Mutations in Helicobacter pylori infected patients with chronic gastritis, intestinal type of gastric cancer and familial gastric cancer.

BACKGROUND: Development of sequential changes of mucous leading to gastric cancer and familial cases of gastric cancer of intestinal type is widely connected with Helicobacter pylori infections. In this study we analysed variants of genes involved in cancerogenesis and inflammatory processes of intestines in patients infected with H.pylori. Our goal was to test whether mutations in these genes predestinate to development of gastric cancer, and whether there is a genetic factor that makes it more likely for infections with H.pylori to cause gastric cancer. As infections with H. pylori are relatively common, discovering such genetic predispositions could be used for establishing risk-groups and for planning treatments. METHODS: Our studies cover analysis of variants in genes involved in cancerogenesis: TP53 (rs11540652, rs587782329, COSM10771), MSH2 (rs193922376), MLH1 (rs63750217), and inflammatory processes of intestine: NOD2 (rs2066847, rs2066842), IL1A (rs1800587) and IL1B (rs1143634) from H.pylori-infected patients. RESULTS: Mutations were more common in the group of patients with gastric cancer of intestinal type and familial cases of gastric cancer in comparison with patients with chronic gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia or gastric cancer (p-value = 0.00824), with the prevalence of p53 mutations in patients with familial gastric cancer vs. patients with other changes of mucosa (p-value = 0.000049). Additionally, gastric cancer patients have mainly genotype TT or CT of the rs2066842 variant of the NOD2 gene. CONCLUSIONS: The lack of statistically significant changes of other interleukin genes involved in inflammatory processes may suggest the presence of H.pylori infection as a potential trigger for the development of the inflammatory process of the mucosa, leading through microbiota dysbiosis to the development of enteric gastric cancer. Mutations in analysed genes correlated with more severe mucosal changes, with a much more frequent presence of TP53 gene mutations, with a limited presence of other mutations in the familial history of gastric cancer.

Be curious: Strategic curiosity drives creativity.

Ivancovsky et al. provide a compelling argument for the role of curiosity in creative thinking. We argue that (a) trait-like curiosity is necessary to engage in creative actions and (b) state-like curiosity might be effectively and strategically induced during interventions. Thus, we posit that curiosity works in an agentic and strategic way in strengthening creativity.

Are cooks more disgust sensitive? Preliminary examination of the food preparation hypothesis.

According to the food preparation hypothesis, sex differences in disgust sensitivity may stem from different sex roles that males and females played in our ancestral times. In current times, these differences may be reflected in varying levels of disgust sensitivity between people who frequently versus rarely engage in meal preparation, or who are versus are not professionally responsible for providing meals for others. To test this reasoning, we conducted a preregistered study with 493 individuals (55% female), with 280 of them working in the restaurant industry. Participants reported their weekly time spent on cooking-related activities and completed the Food Disgust Scale and pathogen subscale of Three Domain Disgust Scale. These measures capture specific, food-related disgust sensitivity, and generalised pathogen disgust sensitivity, respectively. We found that while time spent on cooking was not associated with disgust sensitivity, people professionally engaged in food preparation displayed higher levels of food-related disgust sensitivity. There was no effect of cooking on the generalised pathogen disgust sensitivity. Additionally, we observed sex differences in both types of disgust sensitivity and found that vegetarians exhibited lower disgust sensitivity than meat-eaters. Overall, our findings offer preliminary support for the food preparation hypothesis, and point out that the mechanisms adjusting our disgust sensitivity levels are category-specific, even within the broader pathogen disgust domain.