Search

Aging‐induced cognitive impairment is associated with a loss of metabolic homeostasis and plasticity. An emerging idea is that targeting key metabolites is sufficient to impact the function of other organisms. Therefore, more metabolism‐targeted therapeutic intervention is needed to improve cognitive impairment. We first conducted untargeted metabolomic analyses and 16S rRNA to identify the aging‐associated metabolic adaption and intestinal microbiome change. Untargeted metabolomic analyses of plasma revealed L‐arginine metabolic homeostasis was altered during the aging process. Impaired L‐arginine metabolic homeostasis was associated with low abundance of intestinal Akkermansia muciniphila (AKK) colonization in mice. Long‐term supplementation of AKK outer membranes protein‐Amuc_1100, rescued the L‐arginine level and restored cognitive impairment in aging mice. Mechanically, Amuc_1100 acted directly as a source of L‐arginine and enriched the L‐arginine‐producing bacteria. In aged brain, Amuc_1100 promoted the superoxide dismutase to alleviated oxidation stress, and increased nitric oxide, derivatives of L‐arginine, to improve synaptic plasticity. Meanwhile, L‐arginine repaired lipopolysaccharide‐induced intestinal barrier damage and promoted growth of colon organoid. Our findings indicated that aging‐related cognitive impairment was closely associated with the disorders of L‐arginine metabolism. AKK‐derived Amuc_1100, as a potential postbiotic, targeting the L‐arginine metabolism, might provide a promising therapeutic strategy to maintain the intestinal homeostasis and cognitive function in aging. [ABSTRACT FROM AUTHOR]

BACKGROUND: Several diseases and insects may cause damage to the normal growth of cucumber. Azoxystrobin and meptyldinocap, because of their novel mode of action, are effective against pathogens that have developed reduced sensitivity to other fungicides. Azoxystrobin is persistent in various crops and environments. However, there is a lack of research on the dissipation of these two pesticides, especially meptyldinocap. RESULTS: Analytes could be quantified with decent recoveries of 90–101%, with relative standard deviations (RSDs) of 3.0–10.1%. The terminal residues of meptyldinocap and azoxystrobin in cucumber were all < limit of quantification (LOQ) (0.02 and 0.05 mg kg−1). The half‐lives of meptyldinocap and azoxystrobin were 0.8–1.1 and 1.2–2.8 days, respectively. The processing factors (PFs) for washing were all < 1, but the removal rate for washing was < 29.0%. Peeling had a significant effect on the removal of pesticide. The largest residue reductions were noticed through the pickling process, but special care should be taken regarding residues in the pickling solution as pesticides could transfer to them from cucumber. A more interesting finding was that the degradation of two pesticides was accelerated by the addition of calcium oxide. CONCLUSION: Pesticide residues on cucumber decreased after these processes. These results enable the health‐risks from dietary exposures to pesticide residues to be characterized. They enable maximum residue limits (MRLs) to be established for pesticide residues in food products. They also assist the optimization of food processing with regard to pesticide residue dissipation. © 2019 Society of Chemical Industry [ABSTRACT FROM AUTHOR]