Helicobacter pylori is a spiral-shaped Gram-negative bacterium. It colonizes the gastric mucosa of humans and persists for decades if not treated. Helicobacter pylori infection affects more than half of the world's population and invariably results in chronic gastritis. The cagA gene is present in about 60 to 70% of H. pylori strains; it encodes a high-molecular-weight protein (120 to 140 kDa) and several investigators have noted a correlation between strains that possess cagA and the severity of gastric mucosal inflammation. We examined the relation between cagA status in H. pylori strains and chronic gastritis with inflammatory processes in children from Marília, São Paulo, Brazil. Onehundred-twenty-one children were analyzed histopathologically and by polymerase chain reaction (PCR) to detect H. pylori and cagA. We then looked for an association between cagA presence and inflammatory infiltration. Using histology and PCR, we found 47% H. pylori positive infection; 29 children were diagnosed with chronic gastritis, while 28 showed normal mucosa by histopathological analysis. CagA presence was genotyped in both groups, and an inflammatory infiltrate was studied in all infected children with chronic gastritis. We found cagA strains in 20 of 29 (69%) children with chronic gastritis and 18 of 28 (64%) with normal mucosa, demonstrating a strong relationship between the strains and the inflammatory process. We found a positive association between an inflammatory process associated with H. pylori of cagA+ strains and chronic gastritis development.

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lorazepam administration, we restricted our attention to the time of peak plasma drug level (2.5 hours). The study design had two independent variables: TOMM40 gene (short vs long; between-subjects) and drug administration (placebo vs 0.5 mg vs 1 mg; within-subjects). We measured the difference from baseline in total recall. Results: We conducted a 2 X 3 repeated-measures ANOVA and observed an interaction between drug administration and TOMM40 (p ¼ .022). Pairwise comparisons indicated that poly-T length did not influence memory performance when placebo was administered, but was associated with worse recall when lorazepam was administered, both for 0.5 mg (p ¼ .004) and 1.0 mg (p ¼ .001) doses. Conclusions: Our pilot data suggest that variants of TOMM40 may serve as pharmacodynamic predictors of drug-induced memory dysfunction in e4 negative individuals, most of whom had the e3/e3 genotype. Given that the frequency of e3/e3 in the general population is over 55%, this biomarker could have important clinical implications.

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