Foods are good sources of vitamins, minerals and dietary fibers as well as phytochemicals, which are beneficial for the human body as nutritional supplements. The nutritional value (crude fibers, crude proteins, crude fats, flavonols, carotenoids, polyphenols, glucosinolate, chlorophyll, and ascorbic acid) and nutritional properties (antioxidant activity, anticancer activity, or antimutagenic activity) of foods can be well retained and protected with the appropriate cooking methods. The chemical, physical and enzyme modifications that occur during cooking will alter the dietary phytochemical antioxidant capacity and digestibility. This paper reviewed the recent advances on the effects of domestic cooking process on the chemical and biological properties of dietary phytochemicals. Furthermore, the possible mechanisms underlying these changes were discussed, and additional implications and future research goals were suggested. The domestic cooking process for improving the palatability of foods and increasing the bioavailability of nutrients and bioactive phytochemicals has been well supported.
Loss of GGPPS from childhood mumps infection or deletion in mice results in constitutively activated MAPK and NF-kB signaling that induces spermatogonium apoptosis, macrophage invasion into seminiferous tubules, and sterility.
Preeclampsia (PE) is a major cause of maternal mortality and morbidity worldwide. Although there has been great progress in the understanding of PE, the exact cause for the disease development is still unclear. Recently, studies showed that genetic deletion of ELABELA (ELA, also known as APELA) could induce PE-like symptoms in mice. However, the role of ELA in the disease development of PE remains elusive. Our objective was to measure the changes of ELA levels in maternal serum, urine, and placenta from preeclamptic pregnant women and healthy pregnant women and evaluate the correlation between ELA levels and the occurrence of PE. Additionally, we investigated the effect of ELA on the migration and proliferation of human trophoblast cells. ELA levels are significantly decreased in late-onset PE pregnancies compared with normal pregnancies. The mRNA and protein expressions of ELA and the apelin receptor (APLNR or APJ) in late-onset PE placental tissues are also decreased. Furthermore, our in vitro study showed that the addition of ELA significantly increased the invasion ability and proliferation of trophoblast cells, which were inhibited by the APJ-specific antagonist ML221. Our study identified ELA as significantly decreased in late-onset PE; therefore, it might play an important role in the pathogenesis of late-onset PE.
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