Certain dietary patterns may be related to the risk of CVD. We hypothesised that a plant-centred dietary pattern would be associated with a reduced risk of first myocardial infarction (MI). A case -control study of Norwegian men and postmenopausal women (age 45-75 years) was performed. A FFQ was administered, generally within 3 d after incident MI (n 106 cases). Controls (n 105) were frequency matched on sex, age and geographic location. On the FFQ, 190 items were categorised into thirty-five food groups and an a priori healthy diet pattern score was created. We estimated OR using logistic regression with adjustment for energy intake, family history of heart disease, marital status, current smoking, education and age. Among food groups, the risk of MI was significantly higher per SD of butter and margarine (OR 1·66 (95 % CI 1·12, 2·46)), and lower per SD of tomatoes (OR 0·53 (95 % CI 0·35, 0·79)), high-fat fish (OR 0·57 (95 % CI 0·38, 0·86)), wine (OR 0·58 (95 % CI 0·41, 0·83)), salad (OR 0·59 (95 % CI 0·40, 0·87)), wholegrain breakfast cereals (OR 0·64 (95 % CI 0·45, 0·90)), cruciferous vegetables (OR 0·66 (95 % CI 0·47, 0·93)) and non-hydrogenated vegetable oil (OR 0·68 (95 % CI 0·49, 0·95)). An abundance of cases were found to have a low a priori healthy diet pattern score. A dietary pattern emphasising nutrient-rich plant foods and high-fat fish and low in trans fatty acids was associated with decreased risk of MI among Norwegians.

In a previous study, we characterized a lactose permease mutant (K319N/E325Q) that can transport H+ ions with sugar. This result was surprising because other studies had suggested that Glu-325 plays an essential role in H+ binding. To determine if the lactose permease contains one or more auxiliary H+ binding sites, we began with the K319N/E325Q strain, which catalyzes a sugar-dependent H+ leak, and isolated third site suppressor mutations that blocked the H+ leak. Three types of suppressors were obtained: H322Y, H322R, and M299I. These mutations blocked the H+ leak and elevated the apparent Km value for lactose. The M299I and H322Y suppressors could still transport H+ with beta-d-thiodigalactoside (TDG), but the H322R strain appeared uncoupled for H+/sugar cotransport. Four mutant strains containing a nonionizable substitution at codon 322 (H322Q) were analyzed. None of these were able to catalyze uphill accumulation of lactose, however, all showed some level of substrate-induced proton accumulation. The level seemed to vary based on the substrate being analyzed (lactose or TDG). Most interestingly, a triple mutant, K319N/H322Q/E325Q, catalyzed robust H+ transport with TDG. These novel results suggest an alternative mechanism of lactose permease cation binding and transport, possibly involving hydronium ion (H3O+).

Several factors appear to increase the risk of enzyme elevation events in patients treated with troglitazone.