0 µg·mL-1, 24.4 µg·mL-1, and 15573.0 µg·mL-1, respectively, corresponding to 63.3% decrease, 92.5% decrease, and 47.7-fold increase relative to the EC50 value in SD1-9. Compared with SD1-9, the mycelia of transformants SD1-9C-3, SD1-9C-4, and OESD1-9-1 showed more branches and shorter branches; and the transformants had different pathogenicity to different hosts plants. The expression of the candidate gene RPA190-pc during 10 life-history stages was further studied, the results showed that expression level reached a maximum at the zoospores stage, and it gradually increased with the increase of SD1 and SD1-9 infection time of pepper leaves, indicated that RPA190-pc may be related to the growth and pathogenicity of P. capsici. These results indicate that the expression of RPA190-pc is involved in the regulation of P. capsici resistance to metalaxyl.DapE is an enzyme that belongs to the meso-diaminopimelate/Lysine pathway. It is recognized as an antimicrobial target, hence compounds that inhibit its catalytic activity are required. The principal features considered in the selection of potential inhibitors for this enzyme are compounds containing metal binding groups that could block access of the substrate to the Zinc metal centers and/or block the assembly of the oxyanion hole. We show the interaction of DapE from Enterococcus faecium, Staphylococcus aureus, Klebsiella aerogenes, Pseudomonas aeruginosa and Escherichia coli with flavonoids quercetin, catechin, luteolin, rutin and hesperidin. Flavonoids contain several oxygen atoms distributed along their structure in a pattern that may be considered for the development of new antibiotics. Docking experiments suggest that these compounds containing metal binding groups that interact with metal centers of DapE and binding experiments indicate that glycoside flavonoids are preferred by DapE.The aggregation of islet amyloid polypeptide (IAPP) is implicated in the pathogenesis of type 2 diabetes (T2D). In T2D, this peptide aggregates to form amyloid fibrils; the mechanism responsible for islet amyloid formation is unclear. However, it is known that the aggregation propensity of IAPP is highly related to its primary sequence. Several residues have been suggested to be critical in modulating IAPP amyloid formation, but role of the sole lysine residue at position 1 (Lys-1) in IAPP has not been discussed. In our previous study, we found that glycated IAPP can form amyloid faster than normal IAPP and induce normal IAPP to expedite the aggregation process. To gain more insight into the contribution of Lys-1 in the kinetics of fibril formation, we synthesized another two IAPP variants, K1E-IAPP and K1Nle-IAPP, in which the Lys residue was mutated to glutamate and norleucine, respectively. Interestingly, we observed that the negative or neutral charged side chain at this position was preferred for amyloid formation. The findings suggested this residue may take part in the inter- or intra-molecular interaction during IAPP aggregation, even though it was proposed not to be in part of fibril core structure. Our data also revealed that the inhibitory mechanism of some inhibitors for IAPP aggregation require reaction with Lys-1. Modifications of Lys-1, such as protein glycation, may affect the effectiveness of the inhibitory action of some potential drugs in the treatment of amyloidosis.Although inflammation has a physiological role, unrestrained inflammation can be detrimental, causing tissue damage and disease. Under normal circumstances inflammation is self-limiting with induction of active resolution processes. Central to these is the generation of specialised pro-resolving lipid mediators (SPMs) from eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). see more These include resolvins, protectins and maresins whose activities have been well described in cell and animal models. A number of SPMs have been reported in plasma or serum in infants, children, healthy adults and individuals with various diseases, as well as in human sputum, saliva, tears, breast milk, urine, synovial fluid and cerebrospinal fluid and in human adipose tissue, skeletal muscle, hippocampus, skin, placenta, lymphoid tissues and atherosclerotic plaques. Differences in SPM concentrations have been reported between health and disease, as would be expected. However, sometimes SPM concentrations are lower in disease and sometimes they are higher. Human studies report that plasma or serum concentrations of some SPMs can be increased by increasing intake of EPA and DHA. However, the relationship of specific intakes of EPA and DHA to enhancement in the appearance of specific SPMs is not clear and needs a more thorough investigation. This is important because of the potential for EPA and DHA to be used more effectively in prevention and treatment of inflammatory conditions. If generation of SPMs represents an important mechanism of action of EPA and DHA, then more needs to be known about the most effective strategies by which EPA and DHA can increase SPM concentrations.
Laminaria japonica, a brown seaweed, has been used in Traditional Chinese Medicine (TCM) to treat a variety of diseases including lung cancer.

To demonstrate the effects of Fucoxanthin (FX), a major active component extracted from Laminaria japonica on metastasis and Gefitinib (Gef) sensitivity in human lung cancer cells both in vitro and in vivo.

Invasion and migration of lung cancer cells were detected using the wound healing assay and transwell assay. Epithelial-to-mesenchymal transition (EMT) factors and PI3K/AKT/NF-κB pathways were analyzed by western blotting. RNA interference (RNAi) technology was used to silence TIMP-2 gene expression in A549cells. The anti-metastatic effect of FX was evaluated in vivo in an experimental lung metastatic tumor model. On the other hand, cell counting kit-8 assay was used to study the cell viability of human lung cancer PC9 cells and Gef resistant PC9 cells (PC9/G) after Gef, FX or FX combined with Gef treatment. PC9 xenograft model was established to explore the acancer cells to Gef and this effect may be due to inhibition of tumor cell proliferation and activation of apoptosis.

Collectively, our findings suggested that FX suppresses metastasis of lung cancer cells and overcomes EGFR TKIs resistance. Thus, FX is worthy of further investigation as a drug candidate for the treatment of lung cancer.
Collectively, our findings suggested that FX suppresses metastasis of lung cancer cells and overcomes EGFR TKIs resistance. Thus, FX is worthy of further investigation as a drug candidate for the treatment of lung cancer.see more