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Sweet potatoes are extremely vulnerable to mechanical wounds during harvesting and postharvest handling. It is highly necessary to take measures to accelerate wound healing. The effect of 20 g L-1 of ascorbic acid (AA) treatment on the wound healing of sweet potatoes and its mechanisms were studied. The results validated that AA treatment significantly reduced the weight loss rate and disease index. AA treatment effectively enhanced the formation speed of lignin and SPP at the wound sites, decreased the MDA content, and maintained the cell membrane integrity. AA enhanced the activities of PAL, C4H, 4CL, CAD, and POD and increased the contents of chlorogenic acid, caffeic acid, sinapic acid, ferulic acid, cinnamic acid, p-coumaryl alcohol, sinapyl alcohol, coniferyl alcohol, and lignin. Based on a transcriptomic analysis, a total of 1200 genes were differentially expressed at the sweet potato wound sites by the AA treatment, among which 700 genes were upregulated and 500 genes were downregulated. The KEGG pathway analysis showed that the differentially expressed genes were mainly involved in phenylalanine, tyrosine, and tryptophan biosynthesis; phenylpropanoid biosynthesis; and other wound healing-related pathways. As verified by a qRT-PCR, the AA treatment significantly upregulated the gene expression levels of IbSKDH, IbADT/PDT, IbPAL, and Ib4CL at the wound sties.
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Background: The aim of this study was to explore the clinical relevance of linear measures of Wilson's disease (WD). Methods: Relative values of brain atrophy in 30 patients with WD and 30 healthy volunteers were measured and compared using a manual measurement method. Linear measurement indicators of brain atrophy in patients with and without mental disorders were also compared. In addition, correlations of patients' age, disease duration, and Unified Wilson's Disease Rating Scale (UWDRS) scores with brain atrophy indicators were determined. Results: The results showed that the e-value, Huckman number, Evans index, and lateral ventricular body index were higher in the WD group compared with the control group. The age of patients with WD was negatively correlated with the k-value and significantly positively correlated with the brainstem index. WD duration was prominently positively correlated with the d-value and negatively correlated with the j-value. In addition, neurological function scores were significantly positively correlated with the c-value, e-value, caudate nucleus index, Huckman number, Evans index, and lateral ventricular body index. By contrast, patients with psychiatric symptoms had a higher a-value and fourth ventricular index than those without psychiatric symptoms. Conclusion: Therefore, it can be concluded that patients with WD and those with psychiatric symptoms have more severe brain atrophy compared to normal subjects. The patient's age, disease duration, and neurological function scores were positively correlated with the severity of brain atrophy.
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Polychlorinated biphenyls (PCBs) are potentially hazardous to the environment because of their chemical stability and biological toxicity. In this study, we identified the binding mode of a representative PCB180 to human serum albumin (HSA) using fluorescence and molecular dynamics (MD) simulation methods. PCB180 bound exactly at subdomain IIIA of HSA based on the fluorescence study along with site marker displacement experiments. PCB180 also induced conformational changes that were governed mainly by hydrophobic forces. MD studies and free energy calculations also made important contributions to the understanding of the effects of an HSA-PCB180 system on conformational changes. The simulations on binding behavior proved that PCB180 was located only in subdomain IIIA. Hydrophobic interactions dominated the mode of binding behavior. The results obtained using the two methods correlated well with each other. Our findings provide a framework for elucidating the mechanisms of PCB180-HSA binding, and may also help in further research on the transportation, distribution, and toxicity effects of PCBs when introduced into human blood serum.