Associations between Key words: Helicobacter pylori infection -Interleukin 1 -Lifestyle factorsHelicobacter pylori (HP) infection, a well-known risk factor for stomach cancer, depends largely on sanitary conditions, especially in childhood. [1][2][3] There are still substantial differences in childhood prevalence between developed and developing countries, ranging from 4% to 82% reportedly.2) An increase in infected individuals with age is observed in many developed countries, which is considered to be due to a cohort effect. 1) Although there is no doubt that exposure to the bacterium increases the infection rate in the population, host susceptibility is also an important factor. Even after an ordinary level of HP exposure, uninfected persons still seem to exist in any population. In addition, spontaneous eradication after childhood infection may be influenced by host factors.Polymorphisms of interleukin-1β gene (IL-1B) and interleukin 1 receptor antagonist gene (IL-1RN) were reportedly associated with stomach cancer risk for a population from Poland. 4) IL-1β is a pro-inflammatory cytokine with multiple biological effects, 5) and is induced by HP infection.6) IL-1B has three diallelic polymorphisms at −511, −31, and 3954 base pairs (bp) from the transcriptional start site. Though the differences were not statistically significant, persistent HP infection was observed for 60% of individuals harboring the C/C genotype (n=58) at −31 of IL-1B, for 73% of those with the C/T genotype (n=67), and for 79% of those with the T/T genotype (n=24) in a population from Scotland.4) The T allele at −31 forms a TATA box, suspected of enhancing gene expression. The study reported that the polymorphism at −511 linked tightly with the polymorphism at −31, and therefore quite similar findings on the risks of stomach cancer and HP infection were obtained for IL-1B C−511T. The polymorphism at 3954 was not associated with the risks of stomach cancer and HP infection in the study.4) IL-1RN has a penta-allelic 86-bp tandem repeat polymorphism in intron 2, which was found to affect IL-1β production in vitro, 7) but it was not associated with HP infection. 4) IL-1α is another member of IL-1, which is encoded by IL-1A. It is primarily a cytosolic cytokine. About 10% or 15% is myristoylated and transported to the cell surface (membrane IL-1), but it is not detected in the serum under normal conditions. 5) IL-1A was reported to have three polymorphisms; C−889T, 46-bp variable number of tandem 6 To whom correspondence should be addressed.

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Although nicotine dependence is one of the primary reasons why smokers cannot quit smoking, nicotine cannot explain all of the psychopharmacological effects of tobacco smoke. Accumulating evidence points to potent inhibition of monoamine oxidase (MAO) which metabolizes neurotransmitters relating to additive behaviour. We have therefore investigated the association between smoking behaviour and MAO ( variable number of tandem repeat in the promoter region and A644G) polymorphisms. The genotypes were examined in 504 Japanese outpatients (217 men and 287 women) who visited Aichi Cancer Centre Hospital. The age-adjusted odds ratios (aORs) were estimated by a logistic model. Among males, we did not find a significant association of the smoking habit with either of the polymorphisms. The median Fargastrom test for nicotine dependence (FTND) score among male current smokers was significantly higher with than without the 4-repeat allele (5.8 and 4.7, respectively). The aOR of FTND 6 versus FTND 6 was 2.72 (95% confidence interval 1.13-6.50) for males with the 4-repeat allele. Among females, the aOR of being current smokers compared to never smokers was 0.49 (0.26-0.93) for individuals with the 4-repeat allele. Our results indicate that the polymorphisms of influence the smoking habit for female, as well as the nicotine dependence and smoking initiation for male smokers. These findings among male smokers support the view that MAO affects a smokers' requirement for nicotine and may explain why some people are predisposed to tobacco addiction and why some individuals find it difficult to stop smoking.

This paper lists the genotype frequencies of 50 polymorphisms of 37 genes (ALDH2, ADRB2, ADRB3, COMT, CD36, CXCR2, CCND1, COX2, CYP2A6, CYP17, CYP19, IGF1, IL-1A, IL-1B, IL-1RN, IL-1R1, IL-6, IL-8, IL-10, LEP, Le, L-myc, MPO, MTR, MTHFR, MAO-A, NQO1, OGG1, p53, p73, Se, SRD5A2, TGF-B, TNF-A, TNF-B, XPD, and XRCC1) and 6 sets of combined genotype frequencies for 241 non-cancer Japanese outpatients. Though the genotype frequencies of 25 polymorphisms have already been reported in our previous papers, 15 polymorphisms (CD36 A52C, CXCR2 C785T, CCND1 G870A, IGF1 C/T at intron 2 and G2502T, IL-1A 46-bp VNTR, IL-1R1 C-116T, IL-6 Ins/Del 17C, IL-8 A-278T and C74T, IL- 10 T-819C, LEP A-2548G, SRD5A2 2-bp VNTR, XPD Lys751Gln, and XRCC1 Arg399Gln) and six sets of combined genotype frequencies (IL-1B C-31T and IL-1A C-889T, IL-1B C-31T and IL-1RN 86-bp VNTR, IL-1B C-31T and IL-1R1 C-116T, TNF-A G-308A and TNF-B A252G, SRD5A2 Val89Leu and 2-bp VNTR, and XRCC1 Arg399Gln and XPD Lys751Gln) were reported in this paper for the first time for Japanese. Although microarray technology will produce this kind of information in near future, this is the first document that reports the genotype/allele frequencies among Japanese for an archival purpose.