = 0.0034,and P < 0.015,respectively).The distribution of the C150T iNOS genotypes among the two study groups was not statistically significant alone,but was impacted by H.pylori infection status.When compared to the non-H.pylori infected group,cancer patients who had a heterozygous CT genotype and were also infected with H.pylori were 2.1 times more at risk of developing GC [odds ratio(OR) = 2.1,P = 0.03] while those with a homozygous TT genotype and infected with H.pylori were 5.0 times more at risk of developing GC(OR = 5.0,P = 0.029).In contrast,this association was not seen in patients in the control group.CONCLUSION:A CT or TT polymorphism at position 150 in the iNOS gene significantly increases the risk of GC and may be a marker for GC susceptibility.Alireza Rafiei Vahid Hosseini Ghasem Janbabai Bahman Fazli Abulghasem Ajami Zahra Hosseini-khah Jeremy J Gilbreath D Scott Merrell 2012World Journal of Gastroenterology2012,18,35:4
3Host-induced epidemic spread of the cholera bacterium显示文摘Scott Merrell D Butler SM Qadri F 2002Nature2002,417,6:1
4Response to Abadi and Kusters, World J Gastroenterol 19: 429-430显示文摘In a recent study, Rafiei et al, reported a link between a C150T polymorphism in the human inducible nitric oxide gene and Helicobacter pylori infection as a risk factor for gastric cancer among an Iranian population. Subsequently, Abadi and Kusters published a letter to the editor questioning the validity of the study because of a supposed flaw in primer design. Here we respond to the claims of Abadi and Kusters and show that the results reported in the original article are valid.Alireza Rafiei Jeremy J Gilbreath D Scott Merrell 2013World Journal of Gastroenterology2013,19,23:0
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