E, 1996, Effects of nitrogen deficiency on accumulation of fructan and fructan metabolizing enzj-me activities in sink and source leaves of barley (Hordeum vatgare).-PhysM. Piant, 97: 339-345.Seedlings of barley (Hordeum vulgare L. cv, Agneta) were grown hydroponicaliy under continuous light, constant temperatare and relative humidity. During the first two weeks, the relative growth rate (RGR) was kept at 25% by limiting only the supply of nitrogen. The cultures were then transferred to nitrogen-free media and the amounts of fructan, starch, sucrose, glucose and fructose in sink and source leaves were measured at 0, 12, 24, 48, 72, 120 and 156 h. The activities of two key enzjmes in fructan metabolism, sucrose:sucrose fructosyltransferase (SST), fructan exohydrolase (FEH), as well as acid invertase were aiso measured in the two types of leaves. The fructan and starch levels in both sink and source leaves increased during nitrogen deficiency. The highest increase in starch was 200% of the control, while for fructans a 700% increase was recorded. The activity of SST increased parallel to fructan accumulation in sink leaves. However, the FEH activitj' was constant and not affected by nitrogen deficiency. The invertase activity both in sink and source leaves was reduced by nitrogen deficiency More fructans, as well as sucrose and fructose, accumulated in source leaves compared to sink leaves both before and after nitrogen starvation. The results show that fructan is the major carbohydrate reserve accumulating under nitrogen deficiency both in sink and source leaves in barley plants. The induction of fructan accumulation in sink leaves caused by nitrogen deficiency is intimately connected with the regulation of SST,

Hydroponically cultivated barley plants were exposed to nitrogen (N)-deficiency followed by N-resupply. Metabolic and genetic regulation of fructan accumulation in the leaves were investigated. Fructan accumulated in barley leaves under N-deficiency was mobilized during N-resupply. The enhanced total activity of fructan-synthesizing enzymes, sucrose:sucrose 1-fructosyltransferase (EC 2.4.1.99) and sucrose:fructan 6-fructosyltransferase (6-SFT; EC 2.4. 1.10) caused by N-deficiency decreased with the mobilization of fructan during N-resupply. The activity of the barley fructan-degrading enzyme, fructan exohydrolyase (EC 3.2.1.80) was less affected by the N status. The low level of foliar soluble acid invertase activity under N-deficiency conditions was maintained during the commencement of N-resupply but increased subsequently. Further analyses by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, western blot and northern blot demonstrated that the fructan accumulation and the total activity of fructan-synthesizing enzymes correlated with the 6-SFT mRNA level. We suggest that the changes in fructan levels under N stress are intimately connected with the regulation of fructan synthetic rate which is mostly controlled by 6-SFT.

Although many studies have discussed the association of abnormally expressed silent information regulator 1 (Sirt1) with the prognosis of patients with a variety of solid carcinomas, they failed to agree on whether excessive Sirt1 indicates a good or poor overall survival for the patients. We conducted the current meta-analysis to illustrate the prognostic value of Sirt1 in solid malignancies. Articles published before December 2016 were searched using Pubmed and Web of Science. The studies were selected for the meta-analysis based on certain criteria. A total of 7,369 cases from 37 studies were included, in which 48.6% of the patients overexpressed Sirt1. The overall survival (OS) and clinical features, such as age and TNM stage, were analyzed using RevMan 5.3 software. Sirt1 overexpression was significantly correlated with the OS (HR: 1.52, 95% CI: [1.23, 1.88], P = 0.0001), especially in liver cancer (HR: 1.78, 95% CI: [1.46, 2.18], P < 0.00001) and lung cancer (HR: 1.80, 95% CI: [1.06, 3.05], P = 0.03), which suggested that the overexpression of Sirt1 indicates poor prognosis of patients with solid cancers.

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Fibroblast growth factor 21 (FGF-21), which is a modulator of glucose and lipid homeostasis, acts as a novel therapeutic reagent for many metabolic perturbations. However, its potential as a treatment for cardiovascular disease, especially atherosclerosis (AS) has not been fully explored. Here, we report that recombinant FGF-21 improves resistance to cell damage from oxidative stress in vitro, and from atherosclerosis in vivo. Human umbilical vein endothelial cells (HUVECs) were induced with H2O2, followed by treatment with high purity recombinant FGF-21. The results indicated that FGF-21 significantly enhanced cell viability and decreased the degree of DNA fragmentation in HUVECs, as caused by H2O2 stress induction. Further studies revealed that FGF-21 inhibited H2O2-induced cell apoptosis by preventing the activation of mitogen-activated protein kinase (MAPK) signaling pathways. In an established rat model, FGF-21 dramatically improved the condition of atherosclerotic rats by decreasing serum levels of total triglyceride (TG), low density lipoprotein cholesterol (LDL-C), and total cholesterol (TC), and by increasing the serum levels of high density lipoprotein cholesterol (HDL-C). FGF-21 also has antioxidant effects in the atherosclerotic rat, such that increased levels of superoxide dismutase, reduced glutathione, and reduced malondialdehyde were observed. These data provide novel insight into the potential use of FGF-21 in the prevention and treatment of human cardiovascular diseases.

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This paper presents a fringe capacitance formula of microstructures. The formula is derived by curve fitting on ANSYS simulation results. Compared with the ANSYS and experimental results, the deviation is within ± 2%. The application to determine the pull-in voltage of an electrostatic micro-beam is demonstrated, which agrees very well with the experimental data. The formula presented is very accurate, yields explicit physical meanings and is applicable to common dimension ranges for MEMS devices.