Interaction between dietary factors and Helicobacter pylori infection in noncardia gastric cancer: a population-based case-control study in China.

BACKGROUND: The aim of this study was to investigate the relationships among Helicobacter pylori, dietary factors, and the risk of noncardia gastric cancer in a hospital-based case-control study in China. METHODS: A case-control study of noncardia gastric cancer was performed at 3 hospitals in Xi'an, China, between September 2008 and July 2010. Participants were 257 men and women with histologically diagnosed primary noncardia gastric cancer and 514 sex- and age-matched (± 5 years) control subjects selected from the communities where the cases were living when diagnosed. A questionnaire was used to obtain information regarding potential risk factors, including diet, and blood samples were obtained to examine H pylori infection status. RESULTS: Positive H pylori status (odds ratio [OR], 3.2; 95% confidence interval [CI], 0.8-5.9) and high consumption of pickled foods (OR, 27.1; 95%, 8.7-79.1) appeared to increase the risk of noncardia gastric cancer, whereas high consumption of vegetables (OR, 0.3; 95% CI, 0.1-0.89), fruits (OR, 0.2; 95% CI, 0.09-0.81), and soya products (OR, 0.04; 95% CI, 0.01-0.3) appeared to decrease the risk. Consumption of meat, cereals, tubers, eggs, oils, nuts, fish, fresh fruit, and red meat was not clearly associated with risk. Effect modification was observed, such that a relatively high consumption of fruit and vegetables appeared to attenuate the association of H pylori with risk of noncardia gastric cancer (p < 0.05). CONCLUSIONS: Our data suggest that noncardia gastric cancer is highly preventable through modifications in dietary habits. Given the prevalence of H pylori infection worldwide, information regarding potential interaction between H pylori and lifestyle factors in gastric cancer development, including the dietary factors examined in our study, may prove valuable in future efforts at prevention.

[Synergistic effect of dichlorvos, dimethoate and malathion mixture on reproduction toxicity in male mice].

OBJECTIVE: To evaluate the reproduction toxicity of the mixture composed of dichlorvos, dimethoate and malathion synergistic effect on male mice, and further explore its possible mechanisms. METHODS: The 105 male mice were divided into 7 groups, including control (0 mg/kg), mix low (10.8 mg/kg), mix medium (21.5 mg/kg), mix high dose (43.0 mg/kg), dichlorvos (5.1 mg/kg), dimethoate (12.6 mg/kg) and malathion (25.3 mg/kg) group. The oral gavage for successive 35 days, and the mice were sacrificed on the 36(th) day. The body weight, and the quantity, activity and morphology of sperms were examined. The levels of sexual hormone were measured, including testosterone (T), follicle stimulating hormone (FSH), luteinizing hormone (LH) and estradiol (E(2)). Pathological changes of testicle and epididymis were observed by morphology, pathology and electron microscope. RESULTS: After 14 days exposure, the body weights of the mice were lower in the mix-high dose group ((22.40 ± 3.07) g) than those in control group ((26.73 ± 2.82) g) (P < 0.05). After 28 days exposure, the body weights of the mice were also lower in the mix-medium dose group ((30.00 ± 4.93) g) than those in control group ((33.13 ± 3.29) g) (P < 0.05). The sperm counts and sperm motility decreased significantly as the toxic concentration arised. Comparing to control group ((373.33 ± 14.65)×10(6)/g weight of epididymis and (75.17 ± 7.68)%), the spermatozoa count and sperm motility had decreased in mix-medium and mix-high dose groups ((321.17 ± 18.19)×10(6)/g weight of epididymis, (225.00 ± 19.67)×10(6)/g weight of epididymis, and (64.67 ± 9.91)%, (57.83 ± 9.66)%), and the sperm abnormality rates were higher in mix-medium and mix-high groups ((43.33 ± 8.66)‰ and (55.00 ± 13.80)‰) comparing to those in control group ((32.67 ± 8.17)‰). Compared to those in control group (FSH (1.41 ± 0.20), E(2)(17.32 ± 2.72), LH (8.75 ± 1.32) and T (3.45 ± 0.80) nmol/L), the serum level of FSH (3.14 ± 0.62) and (3.85 ± 0.37) nmol/L, E(2) (36.81 ± 6.68) and (43.76 ± 9.82) nmol/L in mix-medium and mix-high dose group increased (P < 0.01), while the level of LH (5.21 ± 1.23) and (4.27 ± 1.09) nmol/L and T (1.37 ± 0.38) and (0.73 ± 0.18) nmol/L decreased (P < 0.01). The morphological and ultramicrostructure results of testicle and epididymis indicated that the mature sperm numbers were decreased, and the cacoplastic sperm head and the tail of spermatozoon were observed in mix-high dose groups. CONCLUSION: The dichlorvos, dimethoate and malathion mixture had synergistic reproductive toxicity to the testicle and epididymis structure and function, and thus leading to the process of generation cell cytopoiesis abnormalities, simultaneously the hypothalamus-pituitary-gonad axis were also affected and thus resulted in parasecretion.

[The study of insulin resistance and leptin resistance on the model of simplicity obesity rats by curcumin].

OBJECTIVE: To evaluate the insulin and leptin resistance of curcumin on simplicity obesity rats. METHODS: All 50 SPF grade healthy Sprague-Dawley male initial weaning rats were used for two groups in stratified sampling by weight: 30 in treated group and 20 in control group. They were assigned to the following treatment for 8 weeks: the treated group was fed with high-fat food and the control group was fed with normal food. Eight weeks later, adiposity model rats were prepared. Groups: adiposity model rats were divided into 3 groups: model + low curcumin (1.25 g/kg), model + high curcumin (5.00 g/kg) and a model group. In addition, there also had a normal control and a control + high curcumin (5.00 g/kg) group. Ten rats in every group and all given ground feed. After intragastric administration in different doses of curcumin 4 weeks, the effects and pathological changes were observed by the blood sugar, insulin, leptin and TNF-alpha, pathology and transmission electron microscope of pancreatic gland. RESULTS: Given 4 weeks the different dose of curcumin on the simplicity obesity rats, the significant diminished weight (435.0 +/- 37.6) g and content of lipocyte (4.78 +/- 1.87) g as compared with the obesity model control (492.3 +/- 14.8) g and (8.94 +/- 1.88) g (t values were 4.484 and 4.961 respectively, P < 0.01), level of blood sugar (4.50 +/- 0.09) mmol/L, insulin (7.43 +/- 0.65) mmol/L, leptin (3.40 +/- 0.39) mmol/L and TNF-alpha (2.42 +/- 0.19) ng/ml were significantly decreased than those of adiposity model rats (4.94 +/- 0.12) mmol/L, (9.30 +/- 0.21) mmol/L, (4.40 +/- 0.23) mmol/L and (2.86 +/- 0.49) ng/ml (t values were 8.297, 7.743, 6.247 and 2.368 respectively, P < 0.05), and there was no significant difference with the control group (4.30 +/- 0.14) mmol/L on the level of blood sugar (t = 0.399, P > 0.05). There were a lot of secretory granules with large sphere volume in beta cells of pancreatic island found by transmission electron microscope, and these secretory granules had a higher electron density than those in non-disposed groups. CONCLUSION: By diminishing the sediment of fat, relaxing the lymphatic return, and refraining the apoptosis of beta cells, the curcumin might significantly decrease the level of insulin resistance and leptin resistance caused by the high fat diet.

[Evaluating the impact of the second generation reproductive function on the established selenium and iodine deficiency rat models].

OBJECTIVE: To observe the affection of selenium and iodine deficiency on the reproductive function of male and female F2 rat with the established model. METHODS: Artificial synthesize feeds was used in our research. The healthy SD rat ceased lactation were chosen and randomly divided into three groups of lower selenium, lower iodine and two elements deficiency group and then raised in divided cages. The reproductive test of three generation was taken after evaluating the stability of the model. Meanwhile the fertility impact on the male and female rats in F2 was studied by observing the changes on sperm morphology, serum biochemical indexes, testicle pathology, fertility indexes, embryo osteogenesis and the viscera development. RESULTS: The animal models of lower selenium, lower iodine and the two elements deficiency were established successfully. The stability of three animal models was satisfied during the experiment of three generation reproduce test. Deficiency of selenium, iodine and both of them can all impact the reproductive function of male rats on its morphological index of sperm, biochemical index of sperm and morphological and pathological changes in testicle. They can also impact the reproductive function of female rats on the weight of the second generation of pregnant rats, the embryonic and organic development of the third generation. CONCLUSION: Deficiency of selenium and iodine can all impact the reproductive function on F2 model rats.

Interactions between pork consumption, CagA status and IL-1B-31 genotypes in gastric cancer.

AIM: To explore potential interactions among Helicobacter pylori (H. pylori), CagA status, interleukin (IL)-1B-31 genotypes, and non-cardiac gastric cancer (GC) risk. METHODS: A case-control study of non-cardia GC was performed at 3 hospitals located in Xi'an, China, between September 2008 and July 2010. We included 171 patients with histologically diagnosed primary non-cardia GC and 367 population based controls (matched by sex, age and city of residence). A standardized questionnaire was used to obtain information regarding potential risk factors, including pork consumption. H. pylori CagA status was assessed by enzyme-linked immunosorbent assay, and IL-1B-31 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Multivariate unconditional logistic regression was used to explore potential interactions among the factors. RESULTS: The CagA appeared to confer an increased risk of GC (OR = 1.81, 95%CI: 1.25-2.61). The main associations with IL-1B-31C allele here were 0.98 (95%CI: 0.59-1.63) for CC vs TT and 0.99 (95%CI: 0.64-1.51) for C Carriers vs TT. However, no associations were observed for CagA or IL-1B-31 genotype status among subjects who reported low pork consumption (P for interaction = 0.11). In contrast, high pork consumption and IL-1B-31C genotypes appeared to synergistically increase GC risk (P for interaction = 0.048) after adjusting for confounding factors, particularly among subjects with CagA (OR = 3.07, 95%CI: 1.17-10.79). We did not observe effect modification of pork consumption by H. pylori CagA status, or between H. pylori CagA status and IL-1B-31 genotypes after adjustment for pork consumption and other factors. CONCLUSION: These interaction relationships among CagA, IL-1B-31 and pork consumption may have implications for development of the preventive strategies for the early detection of non-cardiac GC.

Interactions between CagA and smoking in gastric cancer.

AIM: To examine the interactions between cytotoxin-associated gene (CagA) positive Helicobacter pylori infection and smoking in non-cardiac gastric cancer. METHODS: A case-control study (257 cases and 514 frequency-matched controls) was conducted from September 2008 to July 2010 in Xi'an, China. Cases were newly diagnosed, histologically confirmed non-cardiac cancer. Controls were randomly selected from similar communities to the cases and were further matched by sex and age (± 5 years). A face-to-face interview was performed by the investigators for each participant. Data were obtained using a standardized questionnaire that included questions regarding known or suspected lifestyle and environmental risk factors of gastric cancer. A 5 mL sample of fasting venous blood was taken. CagA infection was serologically detected by enzyme-linked immunosorbent assays. RESULTS: Smoking and CagA infection were statistically significant risk factors of non-cardiac cancer. CagA was categorized in tertiles, and the odds ratio (OR) was 12.4 (95% CI: 6.1-20.3, P = 0.003) for CagA after being adjusted for confounding factors when the high-exposure category was compared with the low-exposure category. Smokers had an OR of 5.4 compared with subjects who never smoked (95% CI: 2.3-9.0, P = 0.002). The OR of non-cardiac cancer was 3.5 (95% CI: 1.8-5.3) for non-smokers with CagA infection, 3.5 (95% CI: 1.9-5.1) for smokers without CagA infection, and 8.7 (95% CI: 5.1-11.9) for smokers with CagA infection compared with subjects without these risk factors. After adjusting for confounding factors, the corresponding ORs of non-cardiac cancer were 3.2 (95% CI: 1.5-6.8), 2.7 (95% CI: 1.3-4.9) and 19.5 (95% CI: 10.3-42.2), respectively. There was a multiplicative interaction between smoking and CagA, with a synergistic factor of 2.257 (Z = 2.315, P = 0.021). CONCLUSION: These findings support a meaningful interaction between CagA and smoking for the risk of gastric cancer which may have implications for its early detection.