Although common beans (Phaseolus vulgaris L.) are consumed worldwide, studies on the metabolic fate of phenolic compounds from common beans are still very scarce. The present work aimed to study the bioavailability of phenolic compounds in human plasma and urine, after acute consumption of a single meal of cooked common beans. Blood and urine of seven volunteers were collected before (0 h) and at different time points (1, 2, 4, 6 and 8 h for plasma and 0–2, 2–4, 4–6, 6–8 and 8–24 h for urine) after beans’ intake. Ultra-high performance liquid chromatography-quadrupole-time of flight-MS (UPLC-Q-TOF-MS) was used for quantification. After beans’ intake, 405 (sd 3) g, containing 188 mg of phenolic compounds (expressed as gallic acid equivalents), there was a significant increase (P < 0·05) in the plasma concentration of six metabolites and in the urinary excretion of eleven metabolites. After 1 h post-consumption, metabolites, such as kaempferol-3-O-glucuronide, showed a significant increase in plasma concentration, suggesting kaempferol’s glucuronidation in the upper gastrointestinal tract. More than 50 % of the total amount of metabolites, such as 4-methylcatechol-O-sulphate and dihydrocaffeic acid-3-O-sulphate, were excreted after 8 h post-consumption, indicating colonic bacterial metabolism of the phenolic compounds. Partial least square-discriminant analysis models clearly showed clusters of metabolites, which contributed to extend the list of compounds related to cooked common beans’ human intake at different time points and showed the human inter-individual variability in plasma concentration as well as in urinary excreted metabolites, after cooked common beans’ intake.

The effect of duration of wild oat competition on spring wheat yield and growth was determined in time-of-removal experiments conducted over a three year study period in Saskatchewan, Canada. Failure to remove wild oat reduced wheat yield 28 and 39% at wild oat populations of 64 and 188 plants per m2, respectively. Wheat yield was not reduced by wild oat densities of 64 or 118 plants per m2 until the six- and seven-leaf stage of wild oat, respectively. Removing wild oat at 64 plants per m2 before the seven-leaf stage and 118 plants per m2 before the five-leaf stage did not increase wheat culm or fresh weight production.

Greenhouse and field experiments were conducted to evaluate the efficacy of nicosulfuron, primisulfuron, glyphosate, glufosinate, imazethapyr plus imazapyr, and quizalofop on johnsongrass biomass reduction, rhizome total nonstructural carbohydrate (TNC) content, and subsequent regrowth from rhizomes. In the greenhouse, johnsongrass plants originating from rhizome segments were controlled 88 to 97% with quizalofop, glyphosate, imazethapyr plus imazapyr, nicosulfuron, and primisulfuron and 56% with glufosinate 3 wk after treatment (WAT). Johnsongrass treated with quizalofop, glyphosate, and nicosulfuron did not regrow 6 WAT, whereas plants treated with primisulfuron, imazethapyr plus imazapyr, and glufosinate regrew from the rhizome of the treated plant. Rhizome TNC levels 3 WAT were not reduced by glufosinate or nicosulfuron, but they were reduced 64% by quizalofop, 32% by primisulfuron, 61% by glyphosate, and 29% by imazethapyr plus imazapyr. When rhizome TNC was reduced by 60% or more compared with nontreated plants, johnsongrass did not regrow from the treated rhizomes. In field experiments, nicosulfuron and glyphosate controlled johnsongrass 94 and 99%, respectively, whereas imazethapyr plus imazapyr (79%) and glufosinate (85%) provided less control 6 WAT.