Recursiveness, Switching, and Fluctuations in a Replicating Catalytic Network

A protocell model consisting of mutually catalyzing molecules is studied in order to investigate how chemical compositions are transferred recursively through cell divisions under replication errors. Depending on the path rate, the numbers of molecules and species, three phases are found: fast switching state without recursive production, recursive production, and itinerancy between the above two states. The number distributions of the molecules in the recursive states are shown to be log-normal except for those species that form a core hypercycle, and are explained with the help of a heuristic argument.Comment: 4 pages (with 7 figures (6 color)), submitted to PR

Fast and low cost analysis of dioxin and dioxin-like compounds in marine matrices: final report

0info:eu-repo/semantics/publishe

Interleukin-1 polymorphisms associated with increased risk of gastric cancer

Helicobacter pylori infection is associated with a variety of clinical outcomes including gastric cancer and duodenal ulcer disease. The reasons for this variation are not clear, but the gastric physiological response is influenced by the severity and anatomical distribution of gastritis induced by H. pylori. Thus, individuals with gastritis predominantly localized to the antrum retain normal (or even high) acid secretion, whereas individuals with extensive corpus gastritis develop hypochlorhydria and gastric atrophy, which are presumptive precursors of gastric cancer. Here we report that interleukin-1 gene cluster polymorphisms suspected of enhancing production of interleukin-1-beta are associated with an increased risk of both hypochlorhydria induced by H. pylori and gastric cancer. Two of these polymorphism are in near-complete linkage disequilibrium and one is a TATA-box polymorphism that markedly affects DNA-protein interactions in vitro. The association with disease may be explained by the biological properties of interleukin-1-beta, which is an important pro-inflammatory cytokine and a powerful inhibitor of gastric acid secretion. Host genetic factors that affect interleukin-1-beta may determine why some individuals infected with H. pylori develop gastric cancer while others do no